• Activated T cells (especially helper T cells) secrete cytokines, which are signaling proteins that regulate immune responses.

• Cytokines:

  • Activate B cells to produce antibodies

  • Stimulate macrophages and other immune cells

  • Orchestrate cellular immunity

• Immunoglobulins (a) are secreted by B cells/plasma cells.

• Complement components (b) are mainly produced by liver hepatocytes.

• Histamine (c) is released by mast cells and basophils, not T cells.

• Primary lymphoid organs are where lymphocytes develop and mature:

  • Bone marrow: site of B cell maturation and origin of all blood cells.

  • Thymus: site of T cell maturation.

• Spleen and lymph nodes (a) are secondary lymphoid organs, where immune responses are initiated.

• Liver and spleen (c) are not primary lymphoid organs in adults.

• Tonsils and adenoids (d) are secondary lymphoid tissues in the mucosa-associated lymphoid system.

• Natural killer (NK) cells are part of the innate immune system.

• They recognize and kill virus-infected cells or tumor cells without prior sensitization.

• NK cells destroy target cells by:

  • Releasing perforin, which forms pores in the target cell membrane

  • Releasing granzymes, which enter through the pores and trigger apoptosis

• Producing antibodies (a) is a function of B cells.

• Presenting antigen to T cells (c) is done by dendritic cells or macrophages.

• Activating complement (d) is part of the complement system, not the direct action of NK cells.

• Neutrophils are the first immune cells to arrive at the site of bacterial infection.

• They are a type of granulocyte and phagocyte, capable of engulfing and destroying bacteria.

• Basophils (a) are mainly involved in allergic reactions and inflammation.

• Eosinophils (c) target parasites and play a role in allergic responses.

• T helper cells (d) are part of adaptive immunity and respond later by activating B cells and other immune cells.

• C3b binds to the surface of pathogens and tags them for phagocytosis, a process called opsonization.

• C5a (b) is a potent chemoattractant and anaphylatoxin, attracting immune cells to the site of infection.

• C1q (c) initiates the classical complement pathway.

• C4a (d) is an anaphylatoxin, contributing to inflammation, not opsonization.

• Phagocytic cells engulf and destroy pathogens and debris.

• Neutrophils: Rapidly respond to infections and are highly phagocytic.

• Monocytes/macrophages: Circulate as monocytes and differentiate into macrophages in tissues; professional phagocytes.

• Eosinophils: Phagocytic to some extent, particularly against parasites, though less than neutrophils and macrophages.

• Basophils are primarily involved in allergic responses, not phagocytosis.

• Lymphocytes (B and T cells) are not phagocytic.

• IgG is the most abundant antibody in serum and is the only immunoglobulin class that crosses the placenta, providing passive immunity to the fetus.

• IgM (not IgG) (a) appears first in the primary immune response.

• IgM is larger than IgG (b) because it is a pentamer, whereas IgG is a monomer.

• IgG is not directly detected in saline crossmatches (d); crossmatching usually detects IgM-mediated agglutination.

• The secondary immune response occurs when the immune system encounters the same antigen again.

• Memory B and T cells generated during the primary response allow a faster, stronger, and more effective response.

• Primary response (a) is slower because the immune system is seeing the antigen for the first time.

• Passive immunity (c) provides pre-formed antibodies but does not involve memory.

• Innate immunity (d) is nonspecific and acts immediately but does not improve with repeated exposure.

• IgA is the main antibody found in mucosal secretions such as saliva, tears, respiratory secretions, and breast milk.

• In breast milk, it provides passive immunity to infants by protecting their gastrointestinal and respiratory tracts.

• IgG (a) is the main antibody in blood and extracellular fluid and can cross the placenta.

• IgM (b) is the first antibody produced during an infection.

• IgE (d) is involved in allergic reactions and defense against parasites.

• Clonal deletion is a mechanism of central tolerance in primary lymphoid organs (bone marrow for B cells, thymus for T cells).

• Lymphocytes that strongly recognize self-antigens are eliminated to prevent autoimmune reactions.

• Clonal expansion (a) is the proliferation of lymphocytes after recognizing an antigen.

• Antigen presentation (c) is the display of antigens by APCs to T cells.

• Somatic mutation (d) refers to mutations in B cell antibody genes to improve affinity, not self-tolerance.

• Antigen-presenting cells (APCs) process and present antigens on MHC molecules to T cells to initiate adaptive immunity.

• APCs include:

  • Macrophages (a)

  • Dendritic cells (b)

  • B cells (c)

• Neutrophils (d) are phagocytic cells of the innate immune system but do not efficiently present antigens to T cells.

The first line of defense consists of innate, non-specific barriers that prevent pathogens from entering the body. These include the skin, mucous membranes, stomach acid, and enzymes in tears and saliva. T cells, antibodies, and complement proteins are part of the second or third lines of defense, which act only after a pathogen has breached the initial barriers.

• Innate immunity provides immediate, nonspecific defense against pathogens.

• Physical and chemical barriers include:

  • Skin: physical barrier

  • Lactic acid: chemical barrier in sweat

  • Mucus and cilia: trap and remove pathogens in respiratory and gastrointestinal tracts

• Acquired/adaptive immunity (b & c) involves specific immune responses with memory.

• Autoimmunity (d) refers to immune reactions against self-antigens, not protective barriers.

• MHC class II molecules are expressed only on professional antigen-presenting cells (APCs) such as:

  • Dendritic cells

  • Macrophages

  • B cells

• They present exogenous antigens to CD4+ T helper cells.

• MHC class I (a) is expressed on all nucleated cells, not just APCs.

• CD8 (c) is a marker for cytotoxic T cells.

• CD19 (d) is a marker for B cells, not all APCs.

• B lymphocytes (B cells) are the adaptive immune cells responsible for humoral immunity.

• Upon activation by an antigen (and usually with T helper cell help), B cells differentiate into plasma cells, which secrete antibodies.

• Macrophages (a) are phagocytes and antigen-presenting cells.

• T lymphocytes (b) mediate cellular immunity, not antibody production.

• Neutrophils (d) are phagocytic cells of innate immunity and do not produce antibodies.

• The alternative complement pathway is part of innate immunity and is activated directly by microbial surfaces, such as bacterial cell walls, without the need for antibodies.

• Classical pathway (a) requires antigen-antibody complexes for activation.

• Lectin pathway (c) is activated when mannose-binding lectin binds to carbohydrates on microbial surfaces.

• Adaptive pathway (d) is not an official complement pathway; it refers generally to adaptive immunity.

• The MHC class III region does not encode antigen-presenting molecules like class I or II.

• Instead, it encodes various immune-related proteins, including:

  • Complement components (e.g., C2, C4, and factor B)

  • Cytokines (like TNF-α and TNF-β)

• Antigens (a) are recognized by MHC molecules but not encoded by class III.

• Antibodies (b) are produced by B cells, not MHC genes.

• Lymphocytes (d) are cells, not gene products.

• Interleukin-1 (IL-1) is a pro-inflammatory cytokine produced by activated macrophages.

• It acts on the hypothalamus to raise body temperature, causing fever.

• IL-2 (b) stimulates T cell proliferation.

• IL-4 (c) promotes B cell differentiation and class switching to IgE.

• IL-10 (d) is an anti-inflammatory cytokine that suppresses immune responses.

• Th1 cells produce interferon-gamma (IFN-γ), which activates macrophages to enhance their ability to kill intracellular pathogens like viruses and certain bacteria.

• Th2 cells (b) stimulate B cells and are involved in antibody production, especially IgE.

• Th17 cells (c) are involved in inflammation and defense against extracellular bacteria and fungi.

• Treg cells (d) suppress immune responses and maintain self-tolerance.

• Maternal IgG crosses the placenta during pregnancy and provides passive immunity to the newborn, protecting against infections immediately after birth.

• IgM production (a) by the newborn occurs later as part of active immunity.

• NK cell activation (c) and complement activation (d) are part of innate immunity, which is present at birth but does not provide specific pathogen protection like maternal IgG.

• Activated CD8⁺ cytotoxic T lymphocytes (CTLs) secrete IFN-γ, a cytokine that:

  • Enhances antiviral responses

  • Activates macrophages

  • Promotes Th1-type immune responses

• IL-13 (a) and IL-5 (b) are mainly produced by Th2 cells.

• SDF-1 (c) is a chemokine involved in cell migration, not a major CTL cytokine.

• T lymphocytes (T cells) originate from bone marrow stem cells but mature in the thymus.

• In the thymus, T cells undergo positive and negative selection to ensure they can recognize antigens presented by MHC molecules without attacking self-antigens.

• Bone marrow (a) is the site of B cell maturation and the origin of all lymphoid cells.

• Spleen (b) filters blood and participates in immune responses but does not mature T cells.

• Lymph nodes (d) are sites where immune responses are coordinated, but T cells mature elsewhere.

• Mast cells (in tissues) and basophils (in blood) contain granules filled with histamine.

• During allergic reactions, IgE antibodies bound to these cells recognize allergens, triggering degranulation and release of histamine.

• B lymphocytes (a) produce antibodies, not histamine.

• Macrophages (b) are phagocytes and cytokine producers, not histamine releasers.

• NK cells (d) kill infected or tumor cells, not involved in histamine release.

• The spleen filters blood and removes old red blood cells, cellular debris, and opsonized microbes.

• Its white pulp contains lymphocytes that initiate immune responses, while the red pulp contains macrophages that phagocytose opsonized pathogens.

• Bone marrow (a) is primarily for blood cell production.

• Thymus (b) is the site of T cell maturation.

• Lymph nodes (d) filter lymph, not blood.

• During a primary immune response, the immune system first produces IgM antibodies.

• IgM is a pentamer, making it very effective at agglutinating pathogens and activating complement.

• IgG (a) is produced later and is the main antibody in secondary responses.

• IgA (c) is mainly involved in mucosal immunity.

• IgE (d) is associated with allergic reactions and defense against parasites.

• The DPT vaccine (Diphtheria, Pertussis, Tetanus) contains inactivated toxins or bacterial components that stimulate the recipient’s immune system to produce antibodies.

• This is an example of active immunity because the body actively generates its own immune response, primarily humoral (antibody-mediated).

• Passive immunity (b) would involve receiving pre-formed antibodies, such as from maternal IgG.

• Cell-mediated immunity (c) involves T cells and is less prominent with DPT vaccines.

• Immediate hypersensitivity (d) refers to allergic reactions, not vaccination.

• Nonspecific killing means the immune cell can recognize and kill abnormal target cells (like tumor cells or virus-infected cells) without needing prior exposure or antigen-specific recognition.

• c) Natural Killer (NK) cells: These are lymphocytes of the innate immune system. They are the primary mediators of nonspecific tumor cell killing. They identify stressed cells (e.g., tumor cells) by detecting the absence of “self” MHC class I molecules or the presence of stress-induced molecules on the target cell’s surface. They do not require immunization to function.

Why the other options are incorrect:

• a) Cytotoxic T cells: These are key for killing tumor cells, but their action is highly specific. They recognize tumor-specific antigens presented by MHC class I molecules. This requires prior activation and clonal expansion, making it part of the adaptive immune response.

• b) Helper T cells: These cells do not directly kill tumor cells. Their role is to “help” or regulate other immune cells (like cytotoxic T cells and B cells) by releasing cytokines.

• d) Antibody plus complement: This is a specific mechanism of the humoral immune response. It requires that antibodies first be produced against a specific antigen on the tumor cell. This is not a nonspecific process.

• Innate immunity is present at birth and provides immediate, nonspecific defense against pathogens.

• Components include:

  • Physical barriers: skin, mucous membranes

  • Chemical barriers: stomach acid, enzymes

  • Cellular defenses: neutrophils, macrophages, NK cells

• Adaptive immunity (b) / acquired immunity (d) develops after exposure to antigens.

• Passive immunity (c) is temporary protection gained by receiving antibodies from another individual, e.g., via placenta or breast milk.

• The antigen-binding site of an antibody is located at the tips of the Y-shaped molecule.

• It is formed by the variable (V) regions of both the heavy (VH) and light (VL) chains.

• These regions determine antigen specificity through complementarity-determining regions (CDRs).

• Constant heavy chains (a) and constant light chains (b) form the structural backbone of the antibody.

• The Fc region (d) mediates effector functions like complement activation and binding to Fc receptors but does not bind antigens.

• B cells are lymphocytes that, upon activation by an antigen, differentiate into plasma cells, which are the antibody-secreting factories of the immune system.

• Killer T cells (a), also called cytotoxic T lymphocytes, kill infected cells but do not produce antibodies.

• Bone marrow stem cells (b) give rise to B cells but do not directly secrete antibodies.

• Mast cells (c) release histamine and other mediators in allergic responses, not antibodies.

• During a primary immune response, IgM is the first antibody produced by B cells.

• It is a pentamer, making it highly effective at agglutination and complement activation.

• IgG (a) appears later and dominates in secondary responses.

• IgA (c) is mainly involved in mucosal immunity.

• IgE (d) is associated with allergic reactions and parasitic defense.

• MHC class I molecules are expressed on all nucleated cells and present endogenous antigens to CD8⁺ cytotoxic T cells.

• The human MHC class I molecules are HLA-A, HLA-B, and HLA-C.

• Complement proteins (a) are encoded by MHC class III.

• Cytokines (c) are not MHC molecules.

• HLA-DP, DQ, DR (d) are MHC class II molecules, expressed on antigen-presenting cells for presentation to CD4⁺ T cells.

• After the first exposure to an antigen (e.g., initial vaccination), the immune system mounts a primary response, generating memory B and T cells.

• Upon subsequent exposures (booster doses), these memory cells trigger a secondary immune response, which is faster, stronger, and produces higher-affinity antibodies.

• Clonal deletion (a) removes self-reactive lymphocytes.

• Primary immune response (b) is slower because memory cells are not yet formed.

• Immune tolerance (d) refers to unresponsiveness to self-antigens, not enhanced response.

• Th2 cells produce cytokines such as IL-4, IL-5, and IL-13.

• IL-4 specifically promotes class switching in B cells to produce IgE, which is central to allergic responses.

• Th1 (a) cells activate macrophages and promote cellular immunity.

• Th17 (c) cells are involved in inflammation and defense against extracellular bacteria and fungi.

• Treg (d) cells suppress immune responses and maintain tolerance.

• MHC class II molecules are expressed on antigen-presenting cells (APCs) such as dendritic cells, macrophages, and B cells.

• They present exogenous antigens (from outside the cell) to CD4+ helper T cells.

• MHC class I (a) presents endogenous antigens to CD8+ cytotoxic T cells.

• MHC class III (c) includes genes for complement proteins and some cytokines, not antigen presentation.

• Class IV (d) does not exist in humans.

However, the given options don’t include that exact range — the closest reasonable choice in common exam settings is 10–15%, but since that’s not listed, the most likely intended answer from the provided options is a) 21% (even though it’s slightly higher than the typical 10–15%, it may be the closest available).

T cells make up about 70–80%, NK cells about 5–10%, and B cells about 10–15%.

Given the options:

• 21% → slightly high but possible in some references

• 48% → too high

• 76% → typical for T cells, not B cells

• 89% → far too high

• IgM is the first antibody produced during a primary immune response.

• It is pentameric (five antibody units joined together) in serum, giving it high avidity for antigens.

• IgG (a) is monomeric and the most abundant in serum.

• IgA (c) is monomeric in serum but dimeric in mucosal secretions.

• IgE (d) is monomeric and involved in allergic reactions.

• IgG is the only antibody class that can cross the placenta from mother to fetus.

• It provides passive immunity to the newborn, protecting against infections during the first few months of life.

• IgM (a) is too large (pentamer) to cross the placenta.

• IgA (b) is mainly found in mucosal secretions and breast milk, not in the placenta.

• IgE (d) is involved in allergic reactions and does not cross the placenta.

• CRP is an acute phase reactant produced by the liver in response to IL-6 during infection or inflammation.

• It rises very rapidly, often within 6–8 hours, and can increase up to 100-fold.

• Alpha-1 antitrypsin (a), haptoglobin (b), and ceruloplasmin (d) also rise during inflammation but more slowly and less dramatically than CRP.

• IgE plays a central role in defense against parasitic infections, particularly helminths (worms).

• It binds to mast cells and basophils, triggering degranulation and release of histamine and other mediators that help expel parasites.

• IgA (a) is primarily involved in mucosal immunity.

• IgM (c) is the first antibody produced in primary responses.

• IgG (d) provides long-term systemic immunity and can neutralize pathogens but is less involved in anti-parasitic defense.

• C3b receptors (CR1) and Fc receptors (FcγR) are present on phagocytic cells and some lymphocytes.

• Monocytes/macrophages use these receptors to recognize opsonized pathogens, enhancing phagocytosis.

• B lymphocytes express CR2 (CD21), which binds C3d, and Fc receptors, which help in antigen presentation and B cell activation.

• Both cell types utilize these receptors to interact with opsonized antigens effectively.

• a) Cytotoxic cells: FALSE. Cytotoxic T cells (CD8+ T cells) are a major type of T lymphocyte. Their primary function is to identify and kill virus-infected cells, cancerous cells, and foreign tissue grafts.

• b) Helper cells: FALSE. Helper T cells (CD4+ T cells) are another essential type of T lymphocyte. They “help” orchestrate the immune response by activating B cells, cytotoxic T cells, and macrophages by releasing cytokines.

• c) Phagocytic cells: TRUE. T cells are not phagocytic. They cannot engulf and digest pathogens or debris. Phagocytosis is the primary function of cells of the innate immune system, such as macrophages, neutrophils, and dendritic cells.

• d) Regulatory cells: FALSE. Regulatory T cells (Tregs) are a specialized subset of T lymphocytes. Their function is to suppress the immune response and maintain tolerance, preventing the immune system from attacking the body’s own tissues.

• MHC class I molecules are expressed on all nucleated cells.

• They present endogenous antigens (from inside the cell, e.g., viral proteins) to CD8+ cytotoxic T lymphocytes (CTLs).

• CD8+ T cells then kill infected or abnormal cells.

• MHC class II molecules present exogenous antigens to CD4+ helper T cells.

• B cells recognize free antigens via their B-cell receptor.

• NK cells detect cells with reduced or missing MHC I, leading to killing.

• Acute phase reactants are serum proteins whose levels increase rapidly in response to infection, inflammation, or tissue injury.

• Examples include: C-reactive protein (CRP), fibrinogen, serum amyloid A, and complement proteins.

• Haptens (a) are small molecules that cannot elicit an immune response on their own but can when attached to a carrier.

• Opsonins (c) tag pathogens for phagocytosis.

• Chemotaxins (d) attract immune cells to the site of infection.

• Macrophages are professional phagocytes that recognize opsonized pathogens through receptors for complement component C3b and Fc receptors for antibodies, enhancing phagocytosis.

• CD3 (b) is expressed on T lymphocytes, not macrophages.

• Production of antibodies (c) is a function of plasma cells, derived from B cells.

• High rough endoplasmic reticulum activity (d) is characteristic of plasma cells, which synthesize large amounts of protein (antibodies), not macrophages.

• Cellular Immunity is mediated by T lymphocytes. Its function is assessed by testing the ability of these cells to proliferate and activate in response to specific stimuli.

• Lymphocyte proliferation assays directly measure this ability. A patient’s T cells are stimulated in the lab with antigens or mitogens (like phytohemagglutinin, PHA), and their proliferation is measured, providing a direct assessment of T-cell function.

Why the other options are incorrect:

• a) Skin testing with common antigens (e.g., Candida, tetanus toxoid): This is a good in vivo test for delayed-type hypersensitivity, which is a function of cellular immunity. However, it is an indirect test and can be affected by non-immune factors like skin integrity. Lymphocyte proliferation is a more direct and fundamental measure of cellular immune function.

• b) Isohemagglutinin titers: This test measures pre-formed antibodies against ABO blood group antigens (anti-A, anti-B). This is a measure of humoral (antibody-mediated) immunity, not cellular immunity.

• c) Serum immunoelectrophoresis: This test separates and identifies different types of immunoglobulins (antibodies) in the serum. It is also a test of humoral immunity.

• Polyclonal B cell activation occurs when many B cells are activated non-specifically, without antigen specificity.

• This can be triggered by certain bacterial toxins (superantigens) or viral infections.

• As a result, self-reactive B cells may also be activated, potentially leading to autoantibody production and autoimmune phenomena.

• Inhibiting antibody production (a) is incorrect; polyclonal activation stimulates antibody production.

• T helper cell signals (b) are not required for polyclonal activation.

• Suppressor T cells (c) actually downregulate immune responses, not cause polyclonal activation.

• Haptens are small molecules that are not immunogenic on their own but can elicit an immune response when bound to a larger protein carrier.

• Opsonins (a) tag pathogens for phagocytosis.

• Adjuvants (c) enhance immune responses when mixed with antigens but are not themselves antigens.

• Allergens (d) are substances that trigger allergic reactions, which may or may not be haptens.

• An epitope (also called an antigenic determinant) is the specific part of an antigen that is recognized and bound by an antibody.

• The paratope (b) is the antigen-binding site of the antibody that interacts with the epitope.

• Haplotype (c) refers to a set of linked alleles inherited together.

• Allotype (d) refers to genetic variations in antibody constant regions among individuals.

• Interleukin-2 (IL-2) is produced mainly by activated CD4+ T helper cells.

• It acts as a growth factor to stimulate the proliferation and differentiation of T lymphocytes, including both helper and cytotoxic T cells.

• IL-1 (a) is a pro-inflammatory cytokine that induces fever and activates other immune cells.

• IL-6 (c) is involved in B cell differentiation and inflammation.

• TNF-α (d) is a pro-inflammatory cytokine involved in fever, apoptosis, and inflammation, not specifically T cell growth.

• NADPH oxidase is an enzyme complex in phagocytes (like neutrophils and macrophages) that produces reactive oxygen species (ROS) during the respiratory burst.

• ROS, such as superoxide and hydrogen peroxide, are critical for killing ingested pathogens.

• DNA polymerase (a) and RNA polymerase (c) are involved in nucleic acid synthesis, not pathogen killing.

• Catalase (d) breaks down hydrogen peroxide, so it actually reduces ROS, not generates them.

• Interferons (IFNs) are cytokines produced by virus-infected cells.

• They signal neighboring cells to upregulate antiviral defenses, such as inhibiting viral replication and activating natural killer (NK) cells.

• Stimulating antibody production (a) is mainly a function of T helper cells.

• Promoting phagocytosis of bacteria (c) is done by opsonins and phagocytes, not interferons.

• Neutralizing toxins (d) is the role of antibodies, not interferons.

• The membrane attack complex (MAC) is formed by the terminal complement components: C5b, C6, C7, C8, and multiple C9 molecules.

• MAC creates pores in the target cell membrane, leading to cell lysis.

• C1q (a) is part of the classical pathway initiation.

• C3b (b) acts as an opsonin and helps in C5 convertase formation, but does not form MAC alone.

• C4a (d) is an anaphylatoxin involved in inflammation, not MAC formation.

• IgE is the antibody responsible for allergic reactions and defense against parasitic infections.

• It binds to mast cells and basophils, and upon encountering an allergen, triggers the release of histamine and other inflammatory mediators.

• IgG (a) is involved in opsonization, complement activation, and secondary immune responses.

• IgA (b) provides mucosal immunity in secretions like saliva and breast milk.

• IgM (d) is the first antibody produced in a primary immune response.

• Hybridoma technology is used to produce monoclonal antibodies.

• It involves fusing a B lymphocyte (which produces the desired antibody but has a short lifespan) with a myeloma (cancer) cell that can divide indefinitely.

• The resulting hybridoma combines:

  • Antibody-producing ability from the B cell

  • Immortality from the myeloma cell

• Myeloma–myeloma (a) or lymphocyte–lymphocyte (c) hybrids either do not produce the desired antibody or are short-lived.

• Lymphocyte–granulocyte (d) fusion is not used in hybridoma technology.

• Dendritic cells are antigen-presenting cells (APCs) that capture antigens during innate immune responses and present them to T cells, initiating adaptive immunity.

• NK cells (a) are part of innate immunity and kill infected or tumor cells directly.

• Mast cells (c) mediate allergic and inflammatory responses.

• Neutrophils (d) are frontline phagocytes in innate immunity but do not effectively activate adaptive immunity.

• Natural killer (NK) cells are part of the innate immune system.

• They can recognize and kill virus-infected or tumor cells without prior sensitization.

• They detect cells with reduced MHC class I expression or stress-induced ligands.

• Cytotoxic T lymphocytes (a) require antigen presentation on MHC I and prior activation.

• Th1 cells (c) activate macrophages but do not directly kill virus-infected cells.

• Macrophages (d) phagocytose pathogens but do not specifically kill virus-infected host cells.

• IgG is the most abundant immunoglobulin in serum, making up about 70–75% of total antibodies.

• It provides long-term immunity after infection or vaccination and can cross the placenta to confer passive immunity to the fetus.

• IgM (a) is the first antibody produced during primary response but is less abundant.

• IgA (b) is mainly found in mucosal secretions, not serum.

• IgE (d) is present in very low concentrations in serum and is involved in allergic responses.

• V(D)J recombination is the process by which B cells and T cells randomly assemble gene segments (Variable, Diversity, and Joining) to generate a diverse repertoire of antibodies and T-cell receptors from a limited number of genes.

• Gene splicing (a) generally refers to RNA processing, not antibody diversity.

• Antigenic variation (b) is a mechanism used by pathogens to evade the immune system, not antibody generation.

• Somatic hypermutation (d) occurs after B cell activation to increase antibody affinity, not to generate the initial diversity.

• Opsonization is the process where pathogens are “tagged” with opsonins (antibodies like IgG or complement protein C3b).

• This coating enhances recognition and uptake by phagocytic cells such as macrophages and neutrophils.

• Inhibiting complement activation (a) is the opposite of opsonization.

• Destroying T cells (c) or stimulating basophils (d) are unrelated to opsonization.

• The complement system is a group of plasma proteins that help destroy pathogens and promote inflammation.

• It can be activated by:

  • Classical pathway (a): triggered by antigen-antibody complexes

  • Alternative pathway (b): triggered directly by pathogen surfaces

  • Lectin pathway (c): triggered by mannose-binding lectin binding to pathogen carbohydrates

• There is no “apoptosis pathway” for complement activation; apoptosis is a process of programmed cell death, not a complement-activating pathway.

• Central tolerance is the process by which the immune system learns not to attack self-antigens.

• It occurs in primary lymphoid organs:

  • Bone marrow: B cells that strongly recognize self-antigens are eliminated or inactivated.

  • Thymus: T cells undergo positive and negative selection to remove self-reactive clones.

• Spleen (a), lymph nodes (c), and Peyer’s patches (d) are secondary lymphoid organs, where immune responses are initiated but central tolerance is not established.

• Somatic hypermutation occurs in activated B cells within germinal centers of lymph nodes during repeated antigen exposure.

• It introduces point mutations in the variable region of antibody genes, allowing selection of B cells producing higher-affinity antibodies.

• Antigen presentation (a) is the process by which APCs display antigens to T cells.

• Clonal deletion (c) removes self-reactive lymphocytes to prevent autoimmunity.

• Complement activation (d) is part of innate immunity and does not affect antibody affinity.

• Acquired (adaptive) immunity is characterized by:

  • Specificity: Ability to recognize and target specific antigens.

  • Memory: Faster and stronger response upon subsequent exposures to the same antigen.

• Nonspecific mechanisms (a) describe innate immunity.

• Internal and external protection (b) refers to barriers, part of innate immunity.

• Sensitivity with short-term effects (c) does not capture the long-lasting, memory aspect of adaptive immunity.

• Regulatory T cells (Tregs) are a subset of CD4+ T cells that maintain immune tolerance.

• They suppress the activity of other immune cells to prevent autoimmune reactions and limit excessive immune responses.

• Enhancing antibody production (a) is a function of T helper cells.

• Promoting NK cell activity (c) is not a primary function of Tregs.

• Activating complement (d) is part of the innate immune system, not Treg function.

• Immune complex-mediated tissue injury (Type III hypersensitivity) occurs when antigen-antibody complexes deposit in tissues.

• Neutrophils are recruited to these sites by complement activation (C3a, C5a) and attempt to phagocytose the complexes.

• During this process, neutrophils release enzymes and reactive oxygen species, causing tissue damage.

• Mast cells (a) and basophils (c) are mainly involved in Type I hypersensitivity (allergic reactions).

• Eosinophils (d) target parasites and participate in allergic inflammation, but not primary immune complex injury.

• Haptens are small molecules that are antigenic only when attached to a carrier protein.

• Alone, a hapten can bind specifically to an antibody (react with B cell receptors) but cannot elicit a T cell response because it is not processed and presented on MHC molecules.

• When conjugated to a carrier protein, it can induce both B cell and T cell responses.

• Neutralization occurs when antibodies bind to pathogens or their toxins, preventing them from attaching to or entering host cells.

• Opsonization (b) tags pathogens for phagocytosis.

• Fixing complement (c) activates the complement cascade, leading to lysis or inflammation.

• Triggering apoptosis (d) is a mechanism used by cytotoxic T cells, not antibodies.

• Affinity maturation occurs in germinal centers of lymph nodes during B cell activation.

• It involves somatic hypermutation of the variable regions of antibody genes, followed by selection of B cells producing higher-affinity antibodies.

• Clonal deletion (a) eliminates self-reactive lymphocytes to prevent autoimmunity.

• Antigen presentation (c) is the process by which APCs present antigens to T cells.

• Complement activation (d) is part of innate immunity and does not generate high-affinity antibodies.

• Humoral immunity refers to the aspect of immunity that is mediated by macromolecules found in extracellular fluids, such as secreted antibodies, complement proteins, and certain antimicrobial peptides.

• B lymphocytes (B cells) are the cells that, when activated, differentiate into plasma cells. These plasma cells are factories that produce and secrete large amounts of antibodies (also called immunoglobulins) specific to a particular antigen. These antibodies circulate in the blood and lymph, providing humoral immunity.

Here is why the other options are incorrect:

• a) T helper cells: These cells are crucial for activating B cells and are key players in cell-mediated immunity, but they do not produce antibodies themselves.

• c) Macrophages: These are phagocytic cells that engulf pathogens and are part of the innate immune system. They are antigen-presenting cells but not the primary producers of antibodies.

• d) NK cells: These are part of the innate immune system and are responsible for killing virus-infected cells and tumor cells; they are not involved in antibody production.

• Opsonins are molecules (like IgG antibodies or complement component C3b) that coat pathogens, marking them for enhanced recognition and ingestion by phagocytes such as macrophages.

• Antigen alone (b) may be recognized but is less efficiently phagocytosed without opsonization.

• Haptens (c) are small molecules that are antigenic only when attached to carriers; they do not enhance phagocytosis directly.

• Secretory component (d) is part of IgA antibodies that protect mucosal surfaces, not involved in opsonization.

• CD3 is a pan-T cell marker, expressed on all mature T lymphocytes, including:

  • Helper T cells (CD4⁺)

  • Cytotoxic T cells (CD8⁺)

  • Regulatory T cells (CD4⁺CD25⁺ Tregs)

• Anti-CD3 antibodies in immunofluorescence bind to CD3, allowing detection of the total T cell population.

• Specific subsets (helper, cytotoxic, regulatory) require additional markers like CD4 or CD8.

• Passive immunity occurs when pre-formed antibodies are transferred to an individual rather than being produced by their own immune system.

• Examples:

  • Maternal IgG antibodies crossing the placenta to the fetus.

  • IgA antibodies in breast milk.

• Vaccination (a) and antibody production after infection (c) are examples of active immunity, where the individual’s immune system generates its own antibodies.

• Memory T cell activation (d) is also part of active adaptive immunity.

Here’s the explanation for each option:

• a) Help B cells produce antibodies: FALSE. This is a primary function of Helper T cells (CD4+). They are essential for activating B cells to proliferate and differentiate into antibody-secreting plasma cells.

• b) Secrete immunoglobulins: TRUE. T lymphocytes cannot produce or secrete immunoglobulins (antibodies). This is the exclusive function of B lymphocytes and their mature form, plasma cells.

• c) Release cytokines: FALSE. T cells are major producers of cytokines (e.g., interleukins, interferons). These chemical messengers are crucial for directing and regulating the immune response.

• d) Mediate positive skin reactions: FALSE. A positive delayed-type hypersensitivity skin test (like for tuberculosis) is a classic example of a reaction mediated by T cells (and macrophages).

• CD8⁺ T cells, also called cytotoxic T lymphocytes (CTLs), recognize antigens presented on MHC class I molecules.

• They kill virus-infected cells, tumor cells, and sometimes transplanted cells by releasing perforins and granzymes.

• Delayed-type hypersensitivity (a) is mainly mediated by CD4⁺ Th1 cells.

• Regulatory functions (b) are carried out by CD4⁺ Tregs.

• Helper functions (d) are performed by CD4⁺ T helper cells.

• Cytotoxic T lymphocytes (CTLs, CD8+ T cells) recognize antigens presented on MHC class I molecules of infected or abnormal cells.

• Their main function is to directly kill virus-infected cells or tumor cells by releasing perforin and granzymes.

• Activate B cells (a) is a function of T helper (CD4+) cells.

• Produce antibodies (c) is done by B cells/plasma cells, not CTLs.

• Release histamine (d) is a function of mast cells and basophils, not CTLs.

• B lymphocytes (B cells) are part of the adaptive humoral immune system.

• Upon activation by an antigen (and usually T helper cells), B cells differentiate into plasma cells, which produce and secrete antibodies (immunoglobulins).

• Macrophages (a) are phagocytic cells and antigen-presenting cells.

• T lymphocytes (c) do not produce antibodies; they mediate cellular immunity.

• Monocytes (d) circulate in blood and differentiate into macrophages or dendritic cells, but do not secrete antibodies.

• Memory cells are long-lived B and T lymphocytes generated during the primary adaptive immune response after the first encounter with an antigen.

• They allow the immune system to respond faster and more effectively upon subsequent exposures (secondary response).

• Innate immune response (a) does not produce memory cells; it is nonspecific.

• Complement activation (c) is part of innate immunity and does not generate memory.

• Passive immunity (d) involves receiving pre-formed antibodies, so no memory cells are created.

• Toll-like receptors (TLRs) are pattern recognition receptors (PRRs) that detect pathogen-associated molecular patterns (PAMPs).

• They are expressed on innate immune cells like macrophages, dendritic cells, and neutrophils.

• Activation of TLRs triggers immediate, nonspecific immune responses and also helps activate adaptive immunity.

• Adaptive immunity (a) involves B and T cells responding specifically to antigens.

• Humoral immunity (c) is antibody-mediated and part of adaptive immunity.

• Passive immunity (d) is when antibodies are transferred from another individual (e.g., via breast milk or injection).

• Natural killer (NK) cells are regulated by activating and inhibitory receptors.

• Inhibitory receptors recognize MHC class I molecules on normal cells.

• When NK cells detect normal levels of MHC I, their cytotoxic activity is inhibited, preventing killing of healthy cells.

• If MHC I is downregulated (common in virus-infected or tumor cells), the inhibition is lost, and NK cells release perforins and granzymes to induce cell death.