The Immune System
The
Immune
System
• The immune system is the complex
collection of cells and organs that destroys
or neutralizes pathogens that would
otherwise cause disease or death.
• The immune system is a collection of
barriers, cells, and soluble proteins that
interact and communicate with each other
in extraordinarily complex ways.
• The modern model of immune function is
organized into three phases based on the
timing of their effects.
The Immune
System
•The three temporal
phases:
• Barrier defenses
• Innate immune
responses
• Adaptive immune
responses
Barrier
Defenses
• Physical barriers that
prevent pathogens from
either entering the body,
destroy them after they
enter, or flush them out
before they can establish
themselves in the body’s
soft tissues.
• They are not a response to
infections.
• Associated with the external
surfaces of the body, where
pathogens may try to enter
Barrier
Defenses
• Skin: covered with layers of
dead, keratinized epithelium
prevent bacterial invasion.
• Additionally, sweat and other
skin secretions may lower pH,
contain toxic lipids, and
physically wash microbes
away.
• The mucus layer of the
gastrointestinal tract,
respiratory tract, reproductive
tract, eyes, ears, and nose
traps both microbes and
debris, and facilitates their
removal.
Innate
Immune
Response
•Rapid but nonspecific
response and consists of
a variety of specialized
cells and soluble factors.
Adaptive
immune
response
•Slower but more
specific and effective.
Involves many cell types
and soluble factors but
is primarily controlled by
white blood cells
(leukocytes) known as
lymphocytes, which
help control immune
responses.
The Immune
System
• Innate and adaptive immune
defenses can recognize and deal
with the same pathogens, but the
difference is the intensity and
effectiveness of the response.
• Both responses are intertwined -
not separate responses.
• Each type has a different pathway
of activation.
• Innate immune responses can
alert cells of adaptive immune
responses.
Immune
System Cells
• Immune cells arise in the bone marrow
from the same hematopoietic stem cells
responsible for RBC production.
• These cells can be divided into three
classes based on function:
• Phagocytic cells, which ingest
pathogens to destroy them.
• Lymphocytes, which specifically
coordinate the activities of adaptive
immunity.
• Cells containing cytoplasmic
granules, which help mediate
immune responses against parasites
and intracellular pathogens(viruses).
Immune
System
Cells
Phagocytic
cells
• Three major phagocytic cells:
Macrophages, neutrophils, and
dendritic cells
• Macrophages move through
tissues and squeeze through
capillary walls. *Can evolve to
cooperate with lymphocytes as part of the
adaptive immune response.
• Can be freely roaming through
the body or fixed in certain
tissues.
Phagocytic
cells
• A neutrophil is a phagocytic cell that
is attracted via chemotaxis from the
bloodstream to infected tissues.
Their granules contain a variety of
vasoactive mediators such as
histamine. They play a role in the
adaptive immune response as well.
• A monocyte is a circulating
precursor cell that differentiates into
either a macrophage or dendritic cell,
which can be rapidly attracted to
areas of infection by signal molecules
of inflammation.
Natural
Killer Cells
• NK cells are a type of lymphocyte that
can induce apoptosis(cell death).
• This can be done by two ways:
• NK cells can respond to chemical
signals and eventually sending
apoptotic signal to the cell.
• The granules of the NK cells
release perforins to open a
channel in plasma membrane and
granzymes that goes into the cell
and induce apoptosis from inside.
Inflammator
y Response
• The hallmark of the innate immune
response is inflammation.
• Can be initiated by an infection or tissue
injuries.
• The inflammatory reaction brings in
phagocytic cells to the damaged area to
clear cellular debris and to set the stage for
wound repair.
• This reaction also brings in the cells of the
innate immune system, allowing them to
get rid of the sources of a possible infection.
• This action helps to isolate the site, limiting
the spread of the pathogen.
Inflammato
ry Response
Inflammato
ry Response
• Acute inflammation is a short-term
inflammatory response to an insult to the
body.
• Chronic inflammation is ongoing
inflammation. It can be caused by foreign
bodies, persistent pathogens, and
autoimmune diseases such as rheumatoid
arthritis or lupus.
Soluble
Mediators
of the
Innate
Immune
Response
• A cytokine is signaling molecule that allows
cells to communicate with each other over
short distances.
• Interferons are secreted by cells infected
with viruses. Interferons travel to adjacent
cells and induce them to make antiviral
proteins to defend them against the coming
virus.
• The complement system is a series of
proteins found in the blood plasma. They
can kill the pathogen by fusing digestive
enzymes into it. They can also activate the
adaptive immune system.
The
Adaptive
Immune
Response
• The immune system’s first exposure to a
pathogen is called a primary adaptive
response.
• Upon re-exposure to the same pathogen, a
secondary adaptive response is
generated, which is stronger and faster
that the primary response. This secondary
response is the basis of immunological
memory.
• Self-recognition: the ability to distinguish
between self-antigens, those that are
normally present in the body, and foreign
antigens, those that might be on a
potential pathogen.
The Adaptive
Immune
Response
• Two ways of adaptive
immune responses:
Humoral immunity:
involves release of
antibodies by B cells.
Cellular immunity:
involves interaction with
cells by T cells
Both types need
antigens to be activated.
Antigens
• Identification markers
that can be displayed
on cell surfaces.
• Can be proteins or
toxins within
circulating blood or
lymph
Antigens
• Used by lymphocytes to
detect foreign cells entering
the body.
• Without antigens, there
is no adaptive immune
responses.
• Antigens have antigenic
determinants that can be
detected by one antibody.
• Several antibodies can
bind one antigen
Cell (normal or cancerous),
Bactria, virus, pollen, …etc.
Antigens
B cell
Antibodies
Antigens
• T cells only recognize antigen on the
surface of specialized cells called antigen-
presenting cells (APCs).
• Macrophages, dendritic cells, and B
cells are APCs
• Antigens presented by these cells using a
specific protein known as a major
histocompatibility complex (MHC)
molecule.
• Two distinct types MHC class I and MHC
class II.
• MHC-I presented on all nucleated
cells of the body.
• MHC-II presented only on antigen
presenting cells
Cells of the
Adaptive Immune
Responses
• Adaptive immune system involves
three types of cells
• Two major types of lymphocytes
• B lymphocytes (B cells) in
humoral immunity.
• T lymphocytes (T cells
CD4+ & CD8+) in cellular
immunity
• Recent evidence
suggest NK cells as
well
• Antigen-presenting cells (APCs)
• Macrophages, dendritic
cells, and B cells
• Display antigens on MHC-II
Lymphocytes
Development
•Lymphocytes undergo three processes before
they become active.
• Development: T and B lymphocytes both
develop in the bone marrow (primary
lymphoid organ).
• Maturation: in this process, lymphocytes
learn how to recognize self-antigen (self-
tolerance) and foreign-antigen
• B cells mature in the bone marrow
• T cells mature in thymus
• Activation: in lymph nodes and blood,
lymphocytes recognize the foreign
antigen and trigger the adaptive immune
response
Antigen-
Presenting
Cells (APCs)
• Main function is to present
antigens to lymphocytes.
• Recognize foreign antigen,
engulf them and process
them. They then “display”
the processed antigen
pieces on their surface.
• Major types
• Dendritic cells
• Macrophages
• B cells
T Cell-Mediated
Immune
Responses
• T cells induce cell mediated immune
response.
• Several subtypes: helper, cytotoxic and
regulatory T cells
• Each subtype performs different functions
and in different locations within the body.
• Helper and cytotoxic cells are based on
CD4 or CD8 markers that a cell can display
upon leaving the thymus.
• Regulatory T cells regulate and suppress
the immune response to not spiral out of
control and cause autoimmune diseases.
T Cell-Mediated
Immune
Responses
• CD8 cells: develop to be
cytotoxic T cells (Tc).
• Kill target cells by
inducing apoptosis(cell
death) using the same
mechanism as NK cells.
• Activated by cytokines
released by helper T
cells.
T Cell-Mediated
Immune
Responses
• Target cells for cytotoxic T cells
include:
• Cancer cells
• Virus infected cells
• Foreign cells (organ
transplants and wrong
blood transfusion)
• Cells with parasites
• A small number of the activated
Tc cells turn into memory cells
and remain dormant until a
subsequent recognition of the
same antigen.
T Cell-Mediated
Immune
Responses
• Activated Tc cells, bind
to MHC-I on APCs.
• This binding enables
them to recognize the
antigen.
• Next, they search the
body for cells displaying
the same antigen and
destroy them in a similar
mechanism to NK cells.
T Cell-Mediated
Immune
Responses
• CD4 cells: develop to
be helper T (TH)cells.
• Function by secreting
cytokines that act to
enhance other
immune responses.
• Recognize antigens on
MHC-II, then release
cytokines that activate
cytotoxic T cells.
T Cell-Mediated
Immune
Responses
• The cytokines from
TH(helper) cells attract
TC(cytotoxic) cells to the
infection site, and cause
them to bind to the APCs’
MHC-I
• Small number of the
activated TH cells turn
into memory cells and
remain inactive until the
next recognition of the
same antigen.
B
Humoral-
Mediated
Immune
Response
s
• B cells induce humoral immune response.
The humoral response is a type of adaptive
immunity that relies on B cells and antibodies
to fight off.
• They produce and release antibodies that
attach and neutralize or agglutinate antigens.
• There are five different classes of antibody in
humans: IgM, IgD, IgG, IgA, and IgE. Each one
has specific functions in the immune
response.
• B cells do not recognize antigen in the
complex fashion of T cells.
• B cells can recognize native, unprocessed
antigens and do not require the participation
of MHC molecules and antigen-presenting
cells.
Antibody
Structure
• Antibodies are
glycoproteins consisting of
two types of polypeptide
chains with attached
carbohydrates: the heavy
chain and the light chain.
• The main differences
between the classes of
antibodies are in the light
chain, as they form part of
the antigen-binding site on
the antibody molecules.
Five Classes of
Antibodies and
their Functions
• IgM consists of 5 four-
chain structures.
• IgM is the largest of the
antibody molecules.
• IgM is usually the first
antibody made during a
primary response.
• Very effective antibody
against bacteria at early
stages of a primary
antibody response.
Five Classes of
Antibodies and
their Functions
• IgG is a major antibody of late
primary responses and the
main antibody of secondary
responses in the blood.
• IgG is a monomeric(one
molecule) antibody that clears
pathogens from the blood and
can activate complement
proteins.
• It can cross the placenta to
protect the developing fetus.
• It can exit the blood to the
interstitial fluid to fight
extracellular pathogens.
Five Classes of
Antibodies and
their Functions
• IgA exists in 2 forms, a four-
chain monomer in the blood
and an eight-chain structure,
or dimer.
• It is the only antibody to leave
the interior of the body to
protect body surfaces like
skin and mucous membranes.
• IgA is important to newborns,
because it is present in
mother’s breast milk and can
protect the infant from
disease.
Five Classes of
Antibodies and
their Functions
• IgE is usually associated with
allergies.
• It is present in the lowest
concentration in the blood
• If a person is allergic to
peanuts, there will be
peanut-specific IgE bound to
his or her mast cells.
• In this person, eating
peanuts causes IgE to force
mast cells to release the
content of their granules,
sometimes causing severe
allergic reactions that can
cause death(anaphylaxis).
Five Classes of
Antibodies and
their Functions
• IgD is found on the
surface of B cells.
• IgD is secreted into the
bloodstream and other
bodily fluids, although in
smaller amounts than
other antibody classes
• IgD is typically co-
expressed with IgM on
the surface of mature B
cells
B Cell
Activation
• B cells are developed and mature
in the bone marrow and are
activated by binding to antigens
in the lymph nodes.
• Once they are activated, they
develop into Plasma cells.
• Plasma cells are the B cells that
are committed to produce a
specific antibody against a
specific antigen.
• Plasma cells lifespan are only a
few days until the infection is
gone. Some of the activated B
cells will turn into memory cells.
B Cell
Activation
• Initial exposure to the
foreign antigen is
considered a primary
response.
• A second exposure to
the same antigen
induces a secondary
response, which is
initiated by the memory
cells developed from the
primary response.
Primary versus
Secondary
Responses
• The primary response
is delayed by several
days due to the time it
takes for the B cell to
develop into plasma
cells.
• The level of antibody
produced is low, but it
is sufficient for
immune protection.
Primary versus
Secondary
Responses
• With the secondary
response, there is no
time delay, and the
amount of antibody
made is much higher.
• Thus, the secondary
antibody response
overwhelms the
pathogens quickly and,
in most situations, no
symptoms are felt.
B Cell
Activation
• In a few cases, B cells will
need the T helper cells to
be activated.
• B cell will present the
antigen to TH cell, which in
turn will release cytokines
to activate the B cell.
• Thus, the B cell receives
signals from both its
surface antibody and the T
cell via its cytokines.
Active and
Passive
Immunity
• Active immunity is the resistance to
pathogens acquired during an adaptive
immune response within an individual.
• Naturally acquired active immunity, the
response to a pathogen that naturally
invaded the body.
• Artificially acquired active immunity is
when the pathogen is introduced to the
body as the example of vaccines.
• A vaccine is a killed or weakened
pathogen or its components that, when
administered to a healthy individual,
leads to the development of
immunological memory (a weakened
primary immune response) without
causing much in the way of symptoms.
Active and
Passive
Immunity
• Passive immunity arises from the transfer
of antibodies to an individual without
requiring them to mount their own active
immune response.
*No antigen involved therefore no
immunological memory, and it is only effective
for short period of time.
• Naturally acquired is seen during fetal
development and breast feeding. Antibodies
cross the placenta or passed with milk
protect the fetus/baby from infection for the
first few months of its life.
• Artificially acquired usually involves
injections of immunoglobulins taken from
animals previously exposed to a specific
pathogen.
Humoral
Immunity
Active Passive
Naturally
acquired:
infection
Artificially
acquired:
vaccines
Artificially
acquired:
injection
of
antibodie
s
develope
d outside
Naturally
acquired:
during
pregnancy
and
breastfeedin
g
Active and Passive Immunity
Immunodeficienci
es
• Acquired immune deficiency
syndrome (AIDS)
• A result of human
immunodeficiency virus (HIV)
that targets the helper T cells.
• HIV uses CD4 as the receptor to
get inside cells.
• Treatment for the disease
consists of drugs that target
virally encoded proteins that are
necessary for viral replication,
but are absent from normal
human cells.
Autoimmu
ne Diseases
• Immune cells lose their
tolerance to self-cells and
start to attack them.
• Unknown reason but
severe consequences.
• Treatments are usually
based on resolving the
symptoms using
immunosuppressive and
anti-inflammatory drugs
such as steroids.
Autoimmu
ne
Diseases
(cont.)
Hypersensitivitie
s
• The word “hypersensitivity” simply means
sensitive beyond normal levels of activation.
• The immune system is stimulated and ready
to initiate a complex immune response even
with minimum exposure to antigens.
• Four types based on the way they occur.
Hypersensitivitie
s
• Type I involves the mast cells releasing
histamine
• Type II involves the complement system
and happens with mismatched blood
transfusion
• Type III is when the antibody and antigen
precipitate in blood vessels and cause
inflammation
• Type IV is a delayed hypersensitivity. T
helper cells take extra time to activate
cytotoxic T cells.
References
• Contanzo, L. (2021). Contanzo Physiology. (7th, Ed.) Philadephia: Elsevier.
• Hall, J., & Hall, M. (2020). Guyton and Hall Textbook of medical physiology.
(14th, Ed.) Philadelphia: Saunders.
• Justiz Vaillant, A. A., Sabir, S., & Jan, A. (2024). Physiology, Immune
Response. Statpearls.
• Rice University. (2025, June 4). Anatomy of the Lymphatic and Immune
Systems. Retrieved from Rice University:
https://openstax.org/books/anatomy-and-physiology-2e/pages/21-1-
anatomy-of-the-lymphatic-and-immune-systems
• University of Hawaii. (2024, May). Immunology. Retrieved from University
of Hawaii:
https://pressbooks-dev.oer.hawaii.edu/anatomyandphysiology2021/chapte
r/22-immunology/

Immune_2_nursing_physiology_advance.pptx

  • 1.
  • 2.
    The Immune System • The immunesystem is the complex collection of cells and organs that destroys or neutralizes pathogens that would otherwise cause disease or death. • The immune system is a collection of barriers, cells, and soluble proteins that interact and communicate with each other in extraordinarily complex ways. • The modern model of immune function is organized into three phases based on the timing of their effects.
  • 3.
    The Immune System •The threetemporal phases: • Barrier defenses • Innate immune responses • Adaptive immune responses
  • 4.
    Barrier Defenses • Physical barriersthat prevent pathogens from either entering the body, destroy them after they enter, or flush them out before they can establish themselves in the body’s soft tissues. • They are not a response to infections. • Associated with the external surfaces of the body, where pathogens may try to enter
  • 5.
    Barrier Defenses • Skin: coveredwith layers of dead, keratinized epithelium prevent bacterial invasion. • Additionally, sweat and other skin secretions may lower pH, contain toxic lipids, and physically wash microbes away. • The mucus layer of the gastrointestinal tract, respiratory tract, reproductive tract, eyes, ears, and nose traps both microbes and debris, and facilitates their removal.
  • 6.
    Innate Immune Response •Rapid but nonspecific responseand consists of a variety of specialized cells and soluble factors.
  • 7.
    Adaptive immune response •Slower but more specificand effective. Involves many cell types and soluble factors but is primarily controlled by white blood cells (leukocytes) known as lymphocytes, which help control immune responses.
  • 8.
    The Immune System • Innateand adaptive immune defenses can recognize and deal with the same pathogens, but the difference is the intensity and effectiveness of the response. • Both responses are intertwined - not separate responses. • Each type has a different pathway of activation. • Innate immune responses can alert cells of adaptive immune responses.
  • 9.
    Immune System Cells • Immunecells arise in the bone marrow from the same hematopoietic stem cells responsible for RBC production. • These cells can be divided into three classes based on function: • Phagocytic cells, which ingest pathogens to destroy them. • Lymphocytes, which specifically coordinate the activities of adaptive immunity. • Cells containing cytoplasmic granules, which help mediate immune responses against parasites and intracellular pathogens(viruses).
  • 10.
  • 11.
    Phagocytic cells • Three majorphagocytic cells: Macrophages, neutrophils, and dendritic cells • Macrophages move through tissues and squeeze through capillary walls. *Can evolve to cooperate with lymphocytes as part of the adaptive immune response. • Can be freely roaming through the body or fixed in certain tissues.
  • 12.
    Phagocytic cells • A neutrophilis a phagocytic cell that is attracted via chemotaxis from the bloodstream to infected tissues. Their granules contain a variety of vasoactive mediators such as histamine. They play a role in the adaptive immune response as well. • A monocyte is a circulating precursor cell that differentiates into either a macrophage or dendritic cell, which can be rapidly attracted to areas of infection by signal molecules of inflammation.
  • 13.
    Natural Killer Cells • NKcells are a type of lymphocyte that can induce apoptosis(cell death). • This can be done by two ways: • NK cells can respond to chemical signals and eventually sending apoptotic signal to the cell. • The granules of the NK cells release perforins to open a channel in plasma membrane and granzymes that goes into the cell and induce apoptosis from inside.
  • 14.
    Inflammator y Response • Thehallmark of the innate immune response is inflammation. • Can be initiated by an infection or tissue injuries. • The inflammatory reaction brings in phagocytic cells to the damaged area to clear cellular debris and to set the stage for wound repair. • This reaction also brings in the cells of the innate immune system, allowing them to get rid of the sources of a possible infection. • This action helps to isolate the site, limiting the spread of the pathogen.
  • 15.
  • 16.
    Inflammato ry Response • Acuteinflammation is a short-term inflammatory response to an insult to the body. • Chronic inflammation is ongoing inflammation. It can be caused by foreign bodies, persistent pathogens, and autoimmune diseases such as rheumatoid arthritis or lupus.
  • 17.
    Soluble Mediators of the Innate Immune Response • Acytokine is signaling molecule that allows cells to communicate with each other over short distances. • Interferons are secreted by cells infected with viruses. Interferons travel to adjacent cells and induce them to make antiviral proteins to defend them against the coming virus. • The complement system is a series of proteins found in the blood plasma. They can kill the pathogen by fusing digestive enzymes into it. They can also activate the adaptive immune system.
  • 19.
    The Adaptive Immune Response • The immunesystem’s first exposure to a pathogen is called a primary adaptive response. • Upon re-exposure to the same pathogen, a secondary adaptive response is generated, which is stronger and faster that the primary response. This secondary response is the basis of immunological memory. • Self-recognition: the ability to distinguish between self-antigens, those that are normally present in the body, and foreign antigens, those that might be on a potential pathogen.
  • 20.
    The Adaptive Immune Response • Twoways of adaptive immune responses: Humoral immunity: involves release of antibodies by B cells. Cellular immunity: involves interaction with cells by T cells Both types need antigens to be activated.
  • 21.
    Antigens • Identification markers thatcan be displayed on cell surfaces. • Can be proteins or toxins within circulating blood or lymph
  • 22.
    Antigens • Used bylymphocytes to detect foreign cells entering the body. • Without antigens, there is no adaptive immune responses. • Antigens have antigenic determinants that can be detected by one antibody. • Several antibodies can bind one antigen
  • 23.
    Cell (normal orcancerous), Bactria, virus, pollen, …etc. Antigens B cell Antibodies
  • 24.
    Antigens • T cellsonly recognize antigen on the surface of specialized cells called antigen- presenting cells (APCs). • Macrophages, dendritic cells, and B cells are APCs • Antigens presented by these cells using a specific protein known as a major histocompatibility complex (MHC) molecule. • Two distinct types MHC class I and MHC class II. • MHC-I presented on all nucleated cells of the body. • MHC-II presented only on antigen presenting cells
  • 25.
    Cells of the AdaptiveImmune Responses • Adaptive immune system involves three types of cells • Two major types of lymphocytes • B lymphocytes (B cells) in humoral immunity. • T lymphocytes (T cells CD4+ & CD8+) in cellular immunity • Recent evidence suggest NK cells as well • Antigen-presenting cells (APCs) • Macrophages, dendritic cells, and B cells • Display antigens on MHC-II
  • 26.
    Lymphocytes Development •Lymphocytes undergo threeprocesses before they become active. • Development: T and B lymphocytes both develop in the bone marrow (primary lymphoid organ). • Maturation: in this process, lymphocytes learn how to recognize self-antigen (self- tolerance) and foreign-antigen • B cells mature in the bone marrow • T cells mature in thymus • Activation: in lymph nodes and blood, lymphocytes recognize the foreign antigen and trigger the adaptive immune response
  • 27.
    Antigen- Presenting Cells (APCs) • Mainfunction is to present antigens to lymphocytes. • Recognize foreign antigen, engulf them and process them. They then “display” the processed antigen pieces on their surface. • Major types • Dendritic cells • Macrophages • B cells
  • 28.
    T Cell-Mediated Immune Responses • Tcells induce cell mediated immune response. • Several subtypes: helper, cytotoxic and regulatory T cells • Each subtype performs different functions and in different locations within the body. • Helper and cytotoxic cells are based on CD4 or CD8 markers that a cell can display upon leaving the thymus. • Regulatory T cells regulate and suppress the immune response to not spiral out of control and cause autoimmune diseases.
  • 29.
    T Cell-Mediated Immune Responses • CD8cells: develop to be cytotoxic T cells (Tc). • Kill target cells by inducing apoptosis(cell death) using the same mechanism as NK cells. • Activated by cytokines released by helper T cells.
  • 30.
    T Cell-Mediated Immune Responses • Targetcells for cytotoxic T cells include: • Cancer cells • Virus infected cells • Foreign cells (organ transplants and wrong blood transfusion) • Cells with parasites • A small number of the activated Tc cells turn into memory cells and remain dormant until a subsequent recognition of the same antigen.
  • 31.
    T Cell-Mediated Immune Responses • ActivatedTc cells, bind to MHC-I on APCs. • This binding enables them to recognize the antigen. • Next, they search the body for cells displaying the same antigen and destroy them in a similar mechanism to NK cells.
  • 32.
    T Cell-Mediated Immune Responses • CD4cells: develop to be helper T (TH)cells. • Function by secreting cytokines that act to enhance other immune responses. • Recognize antigens on MHC-II, then release cytokines that activate cytotoxic T cells.
  • 33.
    T Cell-Mediated Immune Responses • Thecytokines from TH(helper) cells attract TC(cytotoxic) cells to the infection site, and cause them to bind to the APCs’ MHC-I • Small number of the activated TH cells turn into memory cells and remain inactive until the next recognition of the same antigen.
  • 34.
    B Humoral- Mediated Immune Response s • B cellsinduce humoral immune response. The humoral response is a type of adaptive immunity that relies on B cells and antibodies to fight off. • They produce and release antibodies that attach and neutralize or agglutinate antigens. • There are five different classes of antibody in humans: IgM, IgD, IgG, IgA, and IgE. Each one has specific functions in the immune response. • B cells do not recognize antigen in the complex fashion of T cells. • B cells can recognize native, unprocessed antigens and do not require the participation of MHC molecules and antigen-presenting cells.
  • 35.
    Antibody Structure • Antibodies are glycoproteinsconsisting of two types of polypeptide chains with attached carbohydrates: the heavy chain and the light chain. • The main differences between the classes of antibodies are in the light chain, as they form part of the antigen-binding site on the antibody molecules.
  • 36.
    Five Classes of Antibodiesand their Functions • IgM consists of 5 four- chain structures. • IgM is the largest of the antibody molecules. • IgM is usually the first antibody made during a primary response. • Very effective antibody against bacteria at early stages of a primary antibody response.
  • 37.
    Five Classes of Antibodiesand their Functions • IgG is a major antibody of late primary responses and the main antibody of secondary responses in the blood. • IgG is a monomeric(one molecule) antibody that clears pathogens from the blood and can activate complement proteins. • It can cross the placenta to protect the developing fetus. • It can exit the blood to the interstitial fluid to fight extracellular pathogens.
  • 38.
    Five Classes of Antibodiesand their Functions • IgA exists in 2 forms, a four- chain monomer in the blood and an eight-chain structure, or dimer. • It is the only antibody to leave the interior of the body to protect body surfaces like skin and mucous membranes. • IgA is important to newborns, because it is present in mother’s breast milk and can protect the infant from disease.
  • 39.
    Five Classes of Antibodiesand their Functions • IgE is usually associated with allergies. • It is present in the lowest concentration in the blood • If a person is allergic to peanuts, there will be peanut-specific IgE bound to his or her mast cells. • In this person, eating peanuts causes IgE to force mast cells to release the content of their granules, sometimes causing severe allergic reactions that can cause death(anaphylaxis).
  • 40.
    Five Classes of Antibodiesand their Functions • IgD is found on the surface of B cells. • IgD is secreted into the bloodstream and other bodily fluids, although in smaller amounts than other antibody classes • IgD is typically co- expressed with IgM on the surface of mature B cells
  • 41.
    B Cell Activation • Bcells are developed and mature in the bone marrow and are activated by binding to antigens in the lymph nodes. • Once they are activated, they develop into Plasma cells. • Plasma cells are the B cells that are committed to produce a specific antibody against a specific antigen. • Plasma cells lifespan are only a few days until the infection is gone. Some of the activated B cells will turn into memory cells.
  • 42.
    B Cell Activation • Initialexposure to the foreign antigen is considered a primary response. • A second exposure to the same antigen induces a secondary response, which is initiated by the memory cells developed from the primary response.
  • 43.
    Primary versus Secondary Responses • Theprimary response is delayed by several days due to the time it takes for the B cell to develop into plasma cells. • The level of antibody produced is low, but it is sufficient for immune protection.
  • 44.
    Primary versus Secondary Responses • Withthe secondary response, there is no time delay, and the amount of antibody made is much higher. • Thus, the secondary antibody response overwhelms the pathogens quickly and, in most situations, no symptoms are felt.
  • 45.
    B Cell Activation • Ina few cases, B cells will need the T helper cells to be activated. • B cell will present the antigen to TH cell, which in turn will release cytokines to activate the B cell. • Thus, the B cell receives signals from both its surface antibody and the T cell via its cytokines.
  • 46.
    Active and Passive Immunity • Activeimmunity is the resistance to pathogens acquired during an adaptive immune response within an individual. • Naturally acquired active immunity, the response to a pathogen that naturally invaded the body. • Artificially acquired active immunity is when the pathogen is introduced to the body as the example of vaccines. • A vaccine is a killed or weakened pathogen or its components that, when administered to a healthy individual, leads to the development of immunological memory (a weakened primary immune response) without causing much in the way of symptoms.
  • 47.
    Active and Passive Immunity • Passiveimmunity arises from the transfer of antibodies to an individual without requiring them to mount their own active immune response. *No antigen involved therefore no immunological memory, and it is only effective for short period of time. • Naturally acquired is seen during fetal development and breast feeding. Antibodies cross the placenta or passed with milk protect the fetus/baby from infection for the first few months of its life. • Artificially acquired usually involves injections of immunoglobulins taken from animals previously exposed to a specific pathogen.
  • 48.
  • 49.
    Immunodeficienci es • Acquired immunedeficiency syndrome (AIDS) • A result of human immunodeficiency virus (HIV) that targets the helper T cells. • HIV uses CD4 as the receptor to get inside cells. • Treatment for the disease consists of drugs that target virally encoded proteins that are necessary for viral replication, but are absent from normal human cells.
  • 50.
    Autoimmu ne Diseases • Immunecells lose their tolerance to self-cells and start to attack them. • Unknown reason but severe consequences. • Treatments are usually based on resolving the symptoms using immunosuppressive and anti-inflammatory drugs such as steroids.
  • 51.
  • 52.
    Hypersensitivitie s • The word“hypersensitivity” simply means sensitive beyond normal levels of activation. • The immune system is stimulated and ready to initiate a complex immune response even with minimum exposure to antigens. • Four types based on the way they occur.
  • 53.
    Hypersensitivitie s • Type Iinvolves the mast cells releasing histamine • Type II involves the complement system and happens with mismatched blood transfusion • Type III is when the antibody and antigen precipitate in blood vessels and cause inflammation • Type IV is a delayed hypersensitivity. T helper cells take extra time to activate cytotoxic T cells.
  • 54.
    References • Contanzo, L.(2021). Contanzo Physiology. (7th, Ed.) Philadephia: Elsevier. • Hall, J., & Hall, M. (2020). Guyton and Hall Textbook of medical physiology. (14th, Ed.) Philadelphia: Saunders. • Justiz Vaillant, A. A., Sabir, S., & Jan, A. (2024). Physiology, Immune Response. Statpearls. • Rice University. (2025, June 4). Anatomy of the Lymphatic and Immune Systems. Retrieved from Rice University: https://openstax.org/books/anatomy-and-physiology-2e/pages/21-1- anatomy-of-the-lymphatic-and-immune-systems • University of Hawaii. (2024, May). Immunology. Retrieved from University of Hawaii: https://pressbooks-dev.oer.hawaii.edu/anatomyandphysiology2021/chapte r/22-immunology/

Editor's Notes