Immunology Practice Questions

Q: In the context of immune response, which of the following cell types does not express MHC class II molecules?

NK cells. ***NK cells*** - **Natural Killer (NK) cells)** are innate lymphocytes that do **NOT express MHC class II molecules** under any circumstances. - NK cells use alternative recognition mechanisms (KIRs, activating receptors) to detect target cells, primarily recognizing the **absence of MHC class I** or stress-induced ligands. - They function in innate immunity without antigen presentation capability. - **This is the best answer** as NK cells never express MHC class II, making them distinctly different from professional APCs. *Cortical macrophages* - **Cortical macrophages** in lymphoid organs are professional **antigen-presenting cells (APCs)** that constitutively express **MHC class II molecules**. - They present processed antigens to CD4+ T helper cells, playing a crucial role in initiating adaptive immune responses. *Medullary macrophages* - **Medullary macrophages** are also professional APCs that constitutively express **MHC class II molecules**. - They participate in antigen presentation and immune surveillance within the medullary regions of lymphoid tissues. *Neutrophils* - Neutrophils are granulocytes that **typically do not constitutively express MHC class II molecules** in their resting state. - However, under certain inflammatory conditions with prolonged stimulation (IFN-γ, GM-CSF), neutrophils can be induced to express low levels of MHC class II. - While neutrophils generally lack MHC class II, **NK cells are the more definitive answer** as they never express MHC class II under any physiological or pathological conditions.

Q: IFN-gamma is produced by

T-cells. ***T-cells*** - **Interferon-gamma (IFN-γ)** is a crucial cytokine primarily produced by **activated T-lymphocytes**, especially **Th1 cells** and **cytotoxic T lymphocytes (CTLs)**. - Natural killer (NK) cells also produce **IFN-γ**, which plays a key role in **antiviral** and **antitumor immunity**, as well as in promoting **Type 1 immune responses**. *Macrophages* - While macrophages are **responsive to IFN-γ** (e.g., becoming activated), they are not the primary producers of this cytokine. - Macrophages primarily produce other cytokines such as **IL-1, IL-6, TNF-alpha**, and **IL-12** in response to infection or inflammation. *Neutrophils* - **Neutrophils** are key phagocytes in the innate immune system and are primarily involved in engulfing and killing pathogens. - They are not known to be a significant source of **IFN-γ** production; their main defensive mechanisms involve **phagocytosis**, **degranulation**, and **NETosis**. *B-cells* - **B-cells** are central to humoral immunity, specializing in **antibody production** and acting as **antigen-presenting cells**. - They generally do not produce **IFN-γ**; instead, their cytokine repertoire includes **IL-10**, **IL-6**, and **lymphotoxin**.

Q: Which of the following is a superantigen ?

TSST. ***TSST*** - **Toxic Shock Syndrome Toxin-1 (TSST-1)** is a classic example of a superantigen produced by *Staphylococcus aureus*. - Superantigens **bind directly to MHC class II molecules and T-cell receptors (TCRs)** outside of the antigen-binding groove, leading to non-specific activation of a large percentage of T cells and a massive release of cytokines. *Cholera toxin* - **Cholera toxin** is an exotoxin produced by *Vibrio cholerae* that causes massive fluid secretion in the intestine by **activating adenylate cyclase** in enterocytes. - It functions by **ADP-ribosylating the Gs alpha subunit**, leading to constitutive activation of cyclic AMP production, but it is not a superantigen. *Diphtheria toxin* - **Diphtheria toxin**, produced by *Corynebacterium diphtheriae*, inhibits protein synthesis in eukaryotic cells by **ADP-ribosylating elongation factor-2 (EF-2)**. - This action leads to cell death and the characteristic pseudomembrane formation in diphtheria, but it does not act as a superantigen. *Vero-cytoxin* - **Vero-cytoxin** (also known as Shiga toxin or Shiga-like toxin) is produced by *E. coli* O157:H7 and other Shiga toxin-producing *E. coli* (STEC). - It inhibits protein synthesis by **cleaving ribosomal RNA**, primarily causing damage to intestinal cells and renal endothelial cells, but it is not a superantigen.

Q: What is the primary use of the Hybridoma technique?

Monoclonal antibodies. ***Monoclonal antibodies*** - The **hybridoma technique** is primarily used to produce **monoclonal antibodies (MAbs)**, which are highly specific antibodies derived from a single B-cell clone. - These antibodies recognize a **single epitope** on an antigen, providing exceptional specificity and uniformity. - The technique involves **fusing a B-lymphocyte** (antibody-producing cell) with a **myeloma cell** (immortal cancer cell) to create a hybridoma that continuously produces identical antibodies. - This is the **gold standard** for producing large quantities of identical, highly specific antibodies for diagnostic and therapeutic use. *Specific antibodies* - While monoclonal antibodies are indeed specific, this term is **too vague** and could refer to any antibody with specificity, including polyclonal antibodies. - **Polyclonal antibodies** are also specific but are produced through conventional immunization, not the hybridoma technique. - The defining characteristic of the hybridoma technique is that it produces **monoclonal** (single clone) antibodies, not just "specific" ones. *Antigen* - An **antigen** is a molecule that elicits an immune response and is used to immunize animals during antibody production. - However, antigens are the **input** for antibody production, not the **product** of the hybridoma technique. *Cytokines* - **Cytokines** are signaling molecules involved in immune cell communication and regulation. - They are not produced by the hybridoma technique, which is specifically designed for **antibody production**.

Q: Rosette formation with sheep RBCs (SRBCs) indicates functioning of -

T-cells. ***T-cells*** - **T-cells** possess specific receptors, like **CD2** on their surface, that can bind to ligands on sheep red blood cells (SRBCs). - This binding leads to the formation of characteristic **rosettes**, where SRBCs cluster around the T-lymphocytes, indicating functional T-cells. *B-cells* - **B-cells** primarily function in **humoral immunity** by producing antibodies and do not typically form rosettes with sheep RBCs. - While B-cells have surface receptors, they are not CD2 and thus do not facilitate this specific type of rosette formation. *Neutrophils* - **Neutrophils** are **phagocytic cells** involved in innate immunity, primarily combating bacterial and fungal infections. - They lack the specific surface receptors (like CD2) required to form rosettes with sheep RBCs. *Monocytes* - **Monocytes** are precursors to macrophages and dendritic cells, involved in phagocytosis and antigen presentation. - They do not possess the necessary surface markers to form rosettes with sheep RBCs.

Q: Cytolytic activity of membrane attack complex is modulated by ?

Factor S (vitronectin). ***Correct Option: Factor S (vitronectin)*** - Vitronectin (S-protein) is a **plasma protein** that directly modulates the **cytolytic activity of the membrane attack complex (MAC)**. - It binds to the **C5b-7 complex** in the fluid phase, preventing its insertion into target cell membranes and thereby blocking the formation of the complete, functional MAC. - By inhibiting membrane insertion of C5b-7, vitronectin prevents the subsequent binding of **C8 and C9**, which are essential for the cytolytic pore formation. - This is a **direct modulation** of MAC's cytolytic activity at the MAC assembly stage. *Incorrect Option: Factor H* - Factor H is a regulatory protein that controls the **alternative pathway** of complement activation by promoting degradation of **C3b**. - By degrading C3b, Factor H prevents formation of **C5 convertase**, thereby reducing downstream MAC formation. - However, Factor H acts **early in the complement cascade** and does not directly modulate the cytolytic activity of already-formed MAC components. - Its effect is on **preventing MAC formation**, not on modulating MAC's cytolytic function itself. *Incorrect Option: Factor I* - Factor I is a **serine protease** that cleaves and inactivates C3b and C4b, requiring cofactors like Factor H or C4bp. - Like Factor H, it regulates complement activation **upstream** of MAC formation. - It does not directly interact with or modulate the cytolytic activity of the MAC. *Incorrect Option: Factor B* - Factor B is a component of the **alternative pathway C3 convertase** (C3bBb). - It **promotes complement activation** rather than modulating MAC's cytolytic activity. - Factor B functions early in the cascade and has no direct role in regulating MAC function.

Q: What are the changes in the variable region of immunoglobulins?

Idiotype. ***Idiotype*** - **Idiotype** refers to the unique set of antigenic determinants in the **variable region** of an antibody molecule, specifically within the **hypervariable regions (complementarity-determining regions, CDRs)**. - These unique determinants allow antibodies to recognize specific antigens and are generated by the specific **V(D)J gene rearrangements** in B cells. *Isotype* - **Isotype** refers to the constant region of an antibody, determining its class (e.g., **IgG, IgM, IgA, IgD, IgE**). - This region defines the antibody's effector functions and has nothing to do with the antigen-binding variability. *Allotype* - **Allotype** refers to minor genetic variations within the **constant region** of an antibody molecule within a species. - These variations are due to different alleles inherited from parents and are not associated with the variable region that binds to antigens. *Epitope* - An **epitope** is the specific part of an **antigen** that an antibody or T-cell receptor recognizes and binds to. - It is a feature of the antigen, not a change within the variable region of the immunoglobulin itself.

Q: Which immunoglobulin is known to be heat-labile?

IgM. ***IgM*** - **IgM** is known for its **heat lability** and is readily denatured at 56°C within a few minutes. - This characteristic is due to its **pentameric structure** held together by disulfide bonds and J chains, which are sensitive to thermal denaturation. - Heat lability of IgM is clinically important in complement fixation tests and other laboratory assays where heat inactivation is performed. - IgM is the first antibody produced in primary immune response and its heat sensitivity distinguishes it from other immunoglobulins. *IgA* - **IgA** exists in monomeric (serum) and dimeric (secretory) forms and shows moderate stability to heat. - Secretory IgA is relatively stable as it needs to function in harsh mucosal environments, though not as heat-resistant as IgG. - Does not exhibit the pronounced heat lability characteristic of IgM. *IgG* - **IgG** is the most stable immunoglobulin and is highly resistant to heat denaturation. - Can withstand temperatures up to 60-70°C without significant loss of activity. - Its monomeric structure with strong intramolecular bonds provides exceptional thermal stability. - Most abundant antibody in serum and has the longest half-life. *IgE* - **IgE** is actually quite stable to heat and can withstand 56°C for extended periods. - While it has a short half-life in serum (2-3 days), this is due to receptor binding rather than heat instability. - Important in type I hypersensitivity reactions and parasitic infections. - Does not show the characteristic heat lability that defines IgM.

Q: Which immunoglobulin is primarily secreted by the intestine?

IgA. **IgA** - **Secretory IgA** is the dominant immunoglobulin in mucosal secretions, including those of the intestine. - It plays a crucial role in providing **local immunity** by preventing microbial adherence and neutralizing toxins on mucosal surfaces. *IgG* - **IgG** is the most abundant immunoglobulin in serum and plays a major role in systemic immunity, including opsonization and complement activation. - While some IgG is found in secretions, it is not the primary immunoglobulin secreted by the intestine. *IgM* - **IgM** is a pentameric immunoglobulin, primarily found in blood and lymph, where it is very effective in activating the complement system and agglutinating antigens. - Although it can be found at mucosal surfaces in small amounts, it is not the principal secreted antibody in the intestine. *IgD* - **IgD** is primarily found on the surface of naive B lymphocytes, where it functions as a B cell receptor. - Its role in secreted form is minimal, and it is not significantly secreted into the intestine or other bodily fluids.

Q: What is the most common genetic factor associated with increased susceptibility to Neisseria infections?

Complement deficiency. ***Complement deficiency*** - Deficiencies in the **terminal complement pathway (C5-C9)**, particularly C5b-C9 (membrane attack complex, MAC), significantly increase susceptibility to disseminated *Neisseria* infections. - The MAC is crucial for lysing Gram-negative bacteria like *Neisseria meningitidis* and *Neisseria gonorrhoeae*, and its absence allows for uncontrolled bacterial proliferation. *Factor H deficiency* - **Factor H** is a regulatory protein of the alternative complement pathway, preventing its overactivation on host cells. - Its deficiency typically leads to conditions like **atypical hemolytic uremic syndrome (aHUS)** and **dense deposit disease**, not primarily increased susceptibility to *Neisseria* infections. *HLA B27* - **HLA-B27** is a human leukocyte antigen strongly associated with a group of autoimmune inflammatory diseases called **spondyloarthropathies**, such as ankylosing spondylitis. - It does not directly impact the immune response to *Neisseria* infections or increase susceptibility to them. *IgA deficiency* - **Selective IgA deficiency** is the most common primary immunodeficiency, characterized by low or absent IgA levels. - Individuals with IgA deficiency are more prone to **recurrent respiratory and gastrointestinal infections**, but not specifically disseminated *Neisseria* infections.

Question 1

In the context of immune response, which of the following cell types does not express MHC class II molecules?

Accepted Answer

NK cells

Answer

Cortical macrophages

Answer

Neutrophils

Answer

Medullary macrophages

Question 2

IFN-gamma is produced by

Accepted Answer

T-cells

Answer

Macrophages

Answer

Neutrophils

Answer

B-cells

Question 3

Which of the following is a superantigen ?

Accepted Answer

TSST

Answer

Cholera toxin

Answer

Diphtheria toxin

Answer

Vero-cytoxin

Question 4

What is the primary use of the Hybridoma technique?

Accepted Answer

Monoclonal antibodies

Answer

Antigen

Answer

Specific antibodies

Answer

Cytokines

Question 5

Rosette formation with sheep RBCs (SRBCs) indicates functioning of -

Accepted Answer

T-cells

Answer

B-cells

Answer

Neutrophils

Answer

Monocytes

Question 6

Cytolytic activity of membrane attack complex is modulated by ?

Accepted Answer

Factor S (vitronectin)

Answer

Factor I

Answer

Factor B

Answer

Factor H

Question 7

What are the changes in the variable region of immunoglobulins?

Accepted Answer

Idiotype

Answer

Isotype

Answer

Epitope

Answer

Allotype

Question 8

Which immunoglobulin is known to be heat-labile?

Accepted Answer

IgM

Answer

IgA

Answer

IgG

Answer

IgE

Question 9

Which immunoglobulin is primarily secreted by the intestine?

Accepted Answer

IgA

Answer

IgG

Answer

IgM

Answer

IgD

Question 10

What is the most common genetic factor associated with increased susceptibility to Neisseria infections?

Accepted Answer

Complement deficiency

Answer

HLA-B27

Answer

IgA deficiency

Answer

Factor H deficiency

Immunology — MCQs

Immunology — MCQs

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