Autoimmune Disease

1/25/22, 9:07 AM Autoimmune disease - Wikipedia
Autoimmune disease
An autoimmune disease is a condition arising from
Autoimmune diseases
an abnormal immune response to a functioning body
part.[1] There are at least 80 types of autoimmune
diseases.[1] Nearly any body part can be involved.[3]
Common symptoms include low grade fever and feeling
tired.[1] Often symptoms come and go.[1]
The cause is unknown.[3] Some autoimmune diseases

such as lupus run in families, and certain cases may be
triggered by infections or other environmental
factors.[1] Some common diseases that are generally
considered autoimmune include celiac disease, diabetes
mellitus type 1, Graves' disease, inflammatory bowel
disease, multiple sclerosis, psoriasis, rheumatoid
arthritis, and systemic lupus erythematosus.[1][4] The
diagnosis can be difficult to determine.[1]
Treatment depends on the type and severity of the

condition.[1] Nonsteroidal anti-inflammatory drugs Young woman with malar rash, typically found in
(NSAIDs) and immunosuppressants are often used.[1] systemic lupus erythematosus (SLE)
Intravenous immunoglobulin may also occasionally be Specialty Rheumatology, immunology,
used.[2] While treatment usually improves symptoms, gastroenterology, neurology,
they do not typically cure the disease.[1] dermatology
About 24 million (~7.5%) people in the United States Symptoms Depends on the condition.
are affected by an autoimmune disease.[1][3] Women Commonly low grade fever,
are more commonly affected than men.[1] Often they feeling tired[1]
start during adulthood.[1] The first autoimmune Usual Adulthood[1]
diseases were described in the early 1900s.[5] onset
Types List of autoimmune diseases
(alopecia areata, celiac disease,
Contents diabetes mellitus type 1, Graves'
disease, inflammatory bowel
Signs and symptoms
disease, multiple sclerosis,
Cancer
psoriasis, rheumatoid arthritis,
Examples systemic lupus erythematosus,
Coeliac disease others)[1]
Inflammatory bowel disease
Medication Nonsteroidal anti-inflammatory
Multiple sclerosis
drugs, immunosuppressants,
Rheumatoid arthritis
intravenous immunoglobulin[1][2]
Systemic lupus erythematosus
Frequency 24 million / 7% (USA)[1][3]
Aplastic anemia
Causes
https://en.wikipedia.org/wiki/Autoimmune_disease 1/15
Genetics
Environmental factors
Pathophysiology
Diagnosis
Antinuclear antibody
Complete blood count
Complement
C reactive protein
Erythrocyte sedimentation rate
Treatment
Epidemiology
Research
Stem-cell therapy
Altered glycan theory
Hygiene hypothesis
Vitamin D Influence on Immune Response
See also
References
Further reading
External links
Signs and symptoms

Autoimmune diseases present similar symptoms across the more
than eighty different types.[6] The appearance and severity of
these signs and symptoms depends on the location and type of
autoimmune response that occurs. An individual may also have
more than one autoimmune disease simultaneously, and display
symptoms of multiple diseases. Signs and symptoms presented,
and the disease itself, can be influenced by various other factors
such as age, hormones, and environmental factors.[7] In general,
the common symptoms are:[8]
Fatigue
Low grade fever
General feeling of unwell (malaise)
Muscle aches and joint pain
Rash on different areas of the skin
The appearance of these signs and symptoms can fluctuate, and when they reappear, it is known as a
flare-up.[8] Such signs and symptoms may aid in diagnosis by supporting the results from biologic
markers of autoimmune diseases.[9]
There are several areas that are commonly impacted by autoimmune diseases. These areas include:
blood vessels, underlying connective tissues, joints and muscles, red blood cells, skin, and endocrine
glands (such as thyroid or pancreas glands).[8]
These diseases tend to have characteristic pathological effects that characterize them as an
autoimmune disease. Such features include damage to or destruction of tissues where there is an
abnormal immune response, altered organ growth, and altered organ function depending on the
location of the disease.[8] Some diseases are organ specific and are restricted to affecting certain
tissues, while others are systemic diseases that impact many tissues throughout the body. Signs and
symptoms may vary depending on which of these categories an individual's disease falls under.[10]
Cancer
Research suggests an overall correlation between autoimmune diseases and cancer, in that having an
autoimmune disease increases the risk or likelihood of developing certain cancers.[11] Autoimmune
diseases cause inflammation through a variety of mechanisms, however, the way in which
inflammation is created does not greatly influence cancer risk.[11] Rather, the cancer risk is largely
dependent on the fact that all autoimmune diseases increase chronic inflammation which has been
linked to cancer.[11] Below are some autoimmune diseases most commonly linked to cancer including
celiac disease, inflammatory bowel disease (Crohn's disease and ulcerative colitis), multiple sclerosis,
rheumatoid arthritis, and systemic lupus erythematosus.[11]
Examples
Following are the few examples of autoimmune diseases. See List of autoimmune diseases for a more
exhaustive list.
Coeliac disease
Coeliac disease presents the strongest associations to gastrointestinal and lymphoproliferative

cancers.[11] In coeliac disease, the autoimmune reaction is caused by the body's loss of immune
tolerance to ingested gluten, found primarily in wheat, barley, and rye.[11] This explains the increased
risk of gastrointestinal cancers, as the gastrointestinal tract includes the esophagus, stomach, small
intestine, large intestine, rectum, and anus, all areas that the ingested gluten would traverse in
digestion.[11] The incidence of gastrointestinal cancer can be partially reduced or eliminated if a
patient removes gluten from their diet.[11][12][13][14][15] Additionally, celiac disease is correlated with
lymphoproliferative cancers.[11]
Inflammatory bowel disease
Inflammatory bowel disease is associated with cancers of the gastrointestinal tract and some
lymphoproliferative cancers.[11] Inflammatory bowel disease (IBD) can be further categorized as
Crohn's disease or ulcerative colitis.[11] In both cases, individuals with IBD lose immune tolerance for
normal bacteria present in the gut microbiome.[11] In this case, the immune system attacks the
bacteria and induces chronic inflammation, which has been linked to increased cancer risk.[11]
Multiple sclerosis
Multiple sclerosis is associated with decreased risk of cancer overall but an increased risk of central
nervous system cancer, primarily in the brain.[11] Multiple sclerosis is a neurodegenerative disease in
which T-cells – a specific type of immune cells – attack the important myelin sheath in brain
neurons.[16] This reduces the nervous system function, creating inflammation and subsequent cancer
of the brain.[11]
Rheumatoid arthritis presents mild, yet significant associations with focal cancers all throughout the
body as well as lymphoproliferative cancers.[11] In rheumatoid arthritis, cells that make up the body's
joints and cartilages become invasive and induce local inflammation.[11] Additionally, the chronic
inflammation and over-activation of the immune system creates an environment that favors further
malignant transformation of other cells. This can explain the associations to cancer of the lungs and
skin as well as the increased risk of other hematologic cancers none of which are directly affected by
the inflammation of joints.[17][18]
Systemic lupus erythematosus
Systemic lupus erythematosus is associated with focal cancers throughout the body and
lymphoproliferative cancers.[11] Systemic lupus erythematosus affects multiple organ systems and is
characterized by a widespread loss of immune tolerance.[19] The chronic inflammation throughout the
entire body promotes the malignant transformation of other cells which contributes to the increased
risk of systemic and lymphoproliferative cancers.[11] Conversely, systemic lupus erythematosus is
correlated with a decrease in some cancers. This is best explained by increased immunosurveillance in
these areas, however, the mechanism for why these areas experience lower incidence is poorly
understood.[11]
Aplastic anemia
In aplastic anemia the body fails to produce blood cells in sufficient numbers. Blood cells are
produced in the bone marrow by stem cells that reside there. Aplastic anaemia causes a deficiency of
all blood cell types: red blood cells, white blood cells and platelets.
Causes
The cause is unknown.[3] Some autoimmune diseases such as lupus run in families, and certain cases
may be triggered by infections or other environmental factors.[1] There are more than 100
autoimmune diseases.[20] Some common diseases that are generally considered autoimmune include
celiac disease, diabetes mellitus type 1, Graves' disease, inflammatory bowel disease, multiple
sclerosis, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus.[1][4]
Genetics
Autoimmune diseases are conditions in which the human immune system attacks healthy human
tissues within the body. The exact genes responsible for causing each autoimmune disease have not
been found. However, several experimental methods such as the genome-wide association scans have
been used to identify certain genetic risk variants that may or may not be responsible.[21] Research
focusing on both genome scanning and family trait inheritance analysis has enabled scientists to
further understand the etiology of autoimmune diseases such as Type 1 diabetes and Rheumatoid
arthritis.[22]
Type 1 diabetes is a condition in which pancreatic β-cells are targeted and destroyed by the
immune system.[23] The condition is a result of neo-natal mutations to the insulin gene (INS)
which is responsible for mediating the production of the insulin in the pancreas.[23] The INS gene
is located on the short arm of chromosome 11p15.5 in between the genes for tyrosine hydroxylase
and insulin-like growth factor II.[24] In addition to chromosome 11, a genetic determinant of type 1
diabetes is a locus called the major histocompatibility complex (MHC) located on chromosome
6p21.[22]
Rheumatoid arthritis: Although there is no complete genetic mapping for this condition, several
genes are thought to play a role in causing RA. The genes that influence the human immune
system contain a TNF receptor associated factor 1(TRAF1). This TRAF1 is located on
chromosome 9q33-34.[25] In addition, B1 genes in the human genome contain an increased
concentration of HLA-DRB1 alleles that are most commonly seen in RA patients.[26] RA can vary
in severity as a consequence of polymorphisms within the genome.[26]
Environmental factors
A range of environmental factors have been recognized as either having a direct role in development,
or being a catalyst to many autoimmune diseases. Current studies "indicate" up to seventy percent of
autoimmune disease are perhaps due to environmental factors, including: chemicals, infection, diet,
and gut dysbiosis. A single set of steps has been identified to be the most likely theory for
autoimmune disease onset still there is of yet no definitive proof.[27]
1. Environmental triggers
2. Reduced oral tolerance
3. Gut dysbiosis
4. Enhanced gut permeability
5. Increased immune reactivity
6. Autoimmunity
Chemicals can be found within the direct environment or in the form of drugs, including: hydrazines,
hair dyes, trichloroethylene, tartrazines, hazardous wastes, and industrial emissions.[28]
UV radiation is found to be a possible cause of development of the autoimmune disease

dermatomyositis,[29] exposure to pesticides plays a role in rheumatoid arthritis development,[30] and
vitamin D has been found to be a key in preventing immune dysfunctions in older populations.[31]
Infectious agents are considered T cell activators, a step needed for activation of autoimmune
diseases. These mechanisms are relatively unknown, but are one of the current alternative theories to
explain autoimmune diseases triggered by infection such as Guillain-Barre syndrome and rheumatic
fever.[32]
Pathophysiology
The human immune system typically produces both T cells and B cells that are capable of being
reactive with self-protein, but these self-reactive cells are usually either killed prior to becoming active
within the immune system, placed into a state of anergy (silently removed from their role within the
immune system due to over-activation), or removed from their role within the immune system by
regulatory cells. When any one of these mechanisms fail, it is possible to have a reservoir of self-
reactive cells that become functional within the immune system. The mechanisms of preventing self-
reactive T cells from being created take place through negative selection process within the thymus as
the T cell is developing into a mature immune cell.
Some infections, such as Campylobacter jejuni, have antigens that are similar (but not identical) to
our own self-molecules. In this case, a normal immune response to C. jejuni can result in the
production of antibodies that also react to a lesser degree with gangliosides of myelin sheath
surrounding peripheral nerves' axons (i.e., Guillain–Barré). A major understanding of the underlying
pathophysiology of autoimmune diseases has been the application of genome-wide association scans
that have identified a degree of genetic sharing among the autoimmune diseases.[33]
Autoimmunity, on the other hand, is the presence of self-reactive immune response (e.g., auto-
antibodies, self-reactive T cells), with or without damage or pathology resulting from it.[34] For this
reason, autoantibodies are a hallmark of most autoimmune disorders.[35] This may be restricted to
certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue in different places (e.g.
Goodpasture's disease which may affect the basement membrane in both the lung and the kidney).
There are many different theories as to how an autoimmune disease state arises. Some common ones
are listed below.
Diagnosis
For a disease to be regarded as an autoimmune disease it needs to answer to Witebsky's postulates
(first formulated by Ernest Witebsky and colleagues in 1957 and modified in 1994):[36][37]
Direct evidence from transfer of disease-causing antibody or disease-causing T lymphocyte white

blood cells
Indirect evidence based on reproduction of the autoimmune disease in experimental animals
Circumstantial evidence from clinical clues
Symptoms of early autoimmune disease are often the exact same as common illnesses, including:
fatigue, fever, malaise, joint pain, and rash. Due to the fact symptoms vary for affected location,
disease causing agents, and individuals, it is difficult for proper diagnosis.[38] Typically, diagnosis
begins with looking into a patient's family's history for genetic predisposition. This is combined with
various tests, as no single test can identify an autoimmune disease.[28]
Antinuclear antibody
A test used to identify abnormal proteins, known as antinuclear antibodies, produced when the body
attacks its own tissues.[38][28] It may test positive in several disorders. This test is most useful for
diagnosing systemic lupus erythematosus, having a 95% positive test rate.[39]
Complete blood count
A test taking measurements on maturity levels, count, and size of blood cells.[28][38] Targeted cells
include: red blood cells, white blood cells, hemoglobin, hematocrit, and platelets. Based on increased
or decreased numbers in these counts, underlying medical conditions may be present; typically,
autoimmune disease is represented by low white blood cell count (Leukopenia). For proper diagnosis,
further testing is needed.[40]
Complement
A test used to measure levels of a protein group of the immune system called complement within
blood. If complement is found in low levels, this may be an indication of disease.[38][28]
C reactive protein
C reactive protein, a protein made in the liver generally increases with inflammation, and may be high
in autoimmune disease.[38][28]
Erythrocyte sedimentation rate
This test measures the rate at which a patient's blood cells descend in a test tube. More rapid descents
may indicate inflammation, a common symptom of autoimmune disease.[28][38]
If these tests are indicative antibody abnormalities and inflammation, further tests will be conducted
to identify the autoimmune disease present.[28]
Treatment
Treatment depends on the type and severity of the condition. The majority of the autoimmune
diseases are chronic and there is no definitive cure, but symptoms can be alleviated and controlled
with treatment.[8] Overall, the aim of the various treatment methods is to lessen the presented
symptoms for relief and manipulate the body's autoimmune response, while still preserving the ability
of the patient to combat diseases that they may encounter.[41] Traditional treatment options may
include immunosuppressant drugs to weaken the overall immune response, such as:[42]
Non-steroidal anti-inflammatory drugs (NSAIDs) to reduce inflammation

Glucocorticoids to reduce inflammation
Disease-modifying anti-rheumatic drugs (DMARDs) to decrease the damaging tissue and organ
effects of the inflammatory autoimmune response
Other standard treatment methods include:[8]
Vitamin or hormone supplements for what the body is lacking due to the disease (insulin, vitamin
B12, thyroid hormone, etc.)
Blood transfusions if the disease is blood related
Physical therapy if the disease impacts bones, joints, or muscles
Because these drugs aim to reduce the immune response against the body's own tissues, there are side
effects of these traditional treatment methods, such as being more vulnerable to infections that can
potentially be life-threatening. There are new advancements in medicine for the treatment of
autoimmune diseases that are currently being researched, developed, and used today, especially when
traditional treatment options fail. These methods aim to either block the activation of pathogenic cells
in the body, or alter the pathway that suppresses these cells naturally.[41][43] The goal for these
advancements is to have treatment options available that are less toxic to the patient, and have more
specific targets.[43] Such options include:
Monoclonal antibodies that can be used to block pro-inflammatory cytokines

Antigen-specific immunotherapy which allows immune cells to specifically target the abnormal
cells that cause autoimmune disease[43]
Co-stimulatory blockade that works to block the pathway that leads to the autoimmune response
Regulatory T cell therapy that utilizes this special type of T cell to suppress the autoimmune
response[41]
Epidemiology
The first estimate of US prevalence for autoimmune diseases as a group was published in 1997 by
Jacobson, et al. They reported US prevalence to be around 9 million, applying prevalence estimates
for 24 diseases to a US population of 279 million.[44] Jacobson's work was updated by Hayter & Cook
in 2012.[45] This study used Witebsky's postulates, as revised by Rose & Bona,[37] to extend the list to
81 diseases and estimated overall cumulative US prevalence for the 81 autoimmune diseases at 5.0%,
with 3.0% for males and 7.1% for females. The estimated community
prevalence, which takes into
account the observation that many people have more than one autoimmune disease, was 4.5% overall,
with 2.7% for males and 6.4% for females.[45] National Health and Nutrition Examination Surveys
conducted in the US from the 1980s to present day, have shown an increase of antinuclear antibodies,
a common biomarker for autoimmune diseases. This shows that there has been an increase in the
prevalence of autoimmune diseases in recent years pointing to a stronger influence of environment
factors as a risk factor for autoimmune diseases.[46]
Research
In both autoimmune and inflammatory diseases, the condition arises through aberrant reactions of
the human adaptive or innate immune systems. In autoimmunity, the patient's immune system is
activated against the body's own proteins. In chronic inflammatory diseases, neutrophils and other
leukocytes are constitutively recruited by cytokines and chemokines, resulting in tissue damage.
Mitigation of inflammation by activation of anti-inflammatory genes and the suppression of

inflammatory genes in immune cells is a promising therapeutic approach.[47][48][49] There is a body of
evidence that once the production of autoantibodies has been initialized, autoantibodies have the
capacity to maintain their own production.[50]
Stem-cell therapy
Stem cell transplantation is being studied and has shown promising results in certain cases.[51]
Medical trials to replace the pancreatic β cells that are destroyed in type 1 diabetes are in progress.[52]
Altered glycan theory
According to this theory, the effector function of the immune response is mediated by the glycans
(polysaccharides) displayed by the cells and humoral components of the immune system. Individuals
with autoimmunity have alterations in their glycosylation profile such that a proinflammatory
immune response is favored. It is further hypothesized that individual autoimmune diseases will have
unique glycan signatures.[53]
Hygiene hypothesis
According to the hygiene hypothesis, high levels of cleanliness expose children to fewer antigens than
in the past, causing their immune systems to become overactive and more likely to misidentify own
tissues as foreign, resulting in autoimmune or allergic conditions such as asthma.[54]
Vitamin D Influence on Immune Response
Vitamin D is known as an immune regulator that assists in the adaptive and innate immune
response.[55][56] A deficiency in Vitamin D, from hereditary or environmental influence, can lead to a
more inefficient and weaker immune response and seen as a contributing factor to the development of
autoimmune diseases.[56] With Vitamin D present, vitamin D response elements (VDRE) are encoded
and expressed via pattern recognition receptors (PRR) responses and the genes associated with those
responses.[55] The specific DNA target sequence expressed is known as 1,25-(OH)2D3.[55] The
expression of 1,25-(OH)2D3 can be induced by Macrophages, Dendritic cells, T-cells, and B-cells.[55]
In the presence of 1,25-(OH)2D3, the immune system's production of inflammatory cytokines are
suppressed and more tolerogenic regulatory T-cells are expressed.[55] This is due to Vitamin D's
influence on cell maturation, specifically T-cells, and their phenotype expression.[55] Lack of 1,25-
(OH)2D3 expression can lead to less tolerant regulatory T-cells, larger presentation of antigens to less
tolerant T-cells, and increased inflammatory response.[55]
See also
List of autoimmune diseases
References
1. "Autoimmune diseases fact sheet" (https://www.womenshealth.gov/publications/our-publications/f
act-sheet/autoimmune-diseases.html). Office on Women's Health. U.S. Department of Health and
Human Services. 16 July 2012. Archived (https://web.archive.org/web/20161005144045/https://w
ww.womenshealth.gov/publications/our-publications/fact-sheet/autoimmune-diseases.html) from
the original on 5 October 2016. Retrieved 5 October 2016.
2. Katz U, Shoenfeld Y, Zandman-Goddard G (2011). "Update on intravenous immunoglobulins
(IVIg) mechanisms of action and off- label use in autoimmune diseases". Current Pharmaceutical
Design. 17 (29): 3166–75. doi:10.2174/138161211798157540 (https://doi.org/10.2174%2F138161
211798157540). PMID 21864262 (https://pubmed.ncbi.nlm.nih.gov/21864262).
3. Borgelt LM (2010). Women's Health Across the Lifespan: A Pharmacotherapeutic Approach (http
s://books.google.com/books?id=riP3pxq2jWAC&pg=PA579). ASHP. p. 579. ISBN 978-1-58528-
194-7. Archived (https://web.archive.org/web/20170908184552/https://books.google.com/books?i
d=riP3pxq2jWAC&pg=PA579) from the original on 2017-09-08.
4. Hohlfeld R, Dornmair K, Meinl E, Wekerle H (February 2016). "The search for the target antigens
of multiple sclerosis, part 1: autoreactive CD4+ T lymphocytes as pathogenic effectors and
therapeutic targets". The Lancet Neurology. 15 (2): 198–209. doi:10.1016/S1474-4422(15)00334-
8 (https://doi.org/10.1016%2FS1474-4422%2815%2900334-8). PMID 26724103 (https://pubmed.
ncbi.nlm.nih.gov/26724103). S2CID 20082472 (https://api.semanticscholar.org/CorpusID:2008247
2).
5. Ananthanarayan R, Paniker CK (2005). Ananthanarayan and Paniker's Textbook of Microbiology
(https://books.google.com/books?id=MXMazr0LRDsC&pg=PA169). Orient Blackswan. p. 169.
ISBN 9788125028086. Archived (https://web.archive.org/web/20170908184552/https://books.goo
gle.com/books?id=MXMazr0LRDsC&pg=PA169) from the original on 2017-09-08.
6. Watson, Stephanie (March 26, 2019). "Autoimmune Diseases: Types, Symptoms, Causes and
More" (https://www.healthline.com/health/autoimmune-disorders). Healthline. Retrieved
November 11, 2020.
7. Smith DA, Germolec DR (October 1999). "Introduction to immunology and autoimmunity" (https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC1566249). Environmental Health Perspectives. 107 Suppl
5 (suppl 5): 661–5. doi:10.1289/ehp.99107s5661 (https://doi.org/10.1289%2Fehp.99107s5661).
PMC 1566249 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566249). PMID 10502528 (https://
pubmed.ncbi.nlm.nih.gov/10502528).
8. "Autoimmune disorders" (https://web.archive.org/web/20160112012705/https://www.nlm.nih.gov/m
edlineplus/ency/article/000816.htm). MedlinePlus Medical Encyclopedia. U.S. National Library of
Medicine. 2016-01-12. Archived from the original (https://www.nlm.nih.gov/medlineplus/ency/articl
e/000816.htm) on 2016-01-12. Retrieved 2020-04-14.
9. National Research Council (US) Subcommittee on Immunotoxicology (1992). Autoimmune
Diseases (https://www.ncbi.nlm.nih.gov/books/NBK235671/). National Academies Press (US).
10. Wang L, Wang FS, Gershwin ME (October 2015). "Human autoimmune diseases: a
comprehensive update". Journal of Internal Medicine. 278 (4): 369–95. doi:10.1111/joim.12395 (htt
ps://doi.org/10.1111%2Fjoim.12395). PMID 26212387 (https://pubmed.ncbi.nlm.nih.gov/2621238
7). S2CID 24386085 (https://api.semanticscholar.org/CorpusID:24386085).
11. Franks AL, Slansky JE (April 2012). "Multiple associations between a broad spectrum of
autoimmune diseases, chronic inflammatory diseases and cancer" (https://www.ncbi.nlm.nih.gov/p
mc/articles/PMC3349285). Anticancer Research. 32 (4): 1119–36. PMC 3349285 (https://www.ncb
i.nlm.nih.gov/pmc/articles/PMC3349285). PMID 22493341 (https://pubmed.ncbi.nlm.nih.gov/2249
3341).
12. Meresse B, Ripoche J, Heyman M, Cerf-Bensussan N (January 2009). "Celiac disease: from oral
tolerance to intestinal inflammation, autoimmunity and lymphomagenesis" (https://doi.org/10.103
8%2Fmi.2008.75). Mucosal Immunology. 2 (1): 8–23. doi:10.1038/mi.2008.75 (https://doi.org/10.1
038%2Fmi.2008.75). PMID 19079330 (https://pubmed.ncbi.nlm.nih.gov/19079330).
S2CID 24980464 (https://api.semanticscholar.org/CorpusID:24980464).
13. Green PH, Fleischauer AT, Bhagat G, Goyal R, Jabri B, Neugut AI (August 2003). "Risk of
malignancy in patients with celiac disease". The American Journal of Medicine. 115 (3): 191–5.
doi:10.1016/s0002-9343(03)00302-4 (https://doi.org/10.1016%2Fs0002-9343%2803%2900302-
14. Volta U, Vincentini O, Silano M (2011). "Papillary cancer of thyroid in celiac disease". Journal of
Clinical Gastroenterology. 45 (5): e44-6. doi:10.1097/mcg.0b013e3181ea11cb (https://doi.org/10.1
097%2Fmcg.0b013e3181ea11cb). PMID 20697293 (https://pubmed.ncbi.nlm.nih.gov/20697293).
15. Catassi C, Bearzi I, Holmes GK (April 2005). "Association of celiac disease and intestinal
lymphomas and other cancers". Gastroenterology. 128 (4 Suppl 1): S79-86.
doi:10.1053/j.gastro.2005.02.027 (https://doi.org/10.1053%2Fj.gastro.2005.02.027).
PMID 15825131 (https://pubmed.ncbi.nlm.nih.gov/15825131).
16. Frohman EM, Racke MK, Raine CS (March 2006). "Multiple sclerosis--the plaque and its
pathogenesis". The New England Journal of Medicine. 354 (9): 942–55.
doi:10.1056/nejmra052130 (https://doi.org/10.1056%2Fnejmra052130). PMID 16510748 (https://p
ubmed.ncbi.nlm.nih.gov/16510748).
17. Turesson C, Matteson EL (2009). "Clinical Features of Rheumatoid Arthritis: Extra-Articular
Manifestations". Rheumatoid Arthritis. Elsevier. pp. 62–67. doi:10.1016/b978-032305475-1.50014-
8 (https://doi.org/10.1016%2Fb978-032305475-1.50014-8). ISBN 978-0-323-05475-1.
18. Khurana R, Berney SM (October 2005). "Clinical aspects of rheumatoid arthritis".
Pathophysiology. 12 (3): 153–65. doi:10.1016/j.pathophys.2005.07.009 (https://doi.org/10.1016%
2Fj.pathophys.2005.07.009). PMID 16125918 (https://pubmed.ncbi.nlm.nih.gov/16125918).
19. Tsokos GC (December 2011). "Systemic lupus erythematosus". The New England Journal of
Medicine. 365 (22): 2110–21. doi:10.1056/nejmra1100359 (https://doi.org/10.1056%2Fnejmra110
20. "Autoimmune Disease List • AARDA" (https://www.aarda.org/diseaselist/). AARDA. 2016-06-01.
Retrieved 2019-03-21.
21. Gregersen PK, Olsson LM (2009). "Recent advances in the genetics of autoimmune disease" (htt
ps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2992886). Annual Review of Immunology. 27: 363–
91. doi:10.1146/annurev.immunol.021908.132653 (https://doi.org/10.1146%2Fannurev.immunol.0
21908.132653). PMC 2992886 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2992886).
22. Hill NJ, King C, Flodstrom-Tullberg M (May 2008). "Recent acquisitions on the genetic basis of
autoimmune disease". Frontiers in Bioscience: A Journal and Virtual Library. 13 (13): 4838–51.
doi:10.2741/3043 (https://doi.org/10.2741%2F3043). PMID 18508549 (https://pubmed.ncbi.nlm.ni
h.gov/18508549).
23. Molven A, Ringdal M, Nordbø AM, Raeder H, Støy J, Lipkind GM, et al. (April 2008). "Mutations in
the insulin gene can cause MODY and autoantibody-negative type 1 diabetes" (https://doi.org/10.
2337%2Fdb07-1467). Diabetes. 57 (4): 1131–5. doi:10.2337/db07-1467 (https://doi.org/10.2337%
2Fdb07-1467). PMID 18192540 (https://pubmed.ncbi.nlm.nih.gov/18192540).
24. Bennett ST, Todd JA (1996). "Human type 1 diabetes and the insulin gene: principles of mapping
polygenes". Annual Review of Genetics. 30: 343–70. doi:10.1146/annurev.genet.30.1.343 (https://
doi.org/10.1146%2Fannurev.genet.30.1.343). PMID 8982458 (https://pubmed.ncbi.nlm.nih.gov/89
82458).
25. Kurreeman FA, Padyukov L, Marques RB, Schrodi SJ, Seddighzadeh M, Stoeken-Rijsbergen G,
et al. (September 2007). "A candidate gene approach identifies the TRAF1/C5 region as a risk
factor for rheumatoid arthritis" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1976626). PLOS
Medicine. 4 (9): e278. doi:10.1371/journal.pmed.0040278 (https://doi.org/10.1371%2Fjournal.pme
d.0040278). PMC 1976626 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1976626).
26. Weyand CM, McCarthy TG, Goronzy JJ (May 1995). "Correlation between disease phenotype
and genetic heterogeneity in rheumatoid arthritis" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC
295811). The Journal of Clinical Investigation. 95 (5): 2120–6. doi:10.1172/JCI117900 (https://doi.
org/10.1172%2FJCI117900). PMC 295811 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC29581
27. Vojdani A (2014). "A Potential Link between Environmental Triggers and Autoimmunity" (https://w
ww.ncbi.nlm.nih.gov/pmc/articles/PMC3945069). Autoimmune Diseases. 2014: 437231.
doi:10.1155/2014/437231 (https://doi.org/10.1155%2F2014%2F437231). PMC 3945069 (https://w
ww.ncbi.nlm.nih.gov/pmc/articles/PMC3945069). PMID 24688790 (https://pubmed.ncbi.nlm.nih.go
v/24688790).
28. "Autoimmune Diseases: Symptoms & Causes" (http://www.childrenshospital.org/conditions-and-tr
eatments/conditions/a/autoimmune-diseases/symptoms-and-causes). Boston Children's Hospital.
Retrieved 23 March 2020.
29. Shah M, Targoff IN, Rice MM, Miller FW, Rider LG (July 2013). "Brief report: ultraviolet radiation
exposure is associated with clinical and autoantibody phenotypes in juvenile myositis" (https://ww
w.ncbi.nlm.nih.gov/pmc/articles/PMC3727975). Arthritis and Rheumatism. 65 (7): 1934–41.
doi:10.1002/art.37985 (https://doi.org/10.1002%2Fart.37985). PMC 3727975 (https://www.ncbi.nl
m.nih.gov/pmc/articles/PMC3727975). PMID 23658122 (https://pubmed.ncbi.nlm.nih.gov/2365812
2).
30. Meyer A, Sandler DP, Beane Freeman LE, Hofmann JN, Parks CG (July 2017). "Pesticide
Exposure and Risk of Rheumatoid Arthritis among Licensed Male Pesticide Applicators in the
Agricultural Health Study" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5744649).
Environmental Health Perspectives. 125 (7): 077010. doi:10.1289/EHP1013 (https://doi.org/10.12
89%2FEHP1013). PMC 5744649 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5744649).
31. Meier HC, Sandler DP, Simonsick EM, Parks CG (December 2016). "Association between Vitamin
D Deficiency and Antinuclear Antibodies in Middle-Aged and Older U.S. Adults" (https://www.ncbi.
nlm.nih.gov/pmc/articles/PMC5135624). Cancer Epidemiology, Biomarkers & Prevention. 25 (12):
1559–1563. doi:10.1158/1055-9965.EPI-16-0339 (https://doi.org/10.1158%2F1055-9965.EPI-16-0
339). PMC 5135624 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5135624). PMID 27543618
(https://pubmed.ncbi.nlm.nih.gov/27543618).
32. Wucherpfennig KW (October 2001). "Mechanisms for the induction of autoimmunity by infectious
agents" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC209539). The Journal of Clinical
Investigation. 108 (8): 1097–104. doi:10.1172/JCI14235 (https://doi.org/10.1172%2FJCI14235).
PMC 209539 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC209539). PMID 11602615 (https://pu
bmed.ncbi.nlm.nih.gov/11602615).
33. Cotsapas C, Hafler DA (January 2013). "Immune-mediated disease genetics: the shared basis of
pathogenesis". Trends in Immunology. 34 (1): 22–6. doi:10.1016/j.it.2012.09.001 (https://doi.org/1
0.1016%2Fj.it.2012.09.001). PMID 23031829 (https://pubmed.ncbi.nlm.nih.gov/23031829).
34. Harrison's Principles of Internal Medicine. Vol. 1–2 (18th ed.). McGraw-Hill Professional. 2011-08-
11. ISBN 978-0-07-174889-6.
35. Chang, Sarah Esther; Feng, Allan; Meng, Wenzhao; Apostolidis, Sokratis A.; Mack, Elisabeth;
Artandi, Maja; Barman, Linda; Bennett, Kate; Chakraborty, Saborni; Chang, Iris; Cheung, Peggie;
Chinthrajah, Sharon; Dhingra, Shaurya; Do, Evan; Finck, Amanda; Gaano, Andrew; Geßner,
Reinhard; Giannini, Heather M.; Gonzalez, Joyce; Greib, Sarah; Gündisch, Margrit; Hsu, Alex
Ren; Kuo, Alex; Manohar, Monali; Mao, Rong; Neeli, Indira; Neubauer, Andreas; Oniyide,
Oluwatosin; Powell, Abigail E.; Puri, Rajan; Renz, Harald; Schapiro, Jeffrey; Weidenbacher,
Payton A.; Wittman, Richard; Ahuja, Neera; Chung, Ho-Ryun; Jagannathan, Prasanna; James,
Judith A.; Kim, Peter S.; Meyer, Nuala J.; Nadeau, Kari C.; Radic, Marko; Robinson, William H.;
Singh, Upinder; Wang, Taia T.; Wherry, E. John; Skevaki, Chrysanthi; Luning Prak, Eline T.; Utz,
Paul J. (December 2021). "New-onset IgG autoantibodies in hospitalized patients with COVID-19"
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8440763). Nature Communications. 12 (1): 5417.
Bibcode:2021NatCo..12.5417C (https://ui.adsabs.harvard.edu/abs/2021NatCo..12.5417C).
doi:10.1038/s41467-021-25509-3 (https://doi.org/10.1038%2Fs41467-021-25509-3).
36. Witebsky E, Rose NR, Terplan K, Paine JR, Egan RW (July 1957). "Chronic thyroiditis and
autoimmunization". Journal of the American Medical Association. 164 (13): 1439–47.
doi:10.1001/jama.1957.02980130015004 (https://doi.org/10.1001%2Fjama.1957.0298013001500
37. Rose NR, Bona C (September 1993). "Defining criteria for autoimmune diseases (Witebsky's
postulates revisited)". Immunology Today. 14 (9): 426–30. doi:10.1016/0167-5699(93)90244-F (htt
ps://doi.org/10.1016%2F0167-5699%2893%2990244-F). PMID 8216719 (https://pubmed.ncbi.nl
m.nih.gov/8216719).
38. "Autoimmune disorders" (https://medlineplus.gov/ency/article/000816.htm). MedlinePlus Medical
Encyclopedia. U.S. National Library of Medicine. Retrieved 23 March 2020.
39. "Antinuclear Antibody (ANA)" (https://labtestsonline.org/tests/antinuclear-antibody-ana).
labtestsonline.org. Retrieved 14 April 2020.
40. "Complete blood count (CBC)" (https://www.mayoclinic.org/tests-procedures/complete-blood-coun
t/about/pac-20384919). www.mayoclinic.org. 19 December 2018. Retrieved 14 April 2020.
41. Rosenblum MD, Gratz IK, Paw JS, Abbas AK (March 2012). "Treating human autoimmunity:
current practice and future prospects" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061980).
Science Translational Medicine. 4 (125): 125sr1. doi:10.1126/scitranslmed.3003504 (https://doi.or
g/10.1126%2Fscitranslmed.3003504). PMC 4061980 (https://www.ncbi.nlm.nih.gov/pmc/articles/P
MC4061980). PMID 22422994 (https://pubmed.ncbi.nlm.nih.gov/22422994).
42. Li P, Zheng Y, Chen X (2017). "Drugs for Autoimmune Inflammatory Diseases: From Small
Molecule Compounds to Anti-TNF Biologics" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5506
195). Frontiers in Pharmacology. 8: 460. doi:10.3389/fphar.2017.00460 (https://doi.org/10.3389%
2Ffphar.2017.00460). PMC 5506195 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5506195).
43. Smilek DE, Ehlers MR, Nepom GT (May 2014). "Restoring the balance: immunotherapeutic
combinations for autoimmune disease" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007402).
Disease Models & Mechanisms. 7 (5): 503–13. doi:10.1242/dmm.015099 (https://doi.org/10.124
2%2Fdmm.015099). PMC 4007402 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007402).
44. Jacobson DL, Gange SJ, Rose NR, Graham NM (September 1997). "Epidemiology and estimated
population burden of selected autoimmune diseases in the United States". Clinical Immunology
and Immunopathology. 84 (3): 223–43. doi:10.1006/clin.1997.4412 (https://doi.org/10.1006%2Fcli
n.1997.4412). PMID 9281381 (https://pubmed.ncbi.nlm.nih.gov/9281381).
45. Hayter SM, Cook MC (August 2012). "Updated assessment of the prevalence, spectrum and case
definition of autoimmune disease". Autoimmunity Reviews. 11 (10): 754–65.
doi:10.1016/j.autrev.2012.02.001 (https://doi.org/10.1016%2Fj.autrev.2012.02.001).
46. Dinse, Gregg E.; Parks, Christine G.; Weinberg, Clarice R.; Co, Caroll A.; Wilkerson, Jesse;
Zeldin, Darryl C.; Chan, Edward K. L.; Miller, Frederick W. (June 2020). "Increasing Prevalence of
Antinuclear Antibodies in the United States" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7255
943). Arthritis & Rheumatology. 72 (6): 1026–1035. doi:10.1002/art.41214 (https://doi.org/10.100
2%2Fart.41214). ISSN 2326-5191 (https://www.worldcat.org/issn/2326-5191). PMC 7255943 (http
s://www.ncbi.nlm.nih.gov/pmc/articles/PMC7255943). PMID 32266792 (https://pubmed.ncbi.nlm.ni
h.gov/32266792).
47. Mukundan L, Odegaard JI, Morel CR, Heredia JE, Mwangi JW, Ricardo-Gonzalez RR, et al.
(November 2009). "PPAR-delta senses and orchestrates clearance of apoptotic cells to promote
tolerance" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2783696). Nature Medicine. 15 (11):
1266–72. doi:10.1038/nm.2048 (https://doi.org/10.1038%2Fnm.2048). PMC 2783696 (https://ww
w.ncbi.nlm.nih.gov/pmc/articles/PMC2783696). PMID 19838202 (https://pubmed.ncbi.nlm.nih.gov/
19838202).
48. Roszer T, Menéndez-Gutiérrez MP, Lefterova MI, Alameda D, Núñez V, Lazar MA, et al. (January
2011). "Autoimmune kidney disease and impaired engulfment of apoptotic cells in mice with
macrophage peroxisome proliferator-activated receptor gamma or retinoid X receptor alpha
deficiency" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038038). Journal of Immunology. 186
(1): 621–31. doi:10.4049/jimmunol.1002230 (https://doi.org/10.4049%2Fjimmunol.1002230).
49. Singh RP, Waldron RT, Hahn BH (July 2012). "Genes, tolerance and systemic autoimmunity" (http
s://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306516). Autoimmunity Reviews. 11 (9): 664–9.
doi:10.1016/j.autrev.2011.11.017 (https://doi.org/10.1016%2Fj.autrev.2011.11.017). PMC 3306516
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306516). PMID 22155015 (https://pubmed.ncbi.n
lm.nih.gov/22155015).
50. Böhm I (May 2003). "Disruption of the cytoskeleton after apoptosis induction with autoantibodies".
Autoimmunity. 36 (3): 183–9. doi:10.1080/0891693031000105617 (https://doi.org/10.1080%2F08
51. Swart JF, Delemarre EM, van Wijk F, Boelens JJ, Kuball J, van Laar JM, Wulffraat NM (April
2017). "Haematopoietic stem cell transplantation for autoimmune diseases". Nature Reviews.
Rheumatology. 13 (4): 244–256. doi:10.1038/nrrheum.2017.7 (https://doi.org/10.1038%2Fnrrheu
m.2017.7). PMID 28228650 (https://pubmed.ncbi.nlm.nih.gov/28228650). S2CID 21264933 (http
s://api.semanticscholar.org/CorpusID:21264933).
52. Drew, Liam (2021-07-14). "How stem cells could fix type 1 diabetes" (https://www.nature.com/artic
les/d41586-021-01842-x). Nature. 595 (7867): S64–S66. Bibcode:2021Natur.595S..64D (https://u
i.adsabs.harvard.edu/abs/2021Natur.595S..64D). doi:10.1038/d41586-021-01842-x (https://doi.or
g/10.1038%2Fd41586-021-01842-x). PMID 34262205 (https://pubmed.ncbi.nlm.nih.gov/3426220
5). S2CID 235907766 (https://api.semanticscholar.org/CorpusID:235907766).
53. Maverakis E, Kim K, Shimoda M, Gershwin ME, Patel F, Wilken R, et al. (February 2015).
"Glycans in the immune system and The Altered Glycan Theory of Autoimmunity: a critical review"
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340844). Journal of Autoimmunity. 57: 1–13.
doi:10.1016/j.jaut.2014.12.002 (https://doi.org/10.1016%2Fj.jaut.2014.12.002). PMC 4340844 (htt
ps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340844). PMID 25578468 (https://pubmed.ncbi.nlm.
nih.gov/25578468).
54. Rook GA (February 2012). "Hygiene hypothesis and autoimmune diseases". Clinical Reviews in
Allergy & Immunology. 42 (1): 5–15. doi:10.1007/s12016-011-8285-8 (https://doi.org/10.1007%2F
s12016-011-8285-8). PMID 22090147 (https://pubmed.ncbi.nlm.nih.gov/22090147).
55. Harrison, Stephanie R.; Li, Danyang; Jeffery, Louisa E.; Raza, Karim; Hewison, Martin (January
2020). "Vitamin D, Autoimmune Disease and Rheumatoid Arthritis" (https://www.ncbi.nlm.nih.gov/
pmc/articles/PMC6960236). Calcified Tissue International. 106 (1): 58–75. doi:10.1007/s00223-
019-00577-2 (https://doi.org/10.1007%2Fs00223-019-00577-2). ISSN 0171-967X (https://www.wo
rldcat.org/issn/0171-967X). PMC 6960236 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC696023
56. Lucas, Robyn; Rodney Harris, Rachael (12 August 2018). "On the Nature of Evidence and
'Proving' Causality: Smoking and Lung Cancer vs. Sun Exposure, Vitamin D and Multiple
Sclerosis" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6121485). International Journal of
Environmental Research and Public Health. 15 (8): 1726. doi:10.3390/ijerph15081726 (https://doi.
org/10.3390%2Fijerph15081726). PMC 6121485 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC
Further reading
Kumar V, Abbas AK, Fausto N, Aster J (2010). Robbins and Cotran Pathologic Basis of Disease
(8th ed.). Elsevier. p. 1464. ISBN 978-1-4160-3121-5.
Asherson R (ed.). Handbook of Systemic Autoimmune Diseases (http://www.elsevier.com/wps/fin
d/bookdescription.cws_home/BS_HSAD/description#description). Elsevier.
External links
Autoimmune disorders (https://curlie.org/Health/Conditions_and_Diseases/Immune_Disorders/Aut
o-Immune) at Curlie
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1/25/22, 9:07 AM Autoimmune disease - Wikipedia

The cause is unknown.[3] Some autoimmune diseases

Treatment depends on the type and severity of the

Signs and symptoms

Coeliac disease presents the strongest associations to gastrointestinal and lymphoproliferative

Inflammatory bowel disease

Systemic lupus erythematosus

UV radiation is found to be a possible cause of development of the autoimmune disease

Direct evidence from transfer of disease-causing antibody or disease-causing T lymphocyte white

Complete blood count

Erythrocyte sedimentation rate

Non-steroidal anti-inflammatory drugs (NSAIDs) to reduce inflammation

Other standard treatment methods include:[8]

Monoclonal antibodies that can be used to block pro-inflammatory cytokines

Mitigation of inflammation by activation of anti-inflammatory genes and the suppression of

Altered glycan theory

Vitamin D Influence on Immune Response

Retrieved from "https://en.wikipedia.org/w/index.php?title=Autoimmune_disease&oldid=1062281174"

This page was last edited on 27 December 2021, at 13:50 (UTC).

Text is available under the Creative Commons Attribution-ShareAlike License;

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