Immunology Practice Questions

Q: All of the following compounds are mitogens that stimulate human T cells to proliferate, EXCEPT:

Lipopolysaccharide. **Explanation:** Mitogens are substances that induce mitosis (cell division) in lymphocytes in a non-specific, polyclonal manner, regardless of their antigen specificity. **1. Why Lipopolysaccharide (LPS) is the correct answer:** LPS (Endotoxin), derived from the cell wall of Gram-negative bacteria, is a potent **B-cell mitogen** in humans. It does not stimulate T-cell proliferation. It acts by binding to Toll-like receptor 4 (TLR4) on B-cells, leading to their activation and polyclonal antibody production. **2. Analysis of Incorrect Options (T-cell Mitogens):** * **Phytohemagglutinin (PHA):** A lectin derived from kidney beans; it is a classic, potent stimulator of **T-cells**. * **Concanavalin A (ConA):** A lectin derived from jack beans; it specifically stimulates **T-cells**. * **Anti-CD3 Antibody:** CD3 is a core component of the T-cell receptor (TCR) complex. Antibodies against CD3 mimic the signal of an antigen, leading to robust, polyclonal **T-cell** activation. **3. High-Yield Clinical Pearls for NEET-PG:** * **T-cell Mitogens:** PHA, ConA, and Anti-CD3. * **B-cell Mitogens:** LPS, Epstein-Barr Virus (EBV), and Staphylococcus aureus Cowan I strain (SAC). * **Pokeweed Mitogen (PWM):** Unique because it stimulates **both** T-cells and B-cells. * **Clinical Use:** Mitogen stimulation tests are used in clinical immunology to assess the functional integrity of a patient’s cellular (T-cell) or humoral (B-cell) immunity, such as in suspected Primary Immunodeficiency Disorders (PIDs).

Q: A child has a history of recurrent infections with organisms having polysaccharide antigens (i.e., Streptococcus pneumoniae and Haemophilus influenzae). This susceptibility can be explained by a deficiency of?

IgG subclass 2. **Explanation:** **Why IgG subclass 2 is correct:** Immunoglobulin G (IgG) is divided into four subclasses (IgG1–IgG4). **IgG2** is the primary antibody responsible for the immune response against **encapsulated bacteria** (e.g., *S. pneumoniae*, *H. influenzae type b*, and *N. meningitidis*). These bacteria possess **polysaccharide capsules** that are T-cell independent antigens. While IgG1 and IgG3 typically respond to protein antigens, IgG2 is specifically specialized for carbohydrate/polysaccharide antigens. Therefore, a selective IgG2 deficiency leads to recurrent sinopulmonary infections with encapsulated organisms, even if total IgG levels appear near normal. **Analysis of Incorrect Options:** * **A. C3 nephritic factor:** This is an autoantibody that stabilizes C3 convertase, leading to continuous C3 consumption. It is associated with Type II Membranoproliferative Glomerulonephritis (MPGN) and partial lipodystrophy, not specific susceptibility to polysaccharide antigens. * **B. C5:** Deficiency of late complement components (C5–C9) specifically predisposes individuals to recurrent **Neisserial infections** (Meningitis and Gonorrhea) due to failure of the Membrane Attack Complex (MAC) formation. * **D. Myeloperoxidase (MPO):** MPO deficiency in phagocytes leads to impaired production of hypochlorous acid. While often asymptomatic, it primarily predisposes patients to disseminated **Candidiasis**, not specifically to encapsulated bacteria. **High-Yield Clinical Pearls for NEET-PG:** * **IgG1:** Most abundant subclass; responds to protein antigens (e.g., Tetanus toxoid). * **IgG2:** Responds to polysaccharide antigens; deficiency is the most common subclass deficiency in children. * **IgG3:** Most effective at activating complement. * **IgG4:** Associated with chronic allergen exposure and IgG4-related systemic diseases. * **Wiskott-Aldrich Syndrome:** Often shows low IgG2 levels along with low IgM and high IgA/IgE.

Q: All of the following are a part of innate immunity except?

T cells. **Explanation:** The immune system is broadly divided into **Innate Immunity** (non-specific, immediate response) and **Acquired/Adaptive Immunity** (specific, delayed response with memory). **Why T cells are the correct answer:** T cells (T lymphocytes) are the hallmark of **Adaptive Immunity**. They possess highly specific receptors (TCRs) generated through genetic rearrangement to recognize specific antigens. They provide cell-mediated immunity and develop "memory," allowing for a faster and more potent response upon re-exposure. Therefore, they are not part of the innate system. **Analysis of Incorrect Options:** * **Complement (A):** These are plasma proteins that act as a chemical barrier. They are activated immediately upon pathogen entry via the alternative or lectin pathways, making them a crucial humoral component of innate immunity. * **NK cells (B):** Natural Killer cells are large granular lymphocytes that provide the first line of defense against virally infected cells and tumors. Unlike T cells, they lack antigen-specific receptors and do not require prior sensitization. * **Macrophages (C):** These are professional phagocytes derived from monocytes. They act as cellular components of innate immunity by engulfing pathogens via non-specific pattern recognition receptors (PRRs). **High-Yield Clinical Pearls for NEET-PG:** * **Innate Immunity Components:** Physical barriers (Skin/Mucosa), Chemical barriers (Complement/Lysozyme), and Cellular components (Neutrophils, Macrophages, NK cells, Dendritic cells). * **Bridge between systems:** Dendritic cells and Macrophages act as a bridge by functioning as Antigen Presenting Cells (APCs) to activate the adaptive system. * **NK Cell Marker:** CD56 is the characteristic marker for NK cells. * **Specificity:** Innate immunity recognizes **PAMPs** (Pathogen-Associated Molecular Patterns) via **PRRs** (like Toll-like Receptors).

Q: What part of an antibody is related to the antigen idiotype?

N-terminal. **Explanation:** The **idiotype** of an antibody refers to the unique set of antigenic determinants (idiotopes) located within the **Variable (V) regions** of the heavy and light chains. These regions form the **antigen-binding site (paratope)**. 1. **Why N-terminal is correct:** The polypeptide chains of an antibody have a polarity. The **N-terminal** (amino-terminal) ends of both the heavy and light chains contain the variable domains ($V_H$ and $V_L$). Since the idiotype is defined by the specific amino acid sequence in these variable domains that determines antigen specificity, the N-terminal is the structural site related to the idiotype. 2. **Why other options are incorrect:** * **Fc fragment:** This is the "Fragment crystallizable" region composed only of constant domains ($C_H2, C_H3$). it mediates biological effector functions (e.g., complement fixation, opsonization) but does not bind antigens. * **Hinge region:** This is a flexible amino acid stretch between the $C_H1$ and $C_H2$ domains that allows the two Fab arms to move; it does not determine idiotype. * **C-terminal:** The Carboxy-terminal ends of the heavy chains are located within the Fc region. They are constant for a given isotype and do not contribute to the unique antigen-binding idiotype. **High-Yield Clinical Pearls for NEET-PG:** * **Isotype:** Determined by the heavy chain constant region (e.g., IgG vs. IgA). * **Allotype:** Allelic variations in constant regions between individuals of the same species. * **Idiotype:** Unique to a specific antibody molecule produced by a single B-cell clone; anti-idiotypic antibodies are used in some therapeutic regulations. * **Papain digestion** cleaves *above* the hinge region to produce 2 Fab and 1 Fc fragment, while **Pepsin** cleaves *below* the hinge to produce one $F(ab')_2$ fragment.

Q: Natural killer (NK) cells provide immunity against which of the following?

Viruses. **Explanation:** **Natural Killer (NK) cells** are a type of cytotoxic lymphocyte critical to the **innate immune system**. They play a major role in the rejection of **virally infected cells** and tumor cells. **Why Viruses is the correct answer:** NK cells function by identifying cells that lack or have "downregulated" **MHC Class I molecules**. Many viruses (such as CMV and HIV) attempt to evade the immune system by inhibiting MHC Class I expression to avoid detection by CD8+ T-cells. NK cells utilize the **"Missing Self" hypothesis**: when their inhibitory receptors do not find MHC Class I on a host cell, they release **perforins and granzymes**, inducing apoptosis in the infected cell. This provides a rapid response before the adaptive immune system is fully activated. **Why other options are incorrect:** * **Bacteria & Fungi:** Immunity against these extracellular or pyogenic pathogens primarily relies on **neutrophils, macrophages, and the complement system** (innate), as well as B-cells/antibodies (adaptive). * **Chlamydia:** While Chlamydia is an intracellular bacterium, the primary defense involves **Th1-mediated responses** and interferon-gamma (IFN-γ) activation of macrophages, rather than direct NK cell-mediated lysis. **NEET-PG High-Yield Pearls:** * **Markers:** NK cells are identified by the presence of **CD56** and **CD16** (FcγRIII) and the **absence of CD3**. * **Antibody-Dependent Cellular Cytotoxicity (ADCC):** Through the CD16 receptor, NK cells bind to IgG-coated target cells and kill them. * **Cytokine Production:** NK cells are a major source of **IFN-γ**, which activates macrophages to kill phagocytosed microbes. * **Origin:** They are derived from the **Common Lymphoid Progenitor (CLP)** but do not require the thymus for maturation.

Q: What is true about IgM?

Fixes complement. ### Explanation **Correct Option: A (Fixes complement)** IgM is the most potent activator of the **Classical Complement Pathway**. It exists primarily as a pentamer (connected by a J-chain), providing multiple binding sites for the C1q component of the complement cascade. A single pentameric IgM molecule bound to an antigen can initiate the cascade, whereas IgG requires at least two molecules in close proximity. **Analysis of Incorrect Options:** * **B. Increased in primary response:** While IgM is the *first* antibody produced in a primary immune response, the statement is technically incomplete or less "true" than its complement-fixing ability in a comparative sense. However, in many exam contexts, IgM is the hallmark of the **acute/primary phase**, while IgG dominates the secondary (anamnestic) response. * **C. The Fab region is composed of the variable region:** This is partially incorrect. The Fab (Fragment antigen-binding) region is composed of **both** the entire variable region (VH and VL) and the first constant region (CH1 and CL). * **D. The Fc region is antibody-binding:** This is incorrect. The **Fab** region binds to the antigen (antibody-binding), while the **Fc** (Fragment crystallizable) region binds to host cell receptors (Fc receptors) and mediates effector functions like complement activation and opsonization. **High-Yield Clinical Pearls for NEET-PG:** * **Structure:** IgM is a **pentamer** in serum (10 binding sites) but a **monomer** on the surface of B-cells (BCR). * **Molecular Weight:** It is the largest immunoglobulin (**"Millionaire Molecule"**), preventing it from crossing the placenta. * **Clinical Significance:** Presence of **IgM in a newborn** indicates intrauterine infection (e.g., TORCH), as maternal IgM cannot cross the placenta. * **Agglutination:** Due to its high valency, IgM is the most efficient antibody for agglutination (e.g., ABO blood grouping).

Q: To which cell does IgE bind?

Mast cells. **Explanation:** The correct answer is **Mast cells**. **Why Mast Cells?** IgE (Immunoglobulin E) is the primary mediator of Type I hypersensitivity reactions. Mast cells and basophils possess high-affinity surface receptors known as **FcεRI**. The Fc portion of the IgE molecule binds to these receptors with extreme tenacity. When an allergen later cross-links these bound IgE molecules, it triggers mast cell degranulation, releasing inflammatory mediators like histamine, leukotrienes, and prostaglandins. **Analysis of Incorrect Options:** * **T cells:** These cells utilize T-cell receptors (TCR) to recognize antigens presented by MHC molecules. They do not possess high-affinity receptors for IgE. * **B cells:** While B cells produce IgE (after class-switching), they primarily express IgM and IgD as membrane-bound receptors. They do not typically bind circulating IgE via FcεRI. * **NK cells:** Natural Killer cells possess **FcγRIII (CD16)**, which binds to **IgG**, facilitating Antibody-Dependent Cellular Cytotoxicity (ADCC), but they do not bind IgE. **High-Yield Clinical Pearls for NEET-PG:** * **Receptor Specificity:** **FcεRI** is the high-affinity receptor (found on Mast cells/Basophils); **FcεRII (CD23)** is the low-affinity receptor (found on B cells and macrophages). * **Prausnitz-Küstner (PK) Reaction:** A classic experiment demonstrating that the "reaginic antibody" (IgE) in serum can sensitize the skin of a non-allergic individual by binding to local mast cells. * **Parasitic Infections:** IgE also plays a role in defense against helminths by coating the parasite; eosinophils then bind to the IgE via Fc receptors to release major basic protein (ADCC).

Q: Which of the following conditions is caused by deficiency of complement C3 and C3b?

Severe recurrent pyogenic infection. **Explanation:** **Core Concept:** Complement **C3** is the central hub of the complement system, where the classical, lectin, and alternative pathways converge. Its primary functions include **opsonization** (via C3b) and the initiation of the **Membrane Attack Complex (MAC)**. **Why C is correct:** C3b acts as a major opsonin, coating bacteria to facilitate phagocytosis by neutrophils and macrophages. A deficiency in C3 or C3b leads to a failure in opsonization and an inability to clear encapsulated bacteria (e.g., *Streptococcus pneumoniae*, *Haemophilus influenzae*). This results in **severe, recurrent pyogenic (pus-forming) infections**, typically starting early in life. **Why other options are incorrect:** * **A. Hereditary Angioneurotic Edema:** This is caused by a deficiency of **C1 esterase inhibitor**, leading to overproduction of bradykinin. * **B & D. SLE and Collagen Vascular Diseases:** Deficiencies in **early components** of the classical pathway (**C1, C4, and C2**) are strongly associated with SLE-like syndromes. This is because these components are essential for the clearance of immune complexes; their absence leads to tissue deposition and inflammation. **High-Yield Clinical Pearls for NEET-PG:** * **C1, C2, C4 deficiency:** Associated with Immune complex diseases (SLE). **C2** is the most common complement deficiency. * **C3 deficiency:** Most severe; leads to recurrent pyogenic infections and Type III hypersensitivity. * **C5–C9 (MAC) deficiency:** Specifically predisposes to recurrent **Neisserial infections** (Meningitis/Gonorrhea). * **CH50 Assay:** Used to screen for classical pathway integrity; **AH50** screens the alternative pathway.

Question 1

All of the following compounds are mitogens that stimulate human T cells to proliferate, EXCEPT:

Accepted Answer

Lipopolysaccharide

Answer

Concanavalin A

Answer

Anti CD3 antibody

Answer

Phytohemagglutinin

Question 2

Recurrent Neisseria infections are not predisposed by which of the following?

Accepted Answer

Early complement component deficiency

Answer

Late complement component deficiency

Answer

Factor D deficiency

Answer

Properdin deficiency

Question 3

A child has a history of recurrent infections with organisms having polysaccharide antigens (i.e., Streptococcus pneumoniae and Haemophilus influenzae). This susceptibility can be explained by a deficiency of?

Accepted Answer

IgG subclass 2

Answer

C3 nephritic factor

Answer

C5

Answer

Myeloperoxidase in phagocytic cells

Question 4

All of the following are a part of innate immunity except?

Accepted Answer

T cells

Answer

Complement

Answer

NK cells

Answer

Macrophages

Question 5

What part of an antibody is related to the antigen idiotype?

Accepted Answer

N-terminal

Answer

Fc fragment

Answer

Hinge region

Answer

C-terminal

Question 6

Natural killer (NK) cells provide immunity against which of the following?

Accepted Answer

Viruses

Answer

Bacteria

Answer

Fungi

Answer

Chlamydia

Question 7

Which of the following cells is primarily involved in T cell independent antigen presentation?

Accepted Answer

B cell

Answer

T cell

Answer

Macrophage

Answer

CD8+ cytotoxic T lymphocyte

Question 8

What is true about IgM?

Accepted Answer

Fixes complement

Answer

Increased in primary response

Answer

The Fab region is composed of the variable region

Answer

The Fc region is antibody-binding

Question 9

To which cell does IgE bind?

Accepted Answer

Mast cells

Answer

T cells

Answer

B cells

Answer

NK cells

Question 10

Which of the following conditions is caused by deficiency of complement C3 and C3b?

Accepted Answer

Severe recurrent pyogenic infection

Answer

Hereditary angioneurotic edema

Answer

Systemic lupus erythematosus (SLE)

Answer

Collagen vascular disease

Immunology — MCQs

Immunology — MCQs

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