Overview of Immunology 2) memory response → body will remember

encountered pathogen from before & thus will

know what to do in its next encounter

❖ HISTORY OF IMMUNOLOGY

[Image of a Coronavirus being surrounded by antibodies or

Immunoglobulins (Ig)]

**SARS-CoV-2 (Severe Acute Respiratory Syndrome

Coronavirus 2) has changed the world and the way we
do things.
→ Our bodies have never encountered this pathogen
before, thus it is a complete stranger to our immune
system, therefore our body has no way of recognizing
this yet prior to its appearance & has no immunity
against it.
→ Our body is constantly waging war as we are
constantly in contact with several pathogens, but most
of them would not make us sick because our bodies
have encountered them before and now recognize
them and know how to attack.
● Immunity
- means “exemption” [e.g. exemption
from disease]
// Immunology started because humans began to
notice that fighting a disease becomes easier the
second time they get it.
//@Img is the great philosopher Thucydides -- he lived
during the plagues of the Peloponnesian wars & wrote
observations about the sickness.
-- Thucydides observed that those who survived the
plague were able to treat & tend to the sick w/o
worrying about catching the disease again ==
survivors of previous infection developed an
immunity to the same disease.
● From Variolation to Vaccination

// Our immune system, in order to respond to a

pathogen/ a foreign object has to be able to first
recognize it.

**Basis of immune responses = recognition of

non-cells or altered cells & our response to such.
// The Chinese & the Turks practiced variolation in the
Immune System Response
past. They ground up scabs from smallpox infected
1) effector response → eat/ phagocytose the
individuals & exposed the resulting powder to
pathogen; destroy it through cytotoxicity or
uninfected ones by blowing it to their nose and/or
overwhelm it. [one arm of immune response]
inserting such into small cuts in the skin.

MKP-- Immunology I BIO 141

[variolation = ancient form of vaccination]
-- Variolation poses a certain risk of ~2-3% mortality
rate in individuals who received such treatment.
-- Despite high risk of variolation, it is still practiced as
mortality rate from such is lower than the overall
15-20% mortality rate of the smallpox disease.
// Royalty (e.g. Lady Mary Wortley Montagu) had
observed the variolation process during her stay in
Turkey & brought the technique in England.
● Edward Jenner (1798) & the smallpox vaccine
//Variolation is different from the vaccination practice
conducted today as variation exposes individuals to
the same pathogen thus having higher risk (2-3%
mortality rate). In modern vaccination (as pioneered
by Jenner), a different (mostly lighter) strain of virus is
used.
→ variolation -- expose individuals w/ same strain as
the causal agent of disease (e.g. smallpox w/
smallpox)
→ vaccination -- expose individuals w/ lighter strain
than causal agent of disease (e.g. cowpox w/
smallpox)
MKP-- Immunology I BIO 141
// Modern vaccination is based on the experiments
done by Edward Jenner where he worked on smallpox.
→ Jenner’s observation == milkmaids who developed
cowpox disease similar to smallpox were found to not
be infected by the disease even when exposed to
such.
// To test his observation -- Jenner inoculated a young
boy w/ material from a cowpox pustule, & later
infected the child w/ smallpox.
→ Result == child did not develop smallpox
→ Findings == Infection w/ cowpox (a different but
related strain to smallpox) allowed child to develop
active immunity against smallpox.
Note: This experiment by Jenner cannot be directly
performed today as it is considered unethical by medical
standards.
// Active immunity is different from Passive immunity
● active immunity = exposure to pathogen/ any
strain related to such allowing for the body to
produce antibodies
● passive immunity = antibodies directly given
Note: Edward Jenner’s experiment is the origin of the
vaccination technique as observed to the term’s etymology.
→ “Vacca” = cow
● Louis Pasteur (1885) & the rabies vaccine
// Pasteur also worked on vaccines, specifically in
developing the rabies vaccine, as well as several
experiments w/ chicken cholera & sheep anthrax.
** Pasteur’s Experiment on Chicken cholera ❖ Immunity through Vaccination
== Prepared fresh culture of bacteria to inject in a normal,
healthy chicken, making it develop cholera.

== However, when he took a break & left the bacterial

culture after a long time, & injected the aged culture into
healthy chickens, he found that they were not infected with
cholera.

== Due to lack of funding, he reused the chicken he injected

w/ aged bacterial culture & though he injected it w/ fresh,
new cultures, he observed that the chicken were not
infected by cholera. While normal healthy chicken not
injected w/ aged culture were infected and died.
// Vaccination - deliberate introduction of an
Results: immunogen.
➢ Aged cholera culture → injected to healthy
chicken == not infected ❖ Immunogen
- anything w/c will trigger the immune
➢ Fresh cholera chicken → injected to chicken response. (e.g. -- as follows)
injected w/ aged culture == not infected
→ Attenuated pathogen (live, replicating, but not
➢ Fresh cholera culture → injected to healthy pathogenic) - e.g. when inoculate is left to die and
chicken == infected & died were used for vaccination [rabies vaccine]

// Aging weakened or attenuated the bacteria → Killed inactivated pathogen

→ Subunit (derived from/ parts of a pathogen)

**Discovery of Rabies Vaccine (Passive immunity)
// Young boy bitten by a rabid dog
→ Pasteur then inoculated young boy w/ series of
weakened/attenuated rabies virus from rabid rabbit
→ Young boy didn’t develop rabies & survived.
→ Recombinant (viral antigen produced in a host cell
& purified)
→ Peptides (synthetic fragments of antigen)

→ Vectored (viral pathogen expressed on a safe virus)

**Despite accidental discovery of vaccines, Jenner &
Pasteur still didn’t know the principle behind vaccination
→ Nucleic Acid (DNA or RNA coding for a viral protein
during that time.
& injected directly into body)

//Vaccination in the 20th Century is considered as one Route:

of the top ten achievements of public health
● Immunization
[a process to promote Immunity]
- important in eradicating a lot of
infectious diseases.
// As a result, vaccination programs have eliminated a
lot of infectious diseases (e.g. early childhood
diseases) w/ high risk of death.
- varies depending on type of pathogen & route
of infection
→ Injection (in the muscle [intramuscular] or under
the skin [intradermal]), nasal spray, oral drops/ aerosol
- these copies/mimic the way the pathogens
are naturally encountered.

MKP-- Immunology I BIO 141

 ❖ Effectivity of Vaccines
-- Can be seen from table how vaccines have almost
completely eradicated various early childhood diseases (e.g.
MMR, smallpox, diphtheria etc.) w/c otherwise have very
high mortality
● Immunization
- promotes active immunity
- trains the cells of the immune system
to recognize the virus as opposed to
passive immunity.
[passive immunity - antibodies are introduced]
-- e.g. injection of antivenom w/c are antibodies that
neutralize snake venom or anti-tetanus w/a are
antibodies w/c will neutralize the tetanus toxin]
[e.g. newborns receiving maternal antibodies w/c can
protect them during first few weeks after birth]
Q: What is the consequence of eradication of
diseases in vaccination programs if such is the goal?
- If universal vaccination is stopped/
discontinued, reintroduction of such
eradicated infections may occur due to a lack
of immunity in future generations.
//Universal vaccination should be continued to
procure herd immunity -- wherein infection of diseases
is eradicated in a population.
MKP-- Immunology I BIO 141
❖ Success of the Polio Vaccine
-- Polio == one of the most successful worldwide vaccination
programs. [@img, can be seen how compared to 1988
where a lot of countries (colored orange) still have polio
cases. In 2005, only a couple countries still had such cases &
in August 2020, Africa was already declared polio free.]
// September 2019 -- Polio outbreak in the Philippines
caused by vaccine derived polio w/c mutated from
oral vaccine containing an attenuated form of the
virus.
-- These mini outbreaks of Polio are a result of low
vaccination rates against the disease.
Note:
-- Live attenuated vaccines are commonly used as it is
the easiest to administer.
-- Killed virus - needs to be delivered through injection
& requires more qualified technicians w/c needs more
resources.
[Administration of killed virus is much required if the
goal is to completely eradicate all types of polio
infection globally]
→ Ultimate goal of eradication = polio-free world w/c
would not require vaccine anymore
**Consequence == if vaccine is not administered no
more, & a strain of polio virus is still present -- polio
infection then can always re-emerged & re-infect
unvaccinated population.
 ❖ Challenges of Vaccination Programs // Vaccine hesitancy → Drop in vaccination rates
→ Measles infection outbreak
(82% → 21% vaccine confidence of the population)

// Despite its contribution to public health, opposition to

vaccination has existed even during Jenner’s time

// 1998 -- Scientific Journal, Lancet, released an article

where they associated vaccines w/ autism

-- Though the article was debunked & retracted, the

damage was already done, causing increased vaccine
hesitancy during the 1990s.

// Anti-vaccination & Vaccine Hesitancy == one of the top

10 threats to global health (WHO 2019) along w/ other
threats related to immune system response

→ Vaccine Hesitancy in the Philippines became

prominent after the Dengvaxia (dengue vaccine)
controversy w/c was used as a political issue.

Note: Research in vaccine improvement &

development can be blown out of proportion & public // Vaccine design -- one of the challenges of vaccine
opinions formed based on how the news is recorded programs [e.g. dengue vaccine took over a decade to
than what it actually means. be designed due to characteristic of the virus itself]

● Vaccine Hesitancy -- delay in acceptance/ → Dengue vaccine failure == delayed vaccine release
refusal of vaccines despite availability of safe & failed application (e.g. Dengvaxia scare)
vaccination practices
MKP-- Immunology I BIO 141
 5) Release & Distribution
6) Vaccination process begins

Note: This process is for an already perfected flu vaccine

due to several years of prior development & application.

//Vaccine development is different for new/emerging

viruses or diseases (e.g. Covid-19) as more funding and
research is required for such.

// Problem in vaccine administration & type of

vaccine depending on type of pathogen it fights
against as challenges in vaccine programs.

→ Flu vaccines (for ex.) have to be taken annually

because of several strains of the influenza virus.

→ Flu vaccines -- developed towards a specific strain

as predicted by epidemiologists. // Vaccination as a practical & familiar way to
introduce immunology -- especially since it is a
● Flu vaccinations == killed virus & nasal sprays
product of studying immunology and/or our immune
w/c are a mixture of attenuated live virus
response.
// Several strains of flu virus → flu can be obtained
// Study of immunology is to understand how we can
from other influenza virus strains besides the specific
be immune and protect our body from foreign and/or
strain a vaccine is designed against.
altered substances/cells.
// Flu symptoms are also general, thus a different
**What do we want immunity from?
virus/infection may have caused this, thus the flu
- immunity from infections by pathogens
vaccine may not work.
[pathogens can be unicellular, multicellular etc.]
❖ WHO global influenza surveillance network [every living thing on earth is subject to infections]

❖ Major Forms of Pathogens

// Flu vaccine timeline -- begins a year before actual

implementation.
1) Viruses
1) Epidemiologists predict strains w/c will be
2) Bacteria
prevalent the coming year
3) Protozoa (Unicellular eukaryotes)
2) Production of vaccine begins
Multicellular Pathogens
3) Testing of Vaccine & Licensure
4) Parasitic worms (Helminths)
4) Production
5) Fungi
MKP-- Immunology I BIO 141
// Immunity is beyond the scope of vaccination
against infectious pathogens w/c are mostly
microorganisms.
// Since we live w/ microorganisms everyday, how
does our immune system respond to those organisms
w/c are helpful & beneficial.
❖ Immune Response
**Composed of 2 interconnected Systems
1) Innate Immune Responses
2) Adaptive Immune Responses
● Innate Immune Responses
- first line of defense
- existing/ in place response
- immediate response
● Adaptive Immune Responses
- activates when innate response
doesn’t work
- flexible & dynamic response
//Dynamic relationship or integration of both innate &
adaptive immune response gives a whole immunity
against pathogens w/c can cause diseases.
// Division into innate & adaptive immune response
== very traditional classification of immune responses
& we are currently seeing more & more overlaps &
interconnections bet. the two immune responses as
immunology research reveals more details.
MKP-- Immunology I BIO 141
// Immune responses as walls against infections
// Bodily immune response = have several
walls/defense in place so as to protect the self &
lessen the risk of exposure or infection from
pathogens.
● Innate Immunity
→ Comprised of both anatomical & chemical barriers
(e.g. Mucus, saliva. Stomach acids, skin etc.)
→ May have RNA systems (e.g. apoptosis, CRISPRs,
autophagy etc.)
→ May have innate immune cells (e.g. NK cells,
complement proteins etc. w/c attack a pathogen once
recognized)
● Adaptive immune response
(acquired immunity, a later response)
→ tailored towards specific antigens
→ memory put into place
Note: Recent research shows that innate immune
response do have a kind of memory but is very
different from memory of adaptive immune response
w/c allow you to have a faster & increased response
upon subsequent exposure to the same pathogen.
--Inflammation has been seen in recent years to be
important component of the immune response [both
protective & pathogenic in nature]

Note: Innate & Adaptive Immune System don’t
operate independently of each other. They are
interconnected & intertwined.
-- Both of them are required for a complete immune
response.
❖ Comparison between Innate & Adaptive
Immune Responses
→ naturally in place
→ immediate response (mins-hrs)
→ not specific, limited to recognizing general
molecular patterns (PAMPs/DAMPs etc.)
→ No strict memory [but still has some type of
remembering]
→ Identical response to repeat infections [due to little
remembering]
→ Has various components (e.g. anatomical &
physiological barriers, WBC [phagocytes, NKCs,
granulocytes etc.], Soluble components [e.g.
antimicrobial molecules], complement proteins etc)
→ Components of innate immune system recognizes
PAMPs & DAMPs [have Pattern Recognition Receptors
(PRRs)]

//Cytokines - often heard in immunology

→ are soluble signaling molecules w/c can mediate
responses bet. the components of innate immunity &
adaptive immunity, as well as between innate &
Main Criteria of Identifying bet. Innate & Adaptive
adaptive immunity.
Immune Responses:
1) Response Time -- how fast the response is
2) Specificity -- how specific the response is
3) Memory -- whether there is memory from the
response
4) Response to repeat infection -- does response
improve or become better?
5) Major Components

Innate Adaptive

Response Time Immediate Takes time (hrs-days)

(mins-hrs) @Img: shows light micrograph of the cross section through the
wall of the human intestine showing the villi
Specificity recognize general recognize specific
patterns, limited patterns, tailored
→ Innate immunity can have physical, chemical,
Memory none (doesn’t remembers attack
differentiate into of foreign
mechanical, anatomical & cellular defenses.
memory cells)
substance
(differentiate into
- Physical == e.g. skin
memory cell) - Chemical == digestive enzymes, mucosal
secretions etc.
Response to repeat response is identical Response becomes
or doesn’t change stronger in
- Mechanical == ciliary movements in
infection
succeeding infection respiratory tract, cough reflex etc.
to the same causal
agent - Anatomical
- Cellular == WBC, gut microflora
Major components

❖ Innate Immunity
MKP-- Immunology I BIO 141
→ Gut microflora -- promotes immunity by
preventing pathogenic bacteria from taking over the
body.

→ @Microvilli
-- have mucus secreting, goblet cells
[note: mucus can trap any microorganisms/ potential
pathogens]
-- have crypt where paneth cells reside
[paneth cells - secrete large quantities of antimicrobial
proteins]

Note: A lot of pathogens are encountered through the

respiratory tract or through the gut/ food that we eat. ● Inflammation
- soluble factors produced by immune
cells will recruit other immune cells &
draw fluid to the side of infection,
providing help for pathogen
eradication.

→ The presence of bacteria will cause histamine

release w/c causes vasodilation

→ Due to vasodilation, fluids can leak out through

● Phagocytosis
- Important component of the innate
immune response
Q: How does the WBC sense the presence of the
bacteria?
→ Pattern Recognition Receptors (PRRs) on
phagocytes recognize PAMPs on target cells.
→ This allows the WBC to recognize & bind to their
targets for phagocytosis.
[Ex. of PAMPs == peptidoglycan in bacteria]
-- Since our cells don’t have peptidoglycan, WBC or
phagocytes in the body, pathogens w/ this PAMP then
can be recognized as a foreign substance.
leaky capillaries w/c can contain soluble molecules
[e.g. complement proteins w/c can directly affect
immunity and/or destroy the target]
→ They can also produce signaling molecules
[e.g. chemokines] w/c will attract other white blood
cells [e.g. neutrophils, macrophages] to the site of
infection.
Note: In medicine, the four cardinal signs of
inflammation:
- Calor
- Dolor
- Rubor
- Tumor
// [heat, pain, redness, & swelling]
-- can notice these signs even in small insect bites

// Phagocytosis leads to a respiratory burst where you

have a production of highly toxic oxygen-derived
compounds w/c can help break down the
phagocytosed area.

MKP-- Immunology I BIO 141


● Complement Proteins
- a set of soluble serum proteins that
bind to PAMPs & initiate a cascade of
labeling & destruction events.
// A series of proteins w/c work in domino fashion ==
activation of one protein activates a complement
cascade w/c often leads to the lysis of the target.
[great example of the link bet. innate & adaptive
response]
❖ Adaptive Immune Response
● Adaptive immunity
→ takes longer time for response (hrs-days)
[this is because it is triggered by innate immune
response & also due to several processes before
having the effector function of the adaptive immunity]
→ very diverse compared to innate immunity
[diverse due to antigen specific receptors expressed
by cells of adaptive immunity] [e.g. B-cells produce Ig]
[T-cells produce T-cell receptors] Ig = immunoglobulins
//T-cell receptors & immunoglobulins recognize very
specific molecular patterns referred to as antigens
MKP-- Immunology I BIO 141
→ Adaptive immunity is also very dynamic == there is
improvement in response over time
→ There is memory == has memory cells w/c can last
throughout your entire lifetime to help recognize
subsequent encounters w/ the same pathogen.
→ Due to memory, response to repeat infection thus
is both more rapid & higher compared to 1st response
→ Major cellular components:
- Lymphocytes [e.g. T-cells & B-cells]
// The major cellular components of adaptive
immunity are the B-cells & T-cells & they recognize
the target through antigen specific receptors.
[Ex: Have a pathogen/virus & virus infected host cells]
→ The presence of the virus & the altered
virus-infected host cells can trigger innate immune
responses.This leads to triggering of the adaptive
immune responses
== B-cells can be activated so that they secrete
antibody w/c can recognize viruses
== T-cells can be activated so that they recognize
virus-infected cells, attacking them & preventing the
production of more viruses.
// Adaptive immunity is very specific in its recognition
of its targets & can recognize a diversity of targets. It
also has memory & it depends on the two
lymphocytes [B-cells & T-cells].
 // Key to the diversity of the molecular patterns that
the B- & T-cells recognize == expression of antigen
specific receptors.

// In your B-cells & T-cells → have genes w/c encode

antibody genes [e.g. Immunoglobulin (Ig) genes &
T-cell Receptors (TCRs)] undergoing random gene
rearrangement.

-- Note: This is a very special case known only from

the B- & T-cells precursors. They are the only known
site-specific DNA rearrangement in vertebrates.
// B- & T-cells originate & develop in primary (central)
lymphoid organs.
// Site-specific DNA rearrangement -- only happens in
→ All your blood cells will arise from hematopoietic/ their development in the primary lymphoid organs so
hemopoietic tissues in your bone marrow. that as they mature, they express a diversity of
receptors recognizing an equally diverse number of
→ Some of these hematopoietic stem cells (HSCs) will antigenic patterns.
follow the lymphoid lineage & develop into B-cells.
// As the B- & T-cells circulate in the body & encounter
→ Some HSCs, on the other hand, will migrate to the
antigen in the secondary or peripheral lymphoid
thymus where they mature as T-cells.
organs, antigens activate lymphocytes w/c express
// HSC -- where blood cells arise from receptors specific to it to expand or undergo rapid
proliferation.
-- B-cells → rise from HSC → lymphoid lineage
-- T-cells → rise from HSC → go to thymus ❖ Activation of B- & T- Cells
// The B- & T-cells then circulate in the system & in the
peripheral lymphoid organs [e.g. lymph nodes]
wherein they encounter your antigen & then are
activated so that they are able to perform their
effector functions.

[Effector functions]
- T-cell mediated immune responses
- Antibody responses

// Activation of B- & T- cells trigger changes in gene

expression. If morphology of B- & T-cells is observed, it
can be seen that their morphology is very similar at
rest. However, when they are activated or undergo an
activation process, changes in gene expression that
allow differentiation morphologically can be seen.

// One of the events that occur upon activation is the

expansion of the endoplasmic reticulum (gray area in
the img) due to the high protein expression &

MKP-- Immunology I BIO 141

secretion of effector B-cells w/c secrete the
antibodies.
→ Effector B-cells == plasma cells
// The T-cells, on one hand, express & secrete high
numbers of cytokines w/c are required for signaling to
B-cells or for cytotoxicity
// When B-cells mature in the primary lymphoid
organs in the bone marrow, they express a single type
of B-cell receptor or antibody w/c is membrane
bound.
→ Activation of B-cells as discussed, in essence,
caused them to differentiate into antibody-secreting
B-cells.
Note: The only difference bet. the surface antibody &
the soluble antibody would be the domains w/c will
encode the transmembrane region.
→ Naive B-cells
- cells that have never been exposed to antigen
MKP-- Immunology I BIO 141
// Exposure of B-cells to the antigen causes them to
proliferate & differentiate into either a population of
antibody-secreting effector cells [plasma cells] or into
memory cells.
// Memory cells are long-lived such that upon second
exposure to antigen the body will have a faster
response due to more memory cells existing to
recognize the pathogen.
// This clonal expansion & differentiation into
memory cells & effector cells is very similar in B-cells
& T-cells. -- The only exception is that for T-cells, they
do not secrete their T-cell receptors, rather they are
always membrane bound.
// In the image, the difference bet. A primary &
secondary response to an injected antigen can be
seen in terms of the amount of antibody produced.
→ Humoral response -- difference in primary &
secondary response to antigen.
Note: the response is called as such because your
antibody is soluble in your blood serum.
// Can be observed that the first immunization w/
antigen A will lead to an increase in antibody secreted
after ~10 days.
// Afterwhich, once the antigen is eliminated, there
will have a drop in the antibody production, however
the memory cells are still existing, such that during the
second immunization there will be both a faster
response (w/in <2 days will have a peak antibody
production), and also have a higher response == more
antibody produced in shorter amount of time.
// Humoral response reflects the phenomenon of
immunologic memory.
→ [In vaccination, this is why there are several
injection of a vaccine e.g. 1st injection & several
booster shots]
● MHC class I proteins
→ presents antigen thru CD8+ cytotoxic T-cells
● MHC class II proteins
→ presents antigen thru CD4+ helper T-cells

-- Goal of booster shots = increase no. of memory cells.

// The effector functions of these two cells [Th cell &

Tc cell] are very different.

→ MHCs play a role in antigen recognition by T-cells

// MHC Class I proteins -- present in all nucleated cells

// T-cell have two major populations [Th cell & Tc cell]:
● helper T- cells (Th cells)
● cytotoxic T-cells (Tc cells)
-- While the two [Th cell & Tc cell] are morphologically
difficult to differentiate from one another.
-- They can be differentiated biochemically via the
expression of cell surface proteins. [Aside from the
antigen-specific T-cell receptors, there is also the
expression of co-receptors for helper & cytotoxic
T-cells].
in the body & specialize in presenting antigens w/c
originate from the cytosol [e.g. spiral proteins
expressed by various infected cells]
// MHC Class II proteins -- specialize in presenting
antigens from extracellular origin w/c has been
phagocytosed by these antigen-presenting cells.
→ For effector functions
- Cytotoxic T-cells (Tc cells) when activated,
produce molecules w/c can cause cytotoxicity
in the target cell.

● CD4 co-receptor: expressed by Th cells - Helper T-cells (Th cells), on one hand, produce
● CD8 co-receptor: expressed by Tc cells cytokines w/c can help activate both the
cytotoxic T-cells & B-cells.
// The antigens w/c are recognized by the T-cell
// These antigen-presenting cells (APCs) are very
receptor are not soluble antigens. Rather they are
important in the role for activating your T-cells
antigens w/c have been processed by antigen-
especially those antigen-presenting cells w/c activate
presenting cells & presented as bound to Major
helper T-cells as they produce cytokines w/c help
Histocompatibility Complex (MHC) proteins.
activate other arms of the adaptive immunity.
→ Types of MHC proteins
[there are several types but focus on ff:]
● MHC class I
● MHC class II

MKP-- Immunology I BIO 141


[Can see in img -- an antigen-presenting cell (darker)
associating w/ a T-lymphocyte, showing a presentation
of antigen on MHC molecules recognized by your TCRs
& CD co-receptors]
● “Professional” APCs [w/c express class II MHC]
1) Macrophages
2) Dendritic cells
3) B-cells
Note: While all nucleated cells express MHC class I
molecules, “professional” APCS [e.g. macrophages,
dendritic cells & B-cells] can all express MHC class II
molecules w//c can help activate helper T-cells.
Note: Adaptive immunity w/c includes your B- & T- cell
responses go hand in hand.
// Immune system & response == vertebrate immune
responses.
→ Two arms of Adaptive Immunity
● Humoral response (B-cell response)
● Cell-mediated response (T-cell response)
MKP-- Immunology I BIO 141
-- In the img, it can be seen that if there are foreign
proteins/ infectious agents w/c are introduced into the
vertebrate body & recognized by antibodies or
Immunoglobulins (Igs) & T-cell receptors.
→ This activates the naive B- & T-cells -- causing them
to proliferate & differentiate.
● Humoral response
→ B-cells will differentiate into memory cells &
effector plasma cells w/c secrete antibody to target
the antigen for elimination
● Cell-mediated response
→ The antigen binding to the T-cell receptor
[presented by proper APCs expressing the MHC mol.]
will cause helper T-cells to secrete cytokines w/c will
activate both the B-cell & the other T-cell responses
→ Cytotoxic T-cells, once activated by antigen
presented on the correct MHC molecule, causes them
to differentiate into cytotoxic cells w/c can lead to the
killing of the target cell [whether infected/altered cells
e.g. cancer cells etc.]
// How innate immune responses come into play first
but may not be enough to clear the infections, thus
they recruit the adaptive immune responses to help
out.
→ @Img -- Can see the virus (yellow @top) being
ingested by (“professional”) antigen-presenting cells
w/c breaks it down & presents a viral peptide to the
helper T-cell.
→ Helper T-cell then produce cytokines for B-cells to
produce antibodies w/c can neutralize the virus.

→ While cytotoxic T-cells produce molecules w/c will

target the infected cells for destruction -- preventing
production of more virus particles.

// Aside from effector (B- & Tc cells) cells, there is also

differentiation into long-lived memory cells → allows
the body to recognize the virus for even an entire
lifetime after having first been introduced to the virus.
// The study of immunology isn’t just about dealing w/
infectious diseases/ pathogens. There are also several
microbes in our body, & our immune system
recognizes them as foreign as they may express the
same Microbe Associated Molecular Patterns (MAPs)
[since not all microbes are pathogens].

→ Ex) Our gut microbiota has been shown to be very

important in providing homeostasis. Balanced &
diverse microbiome has been shown to contribute to
better overall health. While less diverse & balanced
microbiomes have a negative impact on health.

[Microbiome has been shown to have impacts on

immune related conditions e.g. inflammation &
autoimmune disease & even in the non-immune
development of our neurological function]

// Because our microbiota are still foreign cells --

→ How then does our immune response balance
their recognition?

→ How do these helpful bacteria prevent the

Note: Adaptive immune responses are recruited by immune response from eliminating them so that they
the innate immune responses. can contribute to our overall health?

● Immune System beyond infectious diseases

// Look at other conditions affected by our immune

system [e.g. immune dysfunction]

MKP-- Immunology I BIO 141

 ● Immune Dysfunction // Response to common environmental allergen can
→ improper regulation of immune responses will be very serious [aside from discomfort of allergic
cause the system to either attack something it response] as it can lead to blocking due to
shouldn’t or fail to attack something it should. overproduction of mucus.

- hypersensitivities (e.g. allergies, asthma) -- → In essence, because of the inflammation mediated

have hypersensitivity than protection by these molecules it can cause mucus production
- graft rejection vs host disease -- significant causing airways to plug & have difficulty breathing.
because we have medical organ [This happens to asthmathic patients]
transplantation
- immunodeficiencies -- caused by an infectious
agent/ a genetic condition
- autoimmune diseases -- immune system fails
to recognize your cells

// Sometimes the immune system is deficient &

doesn’t work in a correct way. [may be due to a
genetic condition]

● Severe Combined Immunodeficiency (SCID)

-- there is impairment of the B- & T-cell responses
// Allergies == can have symptoms w/ discomfort
because of a non-functional ADA enzyme w/c is
(e.g. wheezing, sneezing, runny nose, watery eyes
required for the cell's development.
etc.)
-- people who have SCID are very prone to disease
// Allergens -- common environmental antigens to w/c
we should not have an immune reaction to [i.e. David Vetter - a famous SCID patient who lived in
[i.e. pollens, milk proteins, shell fish etc.] a plastic bubble, preventing him from coming in
contact w/ normal pathogens to avoid infections.
-- Reaction to these products occurs because your
allergens will bind to a specific type of
// At present, SCID patients can now be injected w/
immunoglobulin (Ig) w/c is recognized by the mast
ADA enzymes to cope. There are also genetic therapy
cell.
treatments for SCID.
→ This causes the mast cells to release compounds
w/c are the mediators of said symptoms of wheezing, Note: David Vetter died at a young age
sneezing etc.

// Normally, these compounds are directed towards

parasites, but in this case, they are triggered by
common environmental antigens.
MKP-- Immunology I BIO 141

// Aside from genetic conditions, there is also
immunodeficiency caused by infectious disease [e.g.
Human Immunodeficiency Virus (HIV)].
// Infections w/ HIV can lead to acquired
immunodeficiency syndrome (AIDS), because the HIV
attacks the T-cells.
// w/o the T-cells, the body becomes very prone to
opportunistic infections w/c the body normally can’t
combat.
Note: AIDS patients often die from simple
complications from pneumonia & other infectious
diseases.
-- This is of great concern because the Philippines still
has a very high rate of HIV.
// When we want to hide allergens & we want our
immune presence to be defficient.
MKP-- Immunology I BIO 141
[eg. We want to hide foreign tissue from our
immune system when we have transplants]
-- There are several common medical transplants;
each of them requires a precise matching bet. donor
and recipient.
→ You have to suppress the immune response to
increase the chances of accepting the graft.
● Corneal Transplants
→ You don’t need immunosuppression bec the cornea
enjoys immune privilege.
[Thus, you don’t need to have matching corneal
donors & recipients]
// In transplants, you have risk of either 1) graft
rejection -- thus the recipient antibodies will attack the
donor graph
// Can also have 2) graft versus host disease. → Any
antibodies left on the graft because it wasn’t perfused
completely will attack the host.

// Since there’s an under supply of organ transplants
available, xenotransplantation then is looked into as
an alternative w/c increases the risk of graft rejection.
→ Xenotransplantation - the process of grafting or
transplantation of living cells, tissues, or organs from
one species to another.
// However, with today’s technologies of genetic
engineering, some of the risk of xenotransplantation
can actually be minimized already.
❖ When immune system targets itself
MKP-- Immunology I BIO 141
● Autoimmunity
- happens when the immune system
targets itself [eg. rheumatoid arthritis]
// Rheumatoid arthritis
→ an autoimmune diseases where the connective
tissue is being attacked and there is severe
inflammation & can be very painful
-- Inflammatory Diseases have also now been related
w/ several other lifestyle & genetic diseases. As such
the study of the inflammatory response is currently a
very active field.
❖ When immune system is both friend & foe
// We can have the immune system both being friend
& foe not only w/ regards to the inflammatory
response but can also be in response to cancer.
→ Immune Response to Cancer
- It was shown that the immune response to
cancer can have both healing &
disease-promotion/inducing characteristics
// Mind Map of some of the key principle of immunology
Glossary/ Abbreviations:
● Immune Response (IR)
● Immunoglobulins (Ig)
● Antibodies (Ab)
● T-cell Receptors (TCRs)
● B-cell Receptors (BCRs)
● Pathogen-Associated Molecular Patterns
(PAMPs)
● Microbial Associated Patterns (MAPs)
● Damage Associated Molecular Patterns
(DAMPs)
● Pattern Recognition Receptors (PRRs)
● Dendritic Cells (DCs)
● Natural Killer Cells (NK Cells)
● Antimicrobial Peptides (AMPs)

MKP-- Immunology I BIO 141