Slide 1:

●​ Antibodies: proteins produced by lymphocytes which are a type of white blood cells.
These antibodies directly attack the antigens of bacteria.
●​ Antigens: the chemical substances found found on the surface of all cells
●​ Specific antibodies have complementary shapes for specific antigens. This property is
similar to how enzymes work. For example, an antibody that attacks a typhoid bacterium
will not affect a pneumonia bacterium.
Functions
●​ Antibodies directly attack the antigens of bacteria or any alien cells or proteins that
invade the body
●​ Antibodies also attach to the pathogen and mark the surface of the pathogen to assist
the phagocytes in finding and ingesting the pathogen
●​ They clump up bacteria together or neutralize the toxins (poisonous proteins) that the
bacteria produce.
Slide 2:
How the body develops immunity?
●​ The body develops immunity after recovering from diseases such as measles or
chickenpox. Additionally the reason why you are very unlikely to get sick with these
diseases again is because some of the lymphocytes that produced the specific
antibodies stay in the lymph nodes as memory cells some time. They divide rapidly and
make more antibodies if the same antigen is detected in the body again.
●​ or getting vaccinated
●​ Lastly, you can also inherit some forms of immunity or gain antibodies from your
mother's milk.
Slide 3
B and T lymphocytes
●​ There are two main types of lymphocyte. Both types undergo rapid cell division in
response to the presence of specific antigens. Although their functions are different they
work together.
B Cells
●​ The B cells (from Bone marrow) become short-lived plasma cells and produce antibodies
that are released into the blood. These antibodies may attack antigens directly or stick to
the surface membrane of infected or unfamiliar cells, for example, cells carrying a virus,
bacteria, cancer cells or transplanted cells.
T cell
●​ ‘Killer’ T cells (from the Thymus gland) have receptor molecules on theirsurface, which
attach them to these surface antibodies. The T cells then kill the cell by damaging its cell
membrane.
●​ ‘Helper’ T cells stimulate the B cells to divide and produce antibodies. They also
stimulate the phagocytes to ingest any cells carrying antibodies on their surfaces

1. Molecular Precision of Antibody Binding

Question: Antibodies have complementary shapes to specific antigens. Given that molecular
interactions such as hydrogen bonding and van der Waals forces contribute to antibody-antigen
binding, explain how slight mutations in the antigen's protein structure (e.g., due to viral
evolution) might lead to immune escape.

Answer:
Antibody-antigen binding relies on a precise lock-and-key mechanism. The antigen's surface
contains epitopes—specific molecular structures recognized by antibodies. If a virus undergoes
antigenic drift (gradual mutations in its surface proteins), even a single amino acid change can
alter the epitope enough to weaken or prevent antibody binding. This means:

Loss of hydrogen bonds or Van der Waals interactions can disrupt antibody recognition.

Conformational changes may hide antigenic sites from the immune system.

Escape mutations allow viruses like influenza and SARS-CoV-2 to evade pre-existing immunity,
requiring frequent updates to vaccines.

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2. Adaptive vs. Innate Immune Coordination

Question: The text discusses B and T lymphocytes, which belong to the adaptive immune
system. How do these cells communicate with the innate immune system (e.g., macrophages,
dendritic cells) to mount an effective response? What signaling molecules are involved?

Answer:
The innate immune system acts as the first line of defense, detecting pathogens using pattern
recognition receptors (PRRs) like Toll-like receptors (TLRs). However, it lacks specificity. To
bridge innate and adaptive immunity:

Dendritic cells engulf pathogens, process antigens, and present them on MHC-II molecules to
naïve T cells in lymph nodes.

Cytokines (e.g., IL-12, IL-4, IFN-γ) direct whether naïve T cells become Th1 (cell-mediated
response) or Th2 (antibody-mediated response) cells.

Macrophages and neutrophils are recruited via chemokines (e.g., CXCL8).

Helper T cells (CD4⁺) release IL-2, stimulating B cell activation to produce antibodies.
Cytotoxic T cells (CD8⁺) respond by recognizing infected cells displaying MHC-I antigen
complexes and inducing apoptosis via perforin and granzymes.

This coordination ensures that the immune response is both immediate (innate) and specific
(adaptive).

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3. Memory Cell Longevity and Immunity Limits

Question: Memory cells ensure long-term immunity, but some diseases (e.g., influenza) require
frequent vaccinations. Why do some memory cells provide lifelong immunity (e.g., measles),
while others degrade or become ineffective over time? What role does antigenic variation play in
this phenomenon?

Answer:
Memory cell longevity varies due to:

Pathogen stability: Measles virus is genetically stable, so its antigens remain recognizable over
a lifetime, leading to durable memory cell protection.

Antigenic variation: Influenza undergoes antigenic drift (small mutations) and antigenic shift
(major reassortment of viral genes), making old memory cells ineffective.

Memory cell survival: Memory B and T cells require periodic antigen exposure or stimulation
from cytokines (e.g., IL-7, IL-15) to remain active. In diseases like pertussis (whooping cough),
memory cells wane, necessitating booster shots.

Immune evasion by pathogens: Some viruses, like HIV, directly attack memory T cells, depleting
immunity over time.

Thus, lifelong immunity depends on pathogen stability, memory cell longevity, and continuous
immune stimulation.

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4. Clonal Selection and Somatic Hypermutation

Question: B cells undergo clonal selection and somatic hypermutation to improve antibody
specificity. Explain how these processes enhance immune response efficiency. What are the
evolutionary advantages and potential risks of somatic hypermutation?

Answer:

Clonal selection ensures that only B cells with highly specific receptors proliferate upon antigen
exposure.

Somatic hypermutation (SHM) occurs in the germinal centers of lymph nodes, introducing
random mutations in the variable regions of immunoglobulin genes.

This leads to affinity maturation, where B cells with the strongest antigen binding survive.

Evolutionary Advantages:

Enhances ability to recognize diverse and rapidly evolving pathogens.

Increases binding strength, improving immune response efficiency.

Potential Risks:

Mutations may generate self-reactive B cells, increasing the risk of autoimmune diseases (e.g.,
lupus).

Some mutations may lead to B cell cancers, such as lymphoma.

Despite risks, SHM ensures long-term adaptive immunity by optimizing antibody affinity.

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5. T Cell-Mediated Cytotoxicity Mechanism

Question: Killer T cells attack infected cells by inducing apoptosis. Describe the molecular
pathway by which cytotoxic T cells recognize infected cells and trigger apoptosis. What proteins
and receptors are involved in this process?

Answer:

1. Recognition:
Cytotoxic T cells (CD8⁺) recognize infected cells displaying MHC-I with viral peptides.

2. Binding and Activation:

TCR (T cell receptor) binds MHC-I → Activation.

3. Apoptosis Induction via Two Pathways:

Perforin-Granzymes: Perforin forms pores in the target cell membrane, allowing granzymes to
enter and activate caspase cascades leading to cell death.

Fas-FasL Pathway: Fas ligand (FasL) on T cells binds Fas receptor (CD95) on the target cell,
triggering caspase-mediated apoptosis.

This prevents viral replication while minimizing inflammatory damage to surrounding tissues.

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6. Immunological Tolerance and Autoimmune Risks

Question: The immune system must distinguish between self and non-self. Explain how T cells
undergo negative selection in the thymus to prevent autoimmunity. What happens if this process
fails?

Answer:

Negative selection occurs in the thymus, where immature T cells encounter self-antigens.

If a T cell strongly binds self-antigens, it undergoes apoptosis to prevent autoimmunity.

Failure of negative selection can lead to autoimmune diseases like:

Type 1 Diabetes: T cells attack pancreatic beta cells.

Multiple Sclerosis: T cells attack the myelin sheath of neurons.

Thus, negative selection is crucial for immune self-tolerance.

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7. Herd Immunity and Epidemiological Thresholds

Question: Vaccination provides individual and herd immunity. Using mathematical models (e.g.,
basic reproduction number R₀), explain how herd immunity thresholds are calculated.

Answer:

Herd immunity threshold is calculated using:

\text{Threshold} = 1 - \frac{1}{R_0}

1 - \frac{1}{15} = 93\%

For high-R₀ diseases, higher vaccination rates are needed to prevent transmission.

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8. Immune Evasion by Cancer Cells

Question: Some cancer cells avoid immune detection by suppressing T cell activity. How do
tumors use immune checkpoint proteins (e.g., PD-L1) to evade immune responses?

Answer:

Tumors overexpress PD-L1, which binds to PD-1 receptors on T cells, inhibiting their activation.

Checkpoint inhibitors (e.g., anti-PD-1 drugs like Keytruda) block this interaction, allowing T cells
to attack cancer.

This is a breakthrough in cancer immunotherapy.

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9. Cross-Reactivity and Molecular Mimicry in Autoimmune Diseases

Question: Some autoimmune diseases are triggered by infections due to molecular mimicry,
where pathogen antigens resemble self-proteins. Explain how this process occurs and provide
an example of a disease caused by molecular mimicry.

Answer:

Molecular mimicry occurs when a pathogen has antigens structurally similar to human proteins.

The immune system generates antibodies and T cells against the pathogen, but these
mistakenly attack self-tissues due to the shared molecular patterns.

Example: Rheumatic Fever

Caused by Streptococcus pyogenes infection (strep throat).

The bacterial M protein is structurally similar to proteins in heart valves and joints.

The immune system attacks the heart, joints, and nervous system, leading to rheumatic heart
disease.

This demonstrates how an immune response against a pathogen can lead to unintended
self-destruction.