CHAPTER 11: IMMUNITY
SUBTOPIC :11.1 IMMUNE RESPONSE
LEARNING OUTCOMES:
a)Define immunity
b)Describe type of immunity
i..Innate:and
ii Adaptive
MAIN IDEAS
EXPLANATION
/KEY POINT
a. Immunity and
types of
immunity
Immunity:
The ability to recognize and destroy foreign or dangerous macromolecules
(Solomon 10th Ed, 2015).
The state of having sufficient biological defenses to avoid infection, disease or
other unwanted biological invasion by foreign organism or other foreign
substance
Types of immunity:
NOTES
MAIN IDEAS
/KEY POINT
EXPLANATION
NOTES
SUBTOPIC :11.2 ANTIBODY
LEARNING OUTCOMES:
a) Describe the general structure of antibody
b) State the classes of antibody based on its structure
MAIN IDEAS /KEY
POINT
General structure of
antibodies and
classes based on its
structure.
EXPLANATION
Antibody:
A specific protein (immunoglobulin) that recognizes and binds to specific antigen which
produced by plasma cells.
Structure of antibodies:
Basic shape of antibody
•
•
•
•
•
•
Y shaped
4 polypeptide chains:
 2 identical light chains
 2 identical heavy chains
Linked by disulphide bridge
Each chain contains:
 variable region (V)
 constant region (C)
The constant region of heavy chains:
 form the base of antibody molecules
 determines the way antibody is secreted & how it is distributed in body fluid
✓ Eg: circulate in body fluid or bind to membranes of mast cells (mast
cells are cells found in connective tissue that store histamine,
inflammatory signaling molecule)
The variable region of the light and heavy chain:
 determine the specificity of an antibody molecules
 amino acid sequence varies extensively from one B cell to another.
 part of heavy-chain V region and a light-chain V region form as asymmetric
binding site for an antigen.
•
Each antibody has 2 antigen-binding sites
 Form by the free tips end of both variable region
Classes of antibody:
i.
IgD
• Found in blood and lymph and on surfaces of B cells
• Single monomer
• Function: act as antigen receptors on the surfaces of B
cells
 Stimulating the differentiation of B cells into plasma cells and memory cells
ii.
IgE
• Bind to mast cells and basophil and stimulate them to produce histamines
• Single monomer
• Function: responsible for allergic reaction but useful
against parasitic worms
iii.
•
•
•
•
IgG
Temporary protection to newborn.
single monomer
Easily cross the walls of blood vessel and enter tissue fluid
e.g.: maternal IgG antibodies can cross the placenta and confer
passive immunity to fetus
iv.
IgM
• Primary antibody response.
• Pentamer:
 Large size
 5 monomers held together by polypeptide called J
(joining) chain
• First antibodies to appear in response to
initial exposure to an antigen
v.
IgA
• Common in mucous membranes and in body
secretions: mucus, saliva, tears, breast milk
• Most abundant in body (IgG most abundant
in serum)
• Dimer: 2 monomers held by J chain
• Functions: prevent the attachment of
pathogens to mucosal surfaces
SUBTOPIC :11.3 LYMPHOCYTE DEVELOPMENT
LEARNING OUTCOMES:
a) Describe B cell and T cell
MAIN IDEAS
/KEY POINT
EXPLANATION
 Lymphocytes originate from stem cell in the bone marrow.
 Early lymphocytes are all a like.
 Later they develop into T and B lymphocytes/cell – depending on
where they continue their maturation.
 Lymphocytes that migrate from the bone marrow to thymus
develop into T cells
 Lymphocytes that remain in the bone marrow and continue their
maturation there become B cells
i. Lymphocytes
Account for 20 – 30 % of circulating leukocytes
(a) B cells
Make up 10-15% of circulating lymphocytes,B cell can be further divided
into:
• Plasma cells
 when stimulated, B cells can differentiate into plasma cells which
produce and secrete antibodies
• Memory B cells
 Subset of B cells that respond to a previously encountered antigen
(b) T cells
Approximately 80% of circulating lymphocytes are classified as T cells
• Cytotoxic T cells
 Attack foreign cells or body cells infected by viruses.
• Helper T cells
 Stimulate the activation and function of both T cells and B cells.
• Suppressor T cells
 Inhibit the activation and function of both T and B cells.
• Memory T cells
 Subset of T cells that respond to a previously encountered antigen
NOTES
SUBTOPIC :11.4 DEVELOPMENT OF ADAPTIVE IMMUNITY
LEARNING OUTCOMES: a) Explain cell mediated immune response
b) Explain Hummoral (Antibody mediated) Immune response.
c) Explain various type of antigen and antibody interactions:
i. neutralization
ii. opsonization
iii. activation of complement system and pore formation.
d) Explain the primary and secondary immune responses.
MAIN IDEAS
/KEY POINT
Two types of
immune
response.
EXPLANATION
Types of immune response:
i. Cell mediated immune response
The branch of adaptive immunity that involves the activation of cytotoxic T
cells, which defend against infected cells.
ii. Humoral (Antibody mediated) immune response
The branch of adaptive immunity that involves the activation of B cells and that
leads to the production of antibodies, which defend against bacteria and viruses
in body fluids.
Components of humoral and cell mediated immune response:
ii. Lymphocytes
Account for 20 – 30 % of circulating leukocytes. B cells and T cells are the major
lymphocytes involved in both immune response.
iii. Major histocompatibility complex (MHC) molecule
A host protein that functions in antigen presentation.
• Glycoprotein and antigen that appears in plasma membrane is capable to
activate T cells.
• Membrane glycoproteins are called MHC proteins/human leukocyte
antigens (HLAs).
• Amino acid sequences and shapes of MHC proteins differs among
individuals.
• For T cell to recognize an antigen, the antigen must be bound to
glycoproteins in the plasma membranes of another cell.
NOTES
MAIN IDEAS
/KEY POINT
EXPLANATION
(a) MHC class I molecule
• Present in plasma membrane of all nucleated cell
• Pick up small peptides from the surrounding cytoplasm and carry them
to the cell surface
• If the cytoplasm contains abnormal peptides or viral proteins, they soon
appear in the plasma membrane
• T cells will recognize them as foreign and be activated
(b) MHC class II molecule
• Present only in the plasma membranes of antigen presenting cell (APC)
and lymphocytes
• APCs are specialized cells responsible for activating T cell defenses
against foreign cells (including bacteria) and foreign proteins
iv. Cytokines
Signaling proteins that regulate interaction between cells in the immune system
(a) Interleukin I (IL-1)
• Primary source: macrophages
• Activates helper T cells
(b) Interleukin 2 (IL-2)
• Source: Helper T cells.
• Activates B cells and cytotoxic T cells
Helper T (TH) cells stimulate the humoral and cell-mediated immune response
1. The macrophage ingest a microbe or other foreign particle and breaks it into
fragments (foreign antigens)
2. MHC class II (self protein) bind to foreign antigens
3. Display them on the cell surface
NOTES
MAIN IDEAS
/KEY POINT
EXPLANATION
4. Helper T cell recognize and bind to the MHC-antigen complex caused APC
release IL-1; and diffuse to the TH cell and stimulate it.
5. Activated TH cell release IL-2. IL-2 makes TH cell itself grow and divide
producing memory cells and additional active TH cells.
6. IL-2 activate B cells and stimulating the humoral immune response
7. IL-2 activate TC cells stimulating the cell mediated immune response
NOTES
MAIN IDEAS
/KEY POINT
EXPLANATION
NOTES
Cell Mediated
Immune
Response
a)Cell
mediated
immune
response
i. Pathogens bearing foreign antigens invade body
ii. Antigen presenting cell @ APC (dendritic cell / macrophage)
phagocytizes pathogen
iii. Foreign antigen binds to the class II MHC protein form MHC- antigen complex
and displayed on surface of APC
iv. TH cell with its antigen receptor and accessory protein, CD4 binds with APC
v. APC releases interleukin 1 (IL-1) to activate TH cell
vi. Activated TH cell release IL-2
vii. TH cell proliferate producing activated TH cells and memory TH cells
viii. Activated helper T cell will release IL-2 and the cytotoxic T (TC) cell
ix. TC cell also becomes active when encounters an appropriate antigens bound to
class I MHC molecule of infected cell.
x. Activated TC undergoes mitotic division producing active TC cells (effector
cells) and memory TC cells.
xi. Activated TC cell migrates to the area of infection and eliminate cells that are
infected by viruses or other intracellular pathogen.
MAIN IDEAS
/KEY POINT
EXPLANATION
xii. Fragments of foreign proteins inside of the cell bind with class I MHC
molecules and then displayed on the cell surface. The MHC-antigen complex
is recognized by TC cells.
xiii. TC cells with accessory protein CD8 binds to the MHC molecule, helping keep
the two cells in contact.
xiv. TC cell may:
release perforin to destroy the target cell’s plasma membrane and
form pores.
Secrete a poisonous lymphotoxin, granzymes to kill the target cell.
It activates genes in the target cell’s nucleus that program the cell to
die (apoptosis).
Humoral immune response
b)Humoral
(Antiody
mediated)im
mune
response
i.
Antigen presenting cell @ APC (dendritic cell / macrophage / B cell)
phagocytizes pathogen and degrades it.
ii.
Fragment of foreign antigen binds to the class II MHC protein forming
MHC-antigen complex and displayed on the surface of APC
iii.
TH cell with its antigen receptor and accessory protein, CD4 binds to the
complex of APC
iv.
APC releases interleukin 1 (IL-1) to activate TH cell
NOTES
MAIN IDEAS
/KEY POINT
EXPLANATION
v.
Activated TH cell releases IL-2
vi.
TH cell proliferates producing activated TH cells and memory TH cells
vii.
Once antigens are bound to B cell receptor (antibody) in the B cell
membrane, the B cell displays those antigens that bound to class II MHC molecule
on the surface of its plasma membrane
viii.
Activated TH bind to the sensitized B cell.
ix.
Activated TH cell will release IL-2 that co-stimulate the sensitized B cell
and trigger its activation.
x.
The activated B cell then proliferates or divides mitotically, producing
memory B cells and plasma cells (effector cells).
xi.
Plasma cells secretes antibodies.
xii.
Antibody-antigen interaction occurs.
xiii.
Triggers processes leading to pathogen destruction
xiv.
Memory B cells are long-lived cells that can give rise to effector cells if the
same antigen is encountered later in life
NOTES
MAIN IDEAS
/KEY POINT
c) Various
types of
antigen and
antibody
interactions:
EXPLANATION
NOTES
Antigen:
• Any foreign molecule that elicits an immune response by binding to receptors of B cells or T cells.
• Usually protein, glycoprotein or polysaccharide
• Epitope/antigenic determinant sites: a small, accessible region of an antigen to which an antigen
receptor or antibody binds
• An antigen may have several different epitopes
• Each epitope is recognized by a different antibody
• Different antibodies can recognize distinct epitopes on the same antigen
MAIN IDEAS
/KEY POINT
EXPLANATION
NOTES
Antigen and antibody interactions:
• An antigen-antibody complex forms when an antibody molecule binds to its corresponding
antigen molecule
• Once the two molecules are in position, hydrogen bonding and other weak chemical forces lock
them together
• Antigen covered with antibodies attract eosinophils, neutrophils and macrophages
• These cells then phagocytize the pathogens
i. Neutralization
• A process in which antibodies bind to proteins on the surface of a virus.
• Viruses and bacterial toxins have specific sites that must bind to target regions on body cells
before they can enter or injure those cells.
• Antibodies bind to those sites, making the virus or toxin incapable of attaching itself to cell.
• Thus, neutralizing the virus/toxins.
ii. Opsonization
• A process by which a particulate antigen becomes more susceptible to phagocytosis by
macrophages and neutrophils.
• A coating of antibodies and complement proteins increase the effectiveness of
phagocytosis.
• Some bacteria have slick plasma membranes or capsules, but opsonization makes it easier
for phagocytes to hang on onto their prey before they engulf it.
MAIN IDEAS
/KEY POINT
EXPLANATION
•
NOTES
Phagocytes can bind more easily to antibodies and complement proteins than they can to
the bare surface of a pathogen.
iii. Activation of complement system and pore formation
• When an antibody molecule binds to an antigen, it forms antigen-antibody complex.
• Portion of the antibody change shape exposing areas that bind complement protein.
• This binding activates the complement system.
• The activated bound complement molecule then forms membrane attack complex.
• Pores formed in plasma membrane, allowing water and ions to rush in.
• The cell swells and lyses, destroy the pathogen.
MAIN IDEAS
/KEY POINT
d.Primary
and
secondary
immune
responses.
EXPLANATION
•
•
•
•
•
•
NOTES
Results from exposure of B cell to an antigen
Includes series of cell division, differentiation and antibody production.
Before stimulation by an antigen, B cells are small lymphocyte.
After activation, B cell undergoes a series of divisions to produce large lymphocyte.
Some enlarge cells become plasma cells to produce antibody.
Others revert back to small lymphocytes become memory B cells.
Primary immune response
• Low concentration of antibodies produced at early stage and peak up one to two weeks after
exposure (test on antibody titer).
• Has lag time: slow reaction during 3- 6 days after the exposure.
• B cells specific for that antigen multiply and develop into plasma cells
• Takes 3-14 days to produce enough antibodies to be effective against antigen.
• Meantime, individual usually develops disease symptoms because the antigen has had time to
cause tissue damage.
MAIN IDEAS
/KEY POINT
EXPLANATION
•
•
•
•
•
•
NOTES
Plasma cells secrete antibody.
Antibody concentration rise and reach the peak in 10 -12 days.
IgM is the first antibody produced and later other classes of antibodies are produced as well.
Primary response lasts several days or weeks.
Concentration of antibodies decrease because plasma cell dies.
Memory B cell left in the body.
Secondary immune response
•
•
•
•
•
•
•
The response of immune system to the second infection for same antigen
Memory cell recognize the same antigen faster.
Within hours after second exposure: memory B cells proliferate & differentiate rapidly into
plasma cells to produce antibody.
IgG mainly antibody produced.
Within 2-3 days, antibody rises steeply, higher than in primary response and remain high for
weeks to months.
Plasma cells functioning for much longer than in primary response.
Memory B cell able to recognize antigen for longer period; may persist for many years and
probably for life or the immunity is long lasting.
SUBTOPIC :11.5 IMMUNIZATION
LEARNING OUTCOMES: a) Define Vaccine
b) State the sources of antigen to make vaccine:
i)Inactivated bacterial toxins:
ii)Killed or weaken pathogens
iii)Genes encoding microbial protein (DNA,RNA and
protein)
c)State the importance of vaccination
MAIN IDEAS
/KEY POINT
a)What is vaccine
EXPLANATION
A commercially produced, weakened or killed antigen associated with a particular
disease that stimulates the body to make antibodies.
Solomon. E.P. Martin, C.E. Martin, D.W., Berg, L.R. (2015) Biology. Cencage
Learning. Pg G-46
Inactivated Bacterial toxin



Some bacteria causes disease by making a harmful protein called
a toxin.
The toxin is taken out and inactivated by using chemical . The
inactivated toxin is called toxoid.
By inactivating the toxin, it no longer causes diseases but triggers
immune response to produce antibodies.
Sources of
antigen to make
vaccine.

Examples: Vaccines for Tetanus,Diphteria,Pertussis
Killed or weaken pathogen



Pathogens are microbes that causes diseases such as
bacteria,viruses,fungi and parasites.
By weakening a pathogen,the ability of the pathogen to reproduce is
limited.Therefore,they does not cause diseases.
A weakened virus vaccine reproduces 20 times lesser than a normal
virus infection.
NOTES











However,it is able to reproduce minimaly to induce the production of
memory B cells.This protects the body against the infection in the
future.
Examples:Vaccine for measless,mumps,rubella (MMR) and
chickenpox
The benefits of producing vaccine through weakened pathogens is, it
provides lifelong protections.
The limitation is, this type of vaccine cannot be given to people with
weak immune system .For instance,people with AIDS or cancer..
By killing a pathogen, the pathogen (viruses) are being inactivated.
Inactivated viruses cannot reproduce or cause diseases.
However, the antigens on the viruses are still recognized by the
immune system and triggers immune response by producing
antibody.
Examples;Vaccines for polio,Hepatitis A and rabies are produced
using inactivated viruses.
The advantages of this method is that vaccine cannot cause even a
mild form of the disease that it prevents.
Also, the vaccine can be given to people with weakened immune systems
The limitation is it typically requires several doses to achieve
immunity.
Genes encoding microbial protein (DNA,RNA and protein)

By injecting and individual with DNA vaccines or RNA vaccines,
The DNA or RNA provides the information to make the viruses from
inside the body.

Vaccinated person use the information to make the spike protein from the
surface of the virus.
Immune system detects the protein as foreign substances and triggers the
immune system.
The RNA vaccine uses mRNA of the the viruses to trigger immune
response.
Example: Pfizer and Moderna COVID-19 vaccines are made this way.



Vaccination is the most effective way to prevent diseases that is caused by
pathogens as it :

Importance of
vaccination


Prevents outbreak of a infectious diseases by forming a herd immunity
when majority of the population is vaccinated.
Protects the body from severe illness and reduce the mortality rate due to
illness.
Reduces economical and social impact of pandemic.
SUBTOPIC :11.6 Health issue related to Immune response
LEARNING OUTCOMES: a)Explain the immune suppression by HIV infection
b)State autoimmune diseases:
i. Systemic Lupus Erythematosus (SLE);
ii. Multiple Sclerosis; and
iii. Diabetes Type I
MAIN IDEAS
/KEY POINT
EXPLANATION









Immune
suppression by
HIV



The human immunodeficiency virus (HIV) is the pathogen that causes
AIDS.
The pathogen attack humoral and cell mediated immune response.
HIV infects helper T cells with high efficiency by binding specifically to
CD4 accessory protein.
HIV also infects cells with low level of CD4.Such as macrophages and
brain cells.
Inside the infected cell the HIV’s RNA genome is reverse- transcribed to
produce DNA which is integrated to host cell’s genome.
By doing this, the viral genome can direct the production of new viruses.
Although body responds to HIV by immune system but some HIV may
still escape.
HIV has a very high mutation rate. Hence it persists inside body.
Altered proteins on the surface of mutated viruses reduces interaction with
antibodies and cytotoxic T cells.
Therefore, the viruses replicates, mutates and evolves within the body.
Over time, an untreated HIV infection not only avoids the adaptive
immune response but also abolishes it
Viral replication and cell death triggered by the virus lead to loss of helper
T cells, impairing both humoral and cell-mediated immune responses.
NOTES
Autoimmune disease: A disease in which the body produces antibodies against its
own cells or tissue. Also called autoimmunity.
Solomon. E.P. Martin, C.E. Martin, D.W., Berg, L.R. (2015) Biology. Cencage
Learning. Pg G-4
In autoimmune diseases, antibodies and T cells attack the body’s own tissue
Systemic Lupus
Erythematosus
(SLE)
In systemic lupus erythematosus (SLE) commonly called lupus, the immune
system generates antibodies against histones and DNA released by the normal
breakdown of body cells.
Symptoms include:




skin rashes
fever
arthritis
kidney dysfunction
Other symptoms depend on the part of the body being attacked by the disease.
Multiple
sclerosis
Multiple sclerosis (MS) is a chronic disease affecting the central nervous system
(the brain and spinal cord). It also known as rheumatoid arthritis. MS occurs when
the immune system attacks nerve fibers and myelin sheathing in the brain and
spinal cord.
This attack causes inflammation, which destroys nerve cell processes and myelin –
altering electrical messages in the brain.
Diabetes Type I
Diabetes Type 1 (T1D) results from the destruction of beta cells in the pancreas
which produce insulin that are wrongfully targeted and killed off by specific
antibodies created by the adaptive immune system.
Therefore, it is known as insulin-dependent diabetes
Symptoms include:
 excessive hunger
 excessive thirst
 blurred vision
 fatigue
 frequent urination
 dramatic weight loss in a short period of time
It is caused by:


Genetics
Exposure to viruses and other environmental factors.