1881 - He applied the same technique vs.

IMMUNOLOGY AND anthrax and then rabies (vaccine)

SEROLOGY
Serology is the application of Immunology; More
on the test that we need for Immunology.
WEEK 1: HISTORY OF IMMUNOLOGY
⮚ 430 B.C – plague in Athens, Thucydides:
Recognized “immune” status.
⮚ 1000 AD- Chinese – immunization by
inhaling dried powders “variolation”.
Dried Powders – it’s from a wound
called “crust” or langib (Those
crust will make as powderized,
after powderization, it inhaled by
Chinese which they believed they’ll
get immune high from those
powder)
⮚ 15 Century- England – smallpox “crusts”
th
Louis Pasteur watching as Joseph Meister
receives attenuated rabies vaccine (1885)
Attenuated – a process to “weaken” the virus.
FIRST INSIGHTS INTO MECHANICS OF
IMMUNITY…
Elie Metchnikoff (1880s)
- discovered phagocytic cells that ingest
microbes and particles, and who
discovered new cytosis.
- Cells conferred immunity.
Emil Von Behring and S. Kitasata (1890)
- They discovered blood sera could transfer
immunity. We can extract the sera from
human beings that produces antibodies
for a certain virus.
- Liquid of blood conferred immunity.

⮚ Louis Pasteur – Father of Immunology SIGNIFICANT MILESTONES IN IMMUNOLOGY

⮚ Jenner – FIRST smallpox vaccine; Vaccine
was invented (Latin VACCA means
“COW”)
STORY: Smallpox and cowpox. The cows
have that cowpox. Jenner notices that
cowpox (milkmaid) doesn’t infect the
smallpox, so there’s a possibility that they
are immune to the smallpox. So, Jenner
experimented on an 8-year-old kid; he
extracted the cowpox from one cow, then
injected it into the kid. After the injection
on a boy, Jenner exposed that 8-year-old
boy to smallpox. What happened is that
that 8-year-old boy didn’t get the
smallpox; that’s why the smallpox is from
the cow pox.
Pasteur inoculating sheep at Msr. Rossignol’s
farm – May,1881
1879 – discovered that aged bacterial cultures
of Pasteurella lost virulence. Referred to injection
of weakened culture as a “vaccine” in honor of
Jenner.

AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE


TYPE OF IMMUNITY
Innate Immunity
WEEK 2: IMMUNOLOGY
Immunology
⮚ Stems from Latin word – immunis =
EXEMPT = protection from disease.
⮚ Study of a host’s reactions when foreign
substances
⮚ Systems responsible for the recognition
and disposal of foreign (nonself) material
⮚ T and B lymphocytes, immunoglobulins
(antibodies), complement, and
hematopoietic cells.
Roles and Functions of Immunology
⮚ Defending the body against infections
⮚ Recognizing and responding to foreign
antigens
⮚ Defending the body against the
development of tumors
⮚ The desirable consequences of immunity
include natural resistance recovery and
acquired resistance to infectious disease.
⮚ (Once your body encounters infections,
you can/can’t have the resistance, there’s
function in our body to have the
resistance if your body produces
antibodies)
AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE
⮚ A deficiency of dysfunction of the immune
system can cause many disorders. Ex.
Autoimmune Disorder
1. Born with it, do not need prior exposure.
2. First line of defense
a. Physical barriers, such as epithelial
cells (intact skin), trapping of
bacteria in:
o Mucus adheres on the nose
and nasopharynx that traps
microorganisms, which can be
expelled by coughing or
sneezing,
o Sebum (oil) produced by the
sebaceous glands of the skin
and lactic acid in sweat;
possess antimicrobial
properties.
o Earwax (cerumen) protects the
auditory canals from harsh
environments.
o Tears and saliva contain
Immunoglobulin A (IgA)
b. Chemicals secreted by cells and
tissues, such as acidic pH of skin
surface, complement, interferons,
lysozymes (is an enzyme that
attacks and destroys the cell wall
of susceptible bacteria, particularly
certain gram-positive bacteria) etc.
3. Second line of defense
a. Phagocytosis – the process of a
white blood cell (WBC) engulfing
bacteria
b. Inflammation – nonspecific
response to tissue damage that
includes:
o Chemical release
o Cellular movement
o Elimination of foreign
material
o Tissue repair
 c. Complement system – enhances
phagocytosis, stimulates
inflammatory response, and lyses
foreign cells.
Adaptive Immunity
1. Acquired only after a specific challenge is
encountered and responds, means you
are NOT BORN WITH IT.
2. Two responses:
a. Cell-mediated immunity
o More important in protection
against intracellular pathogens
o Natural Killer (NK) cells: Some
activity against tumor cells
o T helper cells
o Cytotoxic T lymphocytes (CTLs)
o Cytotoxins
b. Humoral-mediated immunity
o More important in protection
against extracellular
pathogens.
o Antibody production by plasma
cells.
3. Could be ACTIVE or Passive immunity.
a. ACTIVE IMMUNITY
o Natural – the host is EXPOSED
to foreign immunogen as a
result of infection, and the
host’s immune cells
manufacture specific products
to eliminate foreign
immunogen. (Ex. Miss Julia is a
healthy person and interacts
(exposed) with a sick person,
AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE
then gets sick because of that
person, and her body reacts to
that virus, so Miss Julia gets an
immune response.)
o Artificial – Vaccination; immune
system responds to an altered
(noninfectious) organism.
o Generally, endures for life.
b. PASSIVE IMMUNITY
o Natural – maternal antibody
crosses placenta (IgG) to
protect infant.
o Artificial – immune products
from another animal injected
into the host (e.g., pooled
gamma- globulin)
o Passive immunity short term,
no memory cells produced.
MAJOR FUNCTIONS OF T CELLS AND B CELLS
Antibody (Humoral) -Mediated Immunity (B Cells)
1. Host defense against infection.
2. (Opsonize bacteria, neutralize toxins and
viruses)
3. Allergy (hypersensitivity) e.g., hay fever
anaphylactic shock
4. Autoimmunity
Cell Mediated Immunity
1. Host defense against infection (especially
M. Tuberculosis, fungi, and virus infected
cells)
2. Allergy (hypersensitivity) e.g. poison oak
3. Graft and tumor rejection
4. Regulated of antibody response (help and
suppression)
THE ORGAN OF THE IMMUNE SYSTEM
1. Primary Lymphoid Organs
a. Bone Marrow
o Pre- B lymphocytes develop into
mature B cells.
o Main source of pluripotential
hematopoietic stem cells
o 1300 g to 1500 g
Thymus
o Pre- T lymphocytes develop into
mature T cells.
b. Maturation Site (B cells and T cells)
2. Secondary Lymphoid Organs
a. Spleen
o Purpose – Filter blood
o Contains both T and B cells.
o 2 main types:
⮚ Red Pulp – destroys old
RBCs.
⮚ White pulp – arranged
around Periarteriolar
Lymphoid Sheath (PALS),
attacked Primary Follicles.
Lymph nodes
o B cells migrate to the cortex and T
cells to the para cortex.
o Primary follicle: Many small B cells
o Secondary follicle: After
stimulation, the primary follicle
becomes a secondary follicle. The
germinal center has a small and
large lymphocyte, blast cells,
macrophages, and dendritic cells.
The medulla contains plasma cells
and large lymphocytes.
AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE
b. MALT 1 (mucosal associated lymph
tissue)
o Found in submucosa in
gastrointestinal tract, respiratory
tract, and urogenital tract. These
surfaces interact with the
environment and can begin the
immune response early.
o Peyer’s patch: Specialized MALT
found in the lower ileum.
c. GALT (gut associated lymph tissue)
d. Trap antigen, APC, Lymphocyte
Proliferation
FUNCTIONS OF SECONDARY LYMPHOID
ORGANS
1. Trapping site of pathogens
2. Stand-by areas of T cells, B cells and
phagocytes.
3. Place of encounter for pathogens and the
cells
4. Production of Antibody and Lymphokine,
phagocytosis occurs.
5. Antigenic Dependent Lymphopoiesis.
CELLS OF THE IMMUNE SYSTEM
Monocytes and Macrophages
1. In the peripheral blood, monocyte; in the
tissue, macrophage. Tissue macrophages
include alveolar macrophage (lungs),
Langerhans (skin), Kupffer cell (liver), and
astrocytes and microglia cells (nervous
system), and osteoclast (bone).
2. Functions
a. Phagocytosis of invaders
b. Present immunogens to T helper cells,
the first step in an immune response
c. Release cytokines (monokines) that
affect other cells’ activities.
3. Macrophages have major
histocompatibility complex (MHC) class II,
complement, and antibody Fc receptors
on their surface.
Granulocytes
1. Neutrophils (polymorphonuclear cells or
PMNs)
 o 60-70% of WBCs in circulation
o Function: Phagocytosis and
contributes to inflammatory
response
2. Eosinophils
o 1 -3% of circulating WBCs.
o Mediate IgE allergic response
3. Basophils
o 0 – 1.0% of circulating WBCs
o Has receptors for IgE and granules
responsible for allergic reactions.
PROCESS OF PHAGOCYTOSIS
• The only granulocytes that can perform in
phagocytosis are the neutrophils and
monocytes (macrophage)
1. Chemotaxis
o Cells are guided to the site of
injury by CHEMOATTRACTANT.
o CHEMOATTRACTANT – it is a
change I the direction of the
movement of a motile cell in
response to the concentration
gradient of a specific chemical
(CHEMOTAXIN).
o Examples of Chemoattractant:
a. Antigens – a toxin present
in a foreign substance.
CELL SURFACE RECEPTOR
– detects antigen.
▪ FC receptor
▪ Complement
receptor-specifically
C3.
b. Necrotic cells – limit the
damage/injury of the tissue.
2. Adherence
o Cascade is a sequence of
adhesion and activation events.
o Inflammatory response
a. Inflammatory Mediators:
HISTAMINES,
PROSTAGLANDINS AND
CYTOKINES
b. Promotes inflammation.
3. Engulfment
o Destruction of foreign matter
AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE
a. Eosinophil – kill
parasites.
o Engulfment can be done by
ACTIVE MEMBRANE
INVAGINATION
a. (4.) PHAGOSOME
FORMATION
b. (5.) Meet and fuse
(fusion)
o Hydrophobic microorganisms
ARE EASILY PHAGOCYTIZED.
6. Digestion/Destruction
o Example of destruction:
▪ Degranulation of
neutrophil
▪ Alteration of Ph
▪ Large amount of lipase
in the cytoplasm
MONOCYTE.
WEEK 3: THE ORGAN OF THE IMMUNE
SYSTEM
CIRCULATION OF LYMPHOCYTES
● Mature T lymphocytes survive for several
months or years.
● B lymphocytes survive only for a few
days.
● Lymphocytes move freely between the
blood and lymphoid tissue.
● Clonal expansion:
POSITIVE SELECTION - It recognized
antigens or foreign substances.
 NEGATIVE SELECTION - It recognized
other cells in a foreign substance. (It
means, even on other good cells, they see
it as bad cells)
● VIRGIN OR NAÏVE LYMPHOCYTES: are
cells that have not encountered their
specific antigen. (NO
EXPERIENCED/HAVEN’T YET
EXPERIENCED with a foreign antigen or
substances)
● MEMORY CELLS: are populations of long-
lived T or B cells that have been
stimulated by antigen. (ALREADY
EXPERIENCED OR HAVE ENCOUNTERED
with a foreign antigen)
⮚ Memory B cells carry surface IgG
as their antigen receptor, memory
T cells express the CD45RO
variant of the leukocyte.
DEVELOPMENT OF T LYMPHOCYTES
● Most lymphocytes found in the circulating
blood are T cells derived from bone
marrow progenitor cells that mature in
the thymus gland.
● These cells are responsible for cellular
immune responses and are involved in
the regulation of antibody reactions in
conjunction with B lymphocytes.
● Differentiation of a lymphocytes begins in
the thymus as a THYMOCYTES (means
immature T lymphocytes)
● Early surface markers of T cells: CD44
and CD25 (It dictates what the cell is to
become)
● MATURATION is a complicated process
that lasts for a period of 3 WEEKS.
EARLY THYMOCYTES
a. DOUBLE-NEGATIVE THYMOCYTES
• Early thymocytes LACKING CD4 AND CD8
surface membranes markers.
b. DOUBLE-POSITIVE THYMOCYTES
• Cells with both CD4+ and CD8+, or
double-positive, surface markers
AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE
represent the second stage of thymocyte
development.
LATER CELLULAR DIFFERENTIATION AND
DEVELOPMENT
a. HELPER T LYMPHOCYTE (T- HELPER OR
Th)
● Helper T type 1 (Th1) cells are
responsible for cell-mediated
effector mechanisms.
● Helper T type 2 (Th2) cells play a
greater role in the regulation of
antibody production.
b. T REGULATORY LYMPHOCYTE
• Cells that control autoimmunity in the
peripheral blood
⮚ Types of Treg cells include the
following:
● Natural CD4+ Treg cells
● Th3 cells
● Tr1 cells
● CD8+ Treg cells
c. CYTOTOXIC T LYMPHOCYTE
• are effector cells found in the peripheral
blood that are capable of directly
destroying virally infected target cells.
T LYMPHOCYTES
• 80% of the circulating lymphocytes in the
peripheral blood
• Responsible for immune responses and
are involved in antibody regulation.
⮚ SUBSETS:
● T-helper cells – 70%,
activates immune system.
▪ Th1 – cell mediated.
▪ Th2 – antibody
regulation
● T-suppressors cells – 30%,
suppresses immune system.
● T-cytotoxic cells – kills
specific causative agents.
● T-delayed hypersensitivity

T CELL MATURATION
● Double Negative Thymocytes
● Double Positive Thymocytes
● Mature T cell
● Activated T cell
● Sensitized T cell
● Memory Cell
B LYMPHOCYTES
• Precursor cells in antibody production.
⮚ B cell maturation:
● Pro-B cell (immature B cells)
● Pre-B cell
● Immature B cell
● Mature B cell – marginal B
cells, Follicular
● Activated B cell (stimulated
by foreign antigen)
● Plasma cell - produce
antibodies.
⮚ SUBSETS:
● B1 – CD5 (+)
● B2 – CD5 (-), most common
circulating.
NATURAL KILLER CELLS (NK)
● Aka LARGE GRANULAR LYMPHOCYTES
(LGL)
● Kill infected and malignant cells (mostly
this natural killer cells function in cancer
patient)
● Identified by presence of CD56 and
CD16, absence of CD3 (nakilala ang mga
natural killer cells because of the surface
markers)
● Activated by IL2 and IFN-gamma to
become LAK (Lymphokine-activated killer)
cell.
Other cells that assist in the immune response:
● Dendritic cells present antigen to T cells.
● Langerhans cells: Dendritic cells found in
the dermis and squamous epithelia.
AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE
● Mast cell: Granulocyte resembling
basophil that contains many chemicals
that affect the immune response.
DISORDER OF THE IMMUNE SYSTEM
1. SEPSIS
⮚ SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME (SIRS)
o Extreme reaction to the
infection
o (systemic, means affected all
the organs)
⮚ Criteria for SIRS
o Alteration of body temperature
(>38C or <36C)
o Increased heart rate
o Increased respiratory rate
o Total leukocyte count of >12.0
x 10(9)/L (or >10% immature
forms)
2. ABNORMAL NEUTROPHIL FUNCTION
● Marked decrease of neutrophil
(called as, neutropenia)
● Defective locomotion (means, the
neutrophil not functioning well or
not doing its job)
DISORDER OF NEUTROPHIL
a. CONGENITAL NEUTROPHIL
ABNORMALITIES
1. Chediak-Higashi Syndrome
● Qualitative disorder of
neutrophils (means,
defective because it based
on the quality)
● Familial disorder inherited.
● Neutrophils having giant
granules display impaired
chemotaxis and delayed
killing of ingested bacteria
 (granules ay hindi dapat
lumalaki)
Chediak-Higashi Syndrome in Microscopic Examination
2. Chronic Granulomatous Disease
● Genetic heterogeneous
disorder (not inherited, but
the problem is on genes)
● development of granulomas
● collection of immune cells
that cluster
● Patients with CGD have
infections with catalase-
positive bacteria and fungi
affecting the skin, lungs,
liver, and bones.
3. Myeloperoxidase Deficiency
● Azurophilic granules are
present, but
myeloperoxidase is
decrease.
● If phagocytes are deficient
in myeloperoxidase, the
patient’s phagocytes
manifest a mild to
moderate defect in bacterial
killing and a marked defect
in fungal killing in vitro.
(Means it is a defective
problem, if the
myeloperoxidase is low or
decreases it affects the
phagocytic function of
neutrophil, that’s why it
couldn’t kill or engulf the
AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE
bacterias and fungi
immediately).
4. Complement Receptor 3 deficiency
● The complement receptor 3
(CR3) deficiency is a rare
condition inherited as an
autosomal recessive trait.
● A deficiency of CR3 on
phagocytic cells present as
a leukocyte adhesion (It
means, the neutrophil
doesn’t properly function or
the process of phagocytic
disappears in terms of
adhesion. If no adhesion,
there will be no no
engulfment or digestion
immediately in the foreign
substance.
DISORDER OF MONOCYTE - MACROPHAGES
Another Monocyte-Macrophage Disorders
a. Gaucher’s Disease
● An inherited disease caused by a
disturbance in cellular lipid
metabolism.
● Most frequently affects children.
● It happened to be an enlarged
spleen and liver called
hepatosplenomegaly.
 b. Niemann-Pick Disease • Chain structure: alpha chain and
● Affects infants and children, with beta chain.
an average life expectancy of 5
years. c. MHC III
● Disorder represents a rare • Minor MHC Antigens
autosomal recessive deficiency of • Involves complement components
the enzyme sphingomyelinase, C2, C4 and Factor B
characterized by massive • HLA on RBC: Benett-goodspeed
accumulation of sphingomyelinase.
MHC I MHC II
MAJOR HISTOCOMPATIBILITY COMPLEX Genetic Loci HLA-A,B,C HLA DR, DQ
● Located on the short arm of Chain structure Alpha and B2
CHROMOSOME 6 microglobulin
● Sets of genes that control tissue Cell Distribution All nucleated Predominantly in
histocompatibility. cells APCs
o Referred to as Human Leukocyte Present Ag to CD8+ Tc cells CD4+ Th cells
Antigen (HLA) complex – encoded
by the MHC genes. MHC Region: Class I & II
o Cell surface markers that allow Class I: ABC Class II: D
immune cells to distinguish “self Loci HLA- A, B, C HLA-DN, DO, DP,
from” non-self (to prevent DQ, DR
autoimmunity Distribution Most Nucleated B lymphocytes,
Cell macrophages and
o HLA does help to know that in
other that is
your body, what you are killing are activated by T
not good cells but antigens or lymphocytes.
foreign substances. Function Present antigen Present antigen
to cytotoxic T to helper T
a. MHC I lymphocytes. lymphocytes.
• Present in all nucleated cells.
• Process cytoplasmically derived
antigens and presented to CD8 WEEK 4-5: INFLAMMATION
positive cells. • When there’s an infection, the first thing
• Genetic Loci: HLA- A, B, C,E,F,G,J we notice in our body is in the skin, which
• Chain structure: alpha chain and could be swelling or inflammation in the
B2 microglobulin. wound, injury, and/or in allergic reactions.
• A complex process involving a variety of
b. MHC II cells and signaling proteins that protect
• Present in macrophages, B cells, the body from foreign substances (In
dendritic cells, and Antigen inflammation, our cells are also involved
Presenting Cells (APC) or affected)
• Restricted to immunocompetent • The body’s overall reaction to injury or
cells of immune system. invasion by an infectious agent.
• Process extracellularly derived
antigens and presented to CD4 CARDINAL SIGNS OF INFLAMMATION
positive cells. - These are the signs when you’re having
infection or allergic reactions.
• Genetic Loci: DP DQ, DR, DM, DO
AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE
 • RUBOR – Redness
• CALOR – Increased heat
• TUMOR – Swelling
• DOLOR – Pain
• FUNCTIO LAESA – Loss of function (Ex.
Diabetic patient)
PRINCIPAL COMPONENTS:
• VASODILATION
o This leads to an increase in blood
flow to the infected area.
o Results in redness and warmth
• INCREASED CAPILLARY PERMEABILITY
o Increased contraction of the
endothelial cells lining the vessels
o Results in swelling and pain.
• DIAPEDESIS
o Motility of the cells.
o Mainly involves Neutrophils.
▪ Mobilized 30-60 mins after
injury.
▪ Diapedesis may last 24-
48hrs.
o Macrophages and dendritic cells
migrate to the injured area several
hours after
• Peaks at 16-48hrs
PATHOGEN RECOGNITION RECEPTOR
• The internal defense system is designed
to recognize molecules that are unique to
infectious organisms.
• Able to distinguish pathogens by means
of receptors or PATHOGEN RECOGNITION
RECEPTORS (PRRs)
o They are also found on neutrophils,
eosinophils, monocytes, mast cells,
T cells and epithelial cells.
FUNCTION OF PRRs
• Play a pivotal role as a second line of
defense if microorganisms penetrate
external barriers.
AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE
• Once these receptors bind to a pathogen,
phagocytic cells become activated and
are better able to engulf and eliminate
any microorganisms.
o Activated cells proceed to secrete
proinflammatory cytokines and
chemokines.
o Abe to distinguish self from nonself
by recognizing pathogen
associated molecular patterns
(PAMPs).
a. TOLL LIKE RECEPTOR (TLR)
• Discovered by Charles Janeway
o First discovered receptor in
humans
• The highest concentration of these TLRs
occurs on monocytes, macrophages, and
neutrophils (similarities of these three,
they are all phagocytic)
TOLL LIKE RECEPTOR (TLR) IN HUMANS
• TLR1. TLR2. TLR4, TLR5, and TLR6 are
found on cell surfaces.
• TLR3, TLR7, TLR8, and TLR9 are found in
the endosomal compartment of a cell.
o TLR2 recognizes teichoic acid and
peptidoglycan found in gram-
positive bacteria.
o TLR4 recognizes
lipopolysaccharide, which is found
in gram-negative bacteria.
o TLR5 recognizes the bacteria
flagellin.
o The function of TLR10 is not yet
known.
TOLL LIKE RECEPTOR (TLR) MECHANISMS IN
HUMANS
• TLR binds particular substances.
• This will activate the production of
CYTOKINES and CHEMOKINES.
• Cells will undergo chemotaxis.
• This will enhance phagocytosis and
destruction of pathogens.
 Receptor Substance Target • Promotes phagocytosis by binding to
Recognized microorganism specific of monocytes, macrophages,
TLR Receptors found on cell surfaces and neutrophil.
TLR1 Lipopeptides Mycobacteria • CRP is elevated in the ff conditions:
TLR2 Peptidoglycan, Gram-positive
o Bacterial/Viral infection
Lipoproteins, bacteria,
Zymosan Mycobacteria, o Rheumatic fever
Yeasts o Tuberculosis
TLR4 Lipopolysaccharide, Gram-negative o Malignant disease
fusion proteins, bacteria, RSV o After a heart attack
Mannan fungi
• Rapidly increases within 4-6 hors after
TLR5 Flagellin Bacteria with
flagellae infection, surgery, or trauma to the
TLR6 Lipopeptides, Gram-positive body.
Lipoteichoic acid, bacteria, • Increased CRP is a significant risk
Zymosan Mycobacteria, factor for CVDs:
yeast o Myocardial infarction
o Ischemic stroke
TLR Receptors found on Endosomal o Peripheral Vascular disease in
Compartment patients with cardiovascular
TLR3 Double-stranded RNA RNA viruses disease history
o Atherosclerosis (result of a
TLR7 Single-stranded RNA RNA viruses chronic inflammatory process)
• In chronic inflammation, increased CRP
TLR8 Single-stranded RNA RNA viruses
amounts react with the endothelial
cells that line the vessel walls,
TLR9 Double-stranded DNA DNA viruses,
bacterial DNA predisposing these walls to:
TLR10 Unknown Unknown o Vasoconstriction
o Platelet activation
o Thrombosis (clot formation)
b. ACUTE PHASE REACTANTS
o Vascular inflammation
• Serum constituents increase rapidly
because of infection, injury, or trauma to
➢ SERUM AMYLOID A (SAA)
the tissues.
• Can increase almost a thousandfold in
• Acute-phase reactants act by binding to
response to infection or injury.
microorganisms and promoting
• It is an apolipoprotein synthesized in
adherence.
the liver.
o Molecular weight: 11,685
➢ C- REACTIVE PROTEINS (CRP)
Daltons
• First discovered by Tillet & Francis
o Normal circulating levels are 5-
(1930)
8 ug/mL.
• Precipitate that formed when mixing
• Also act as a chemical messenger
the serum of patients infected with
o It activates monocytes and
Streptococcus pneumonia with a
macrophages to then produce
soluble extract of the bacteria.
products that increase
o Molecular weight: 118,000 –
inflammation.
144,000 Daltons
o Half-life: 18hrs

AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE

 ➢ COMPLEMENT • Fibrinogen is cleaved by thrombin
• Refers to a series of serum proteins to form fibrils that make up a fibrin
that are normally present. clot.
• Mediation of inflammation o The clot increases the strength
o Other functions: of a wound and stimulates
▪ Chemotaxis endothelial cell adhesion and
▪ Opsonization proliferation.
▪ Lysis of cells
CYTOKINES
➢ ALPHA1 – ANTITRYPSIN (AAT) • Are the chemical messengers that
• Molecular weight: 52,000 Daltons regulate the immune system.
• It is a general plasma inhibitor pf • Can be classified as proteins, peptides, or
protease, elastase, and trypsin. glycoproteins.
• Different cytokines:
➢ HAPTOGLOBIN o Chemokines
• Molecular weight: 100,000 o Interferons
Daltons o Interleukins
• Binds irreversibly free hemoglobin o Tumor necrosis factor
released by intravascular Cytokine Principle Source Function
hemolysis. TNFa Macrophages Pro-inflammatory
IL-1 Macrophages Pro-inflammatory
o Acts as antioxidant to protect
IL-2 T cells T cells growth
against oxidative damage from factor
free hemoglobin. IL-10 T cells Anti-inflammatory
IFNy T cells, NK cells Proinflammatory
➢ CERULOPLASMIN TGFB Many Proinflammatory,
• Molecular weight: 132,000 regulatory
Daltons
GENRAL PROPERTIES OF CYTOKINES
• It is the principal copper-
transporting protein in human • Mediate and regulate immune and
plasma. inflammatory responses.
• Act as an enzyme. • Cytokines often have multiple different
o Converts the toxic ferrous ion effects on the same target cell. Some
(Fe2+) to the nontoxic ferric occur simultaneously, whereas others may
form (Fe3+) occur over different time frames (i.e.
minutes, hours, or days).
• Normal adult plasma
concentration: 20-40 mg/dL • Cytokines do not act alone but in
conjunction with many other cytokines
• WILSON’S DISEASE: depletion of
that are included during the process of
ceruloplasmin
immune activation.
➢ FIBRINOGEN
FUNCTION OF CYTOKINES
• Molecular weight: 340,000
• Mediator
Daltons
• Regulation
• Normal concentration: 200-400
mg/dL • Stimulators of immature leukocyte growth
and differentiation
• Control the infection.
AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE
CYTOKINE RECEPTORS
• Lymphokines = released from
lymphocytes
• Monokines = released from monocytes
and macrophages
• Interleukins = secreted by leukocytes that
mainly act on other leukocytes

CYTOKINE FAMILY
• Tumor necrosis factor (TNF)
• Interferon (IFN)
o Established antimicrobial
properties.
o Three types: alpha, beta, gamma
▪ Induced production of
proteins and pathways that
directly interfere with viral
replication and cell division.
▪ Alpha
❖ Used to treat
hepatitis and
Kaposi’s sarcoma,
leukemias and
lymphomas.
❖ Produces rapidly
within 24 hours of
infection.
▪ Beta
❖ Treating multiple
sclerosis
▪ Gamma
❖ Mainly a T cell
product and
produced later, and
mounted NK cells.
• Transforming growth factor (TGF)

AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE

AIRA DIORELA CARE | BS MEDICAL LABORATORY SCIENCE