Immunology Practice Questions

Q: All of the following about NK cells are true, except:

Do not secrete interferon-gamma (IFN-gamma). **Explanation:** Natural Killer (NK) cells are a critical component of the innate immune system. The correct answer is **C** because it is a false statement: **NK cells are major producers of Interferon-gamma (IFN-γ).** Upon activation by IL-12 (from macrophages), NK cells secrete IFN-γ to activate macrophages, creating a bidirectional feedback loop essential for controlling intracellular pathogens. **Analysis of Options:** * **Option A (Derived from large granular cells):** This is true. Morphologically, NK cells are identified as **Large Granular Lymphocytes (LGLs)**. They contain prominent cytoplasmic granules (perforins and granzymes) used to induce apoptosis in target cells. * **Option B (Comprise about 5% of peripheral lymphoid cells):** This is true. NK cells typically constitute **5–15%** of the circulating lymphocyte population in humans. * **Option D (Express IgG Fc receptors):** This is true. NK cells express **CD16**, which is a low-affinity Fc receptor for IgG (FcγRIII). This allows them to bind to antibody-coated target cells and execute **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. **High-Yield Clinical Pearls for NEET-PG:** * **Surface Markers:** NK cells are characterized as **CD3 negative, CD16 positive, and CD56 positive.** * **MHC Restriction:** Unlike T-cells, NK cells are **not MHC-restricted**. They follow the "Missing Self" hypothesis, where they kill cells that have downregulated MHC-I (a common viral/tumor escape mechanism). * **Receptors:** They possess **KIR (Killer Immunoglobulin-like Receptors)** which provide inhibitory signals when they bind to self-MHC-I molecules. * **Origin:** They share a Common Lymphoid Progenitor (CLP) with B and T cells but do not undergo thymic maturation.

Q: Cell-mediated immunity is NOT responsible for which of the following?

Arthus reaction. **Explanation:** The core of this question lies in distinguishing between **Type III** and **Type IV hypersensitivity reactions**. **1. Why Arthus Reaction is the Correct Answer:** The Arthus reaction is a localized **Type III hypersensitivity reaction**. It is mediated by **humoral immunity**, specifically the formation of **antigen-antibody (IgG) complexes** that deposit in vessel walls. This triggers the complement cascade and attracts neutrophils, leading to vasculitis and necrosis. Since it depends on antibodies and not T-cells, it is NOT a manifestation of cell-mediated immunity (CMI). **2. Analysis of Incorrect Options (CMI-mediated):** * **Contact Dermatitis (Option B):** This is a classic **Type IV (Delayed-type) hypersensitivity** reaction. It is mediated by sensitized T-lymphocytes (CD4+ and CD8+) reacting to haptens like nickel or poison ivy. * **Graft Rejection (Option C):** Acute and chronic cellular rejections are primarily mediated by **T-cells** (CD8+ cytotoxic T-cells and CD4+ Th1 cells) recognizing foreign MHC molecules. * **Tumor Rejection (Option D):** The immune system’s primary defense against tumors is **Immune Surveillance**, which relies heavily on CMI, specifically Cytotoxic T-lymphocytes (CTLs), Natural Killer (NK) cells, and activated macrophages. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Hypersensitivity:** **ACID** (Type I: **A**naphylactic; Type II: **C**ytotoxic; Type III: **I**mmune-Complex; Type IV: **D**elayed/Cell-mediated). * **Arthus Reaction vs. Serum Sickness:** Both are Type III. Arthus is **localized** (e.g., post-vaccination swelling), while Serum Sickness is **systemic**. * **Type IV Hypersensitivity Examples:** Mantoux test (Tuberculin), Lepromin test, Sarcoidosis (granuloma formation), and Type 1 Diabetes (beta-cell destruction).

Q: Secondary allograft rejection is primarily mediated by which component of the immune system?

Memory cells. **Explanation:** The correct answer is **Memory cells**. Allograft rejection is a classic example of cell-mediated immunity (CMI). **Why Memory Cells are correct:** When an individual is exposed to a foreign tissue graft for the first time, the immune system undergoes a "Primary Response" (First-set rejection), leading to the formation of sensitized T-lymphocytes and **Memory T-cells**. Upon subsequent exposure to the same donor antigens (a second graft), these pre-existing memory cells recognize the antigens immediately. This triggers a "Secondary Response" known as **Second-set rejection**, which is much faster and more vigorous than the first. This accelerated reaction is the hallmark of immunological memory. **Why other options are incorrect:** * **Antibodies:** While antibodies play a role in Hyperacute rejection (pre-formed antibodies) and some forms of chronic rejection, the classic "Second-set" accelerated rejection is primarily a T-cell mediated process. * **Immune complexes:** These are involved in Type III hypersensitivity reactions (like Serum Sickness or Arthus reaction) but are not the primary mediators of the cellular destruction seen in secondary allograft rejection. **High-Yield Clinical Pearls for NEET-PG:** * **First-set Rejection:** Occurs in 10–14 days (Primary immune response). * **Second-set Rejection:** Occurs in 5–6 days (Secondary immune response mediated by memory T-cells). * **Hyperacute Rejection:** Occurs within minutes to hours; mediated by **pre-formed humoral antibodies** against ABO or HLA antigens. * **Graft vs Host Disease (GVHD):** Occurs when immunocompetent T-cells in the *graft* attack the *host* (common in bone marrow transplants).

Q: A young patient presents with severe recurrent pyogenic bacterial infections, yet has normal T-cell and B-cell numbers. Testing reveals a defect in the CD40 ligand of the patient's CD4 T-helper cells. Which immunoglobulin, characterized by its presence as a monomer on B-cell surfaces, a pentamer in serum, and its initial appearance in the primary immune response, is significantly elevated in this patient?

IgM. **Explanation:** The clinical presentation describes **Hyper-IgM Syndrome (Type 1)**, an X-linked immunodeficiency. The core defect lies in the **CD40 ligand (CD154)** on T-cells, which fails to interact with the **CD40 receptor** on B-cells. This interaction is mandatory for **Isotype Class Switching** and **Somatic Hypermutation**. 1. **Why IgM is correct:** Because B-cells cannot receive the "signal" to switch from producing IgM to other classes (IgG, IgA, or IgE), they continue to produce only IgM. Consequently, serum levels of IgM are normal to significantly elevated, while other isotopes are severely deficient. IgM is the first antibody produced in a primary response, exists as a **monomer** on B-cell surfaces (BCR), and forms a **pentamer** (with a J-chain) in serum. 2. **Why other options are incorrect:** * **IgG:** Levels are low because class switching from IgM to IgG is blocked. IgG is the most abundant serum Ig and crosses the placenta. * **IgA:** Levels are low due to the class-switch defect. IgA is primarily found in secretions (dimer) and protects mucosal surfaces. * **IgD:** While present on B-cell surfaces alongside IgM, it is not the primary antibody elevated in this syndrome and does not exist as a pentamer in serum. **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Most common form is X-linked (CD40L deficiency). * **Clinical Clue:** Recurrent pyogenic infections (due to low IgG) + *Pneumocystis jirovecii* pneumonia (due to T-cell signaling defect). * **Diagnosis:** Flow cytometry showing absent CD154 on activated T-cells. * **Treatment:** IVIG replacement and Hematopoietic Stem Cell Transplant (HSCT).

Q: Which of the following statements regarding IgE antibodies is NOT true?

It can cross the placenta and fix complement.. ### Explanation The correct answer is **D**, as IgE does **not** cross the placenta nor does it fix complement via the classical pathway. #### Why Option D is the Correct Answer (The False Statement) * **Placental Transfer:** Only **IgG** is capable of crossing the placenta to provide passive immunity to the fetus, due to the presence of specific Fc receptors (FcRn) on placental cells. * **Complement Fixation:** The classical complement pathway is activated by **IgM** (most potent) and **IgG** (subclasses 1, 2, and 3). IgE lacks the binding site for C1q and therefore cannot fix complement. #### Why the Other Options are Incorrect (True Statements) * **Option A & B:** IgE is the primary mediator of **Type I Hypersensitivity** (allergic) reactions. It binds to high-affinity receptors (FcεRI) on **mast cells and basophils**. Upon re-exposure to an allergen, cross-linking of IgE triggers degranulation, releasing histamine, leukotrienes, and prostaglandins. * **Option C:** IgE plays a crucial role in **helminthic (parasitic) infections**. It facilitates Antibody-Dependent Cellular Cytotoxicity (ADCC) by recruiting **eosinophils**, which release major basic protein to destroy the parasite. #### NEET-PG High-Yield Pearls * **Heat Lability:** IgE is the most heat-labile immunoglobulin (inactivated at 56°C for 30 minutes). * **Prausnitz-Küstner (PK) Reaction:** Historically used to detect IgE (reaginic antibody) by passive cutaneous anaphylaxis. * **Serum Levels:** IgE has the lowest serum concentration and the shortest half-life (~2 days) among all immunoglobulins. * **Structure:** It is a monomer with an extra constant domain (**CH4**) on its heavy chain.

Q: Which of the following is coded by the HLA III gene?

Complement. The Human Leukocyte Antigen (HLA) complex, located on the short arm of **Chromosome 6**, is divided into three classes. Understanding the distinct functions of these classes is high-yield for NEET-PG. ### **Explanation of the Correct Answer** **Option B (Complement)** is correct because the **HLA Class III** region codes for several secreted proteins involved in the immune response that are *not* cell-surface markers. Specifically, it codes for: * **Complement components:** C2, C4 (C4A and C4B), and Factor B. * **Cytokines:** Tumor Necrosis Factor (TNF-α and TNF-β). * **Heat Shock Proteins (HSP).** Unlike Class I and II, Class III molecules do not participate in antigen presentation but play a vital role in the inflammatory cascade. ### **Analysis of Incorrect Options** * **Options A & C (Graft Rejection / GVHD):** These reactions are primarily mediated by **HLA Class I** (A, B, C) and **HLA Class II** (DR, DQ, DP) molecules. Class I molecules are found on all nucleated cells and are the main targets in acute cellular rejection, while Class II molecules are restricted to antigen-presenting cells and are crucial for T-helper cell activation. * **Option D (Immunoglobulins):** These are produced by B-lymphocytes and are coded by genes located on **Chromosomes 14** (Heavy chains), **2** (Kappa light chains), and **22** (Lambda light chains), not the HLA complex on Chromosome 6. ### **High-Yield Clinical Pearls for NEET-PG** * **Class I HLA:** Coded by A, B, and C loci; presents endogenous antigens to **CD8+ T-cells**. * **Class II HLA:** Coded by DP, DQ, and DR loci; presents exogenous antigens to **CD4+ T-cells**. * **Ankylosing Spondylitis:** Strongly associated with **HLA-B27** (Class I). * **Narcolepsy:** Strongly associated with **HLA-DR2/DQB1*06:02** (Class II). * **Structure:** Class I has one heavy chain and one **β2-microglobulin** (coded on Chromosome 15); Class II has two heavy chains (α and β).

Q: The peptide binding site on Class I MHC molecules is located in which region?

The distal domain of the alpha subunit. ### Explanation **1. Why Option B is Correct:** The Class I MHC molecule is a heterodimer consisting of a heavy **$\alpha$ chain** (encoded by HLA-A, B, or C genes) and a non-covalently linked **$\beta_2$-microglobulin**. The $\alpha$ chain is folded into three domains: $\alpha_1, \alpha_2,$ and $\alpha_3$. The peptide-binding groove (cleft) is formed by the interaction of the **$\alpha_1$ and $\alpha_2$ domains**. These are the **distal domains** (farthest from the cell membrane). This groove typically accommodates short peptides of 8–10 amino acids for presentation to CD8+ T cells. **2. Why Other Options are Incorrect:** * **Option A:** The proximal domain of the $\alpha$ subunit is the **$\alpha_3$ domain**. This region is highly conserved and serves as the binding site for the **CD8 coreceptor** of T cells, not for the peptide itself. * **Option C & D:** These options describe the structure of **Class II MHC** molecules. In Class II MHC, the peptide-binding groove is formed by the interaction of two different chains (the distal $\alpha_1$ and $\beta_1$ domains). In Class I MHC, the $\beta$ subunit ($\beta_2$-microglobulin) does not participate in forming the binding cleft. **3. High-Yield Clinical Pearls for NEET-PG:** * **MHC Class I:** Present on all nucleated cells (absent on RBCs). Presents **endogenous** antigens (e.g., viral or tumor proteins) to **CD8+ Cytotoxic T cells**. * **MHC Class II:** Present only on **Antigen-Presenting Cells (APCs)** like dendritic cells, macrophages, and B cells. Presents **exogenous** antigens to **CD4+ Helper T cells**. * **Rule of 8:** MHC I × CD8 = 8; MHC II × CD4 = 8. * **$\beta_2$-microglobulin:** It is encoded on **Chromosome 15**, while the MHC gene complex is on **Chromosome 6**. It is essential for the surface expression of Class I MHC.

Question 1

Which one of the following hypotheses may be sufficient to explain non-precipitation in an antigen-antibody system?

Accepted Answer

The antibody has been cleaved to divalent Fab' fragments

Answer

The antigen has a multivalent determinant

Answer

The antigen has a single, non-repeated determinant

Answer

The antibody has been cleaved to divalent Fab'2 fragments

Question 2

An immunologist sees a child with a suspected primary immunodeficiency and orders a nitroblue tetrazolium test. What condition is she screening the child for?

Accepted Answer

Chronic granulomatous disease

Answer

Chediak-Higashi syndrome

Answer

Tuftsin deficiency

Answer

Wiskott-Aldrich syndrome

Question 3

All of the following about NK cells are true, except:

Accepted Answer

Do not secrete interferon-gamma (IFN-gamma)

Answer

Derived from large granular cells

Answer

Comprise about 5% of human peripheral lymphoid cells

Answer

Express IgG Fc receptors

Question 4

Cell-mediated immunity is NOT responsible for which of the following?

Accepted Answer

Arthus reaction

Answer

Contact dermatitis

Answer

Graft rejection

Answer

Tumor rejection

Question 5

Secondary allograft rejection is primarily mediated by which component of the immune system?

Accepted Answer

Memory cells

Answer

Antibodies

Answer

Immune complexes

Answer

None of the above

Question 6

A young patient presents with severe recurrent pyogenic bacterial infections, yet has normal T-cell and B-cell numbers. Testing reveals a defect in the CD40 ligand of the patient's CD4 T-helper cells. Which immunoglobulin, characterized by its presence as a monomer on B-cell surfaces, a pentamer in serum, and its initial appearance in the primary immune response, is significantly elevated in this patient?

Accepted Answer

IgM

Answer

IgG

Answer

IgA

Answer

IgD

Question 7

Which of the following statements regarding IgE antibodies is NOT true?

Accepted Answer

It can cross the placenta and fix complement.

Answer

It mediates the release of histamine and other chemical mediators.

Answer

It is the primary antibody involved in allergic reactions.

Answer

It is involved in anti-parasitic immune responses.

Question 8

What region of the immunoglobulin molecule contains the antigen binding site?

Accepted Answer

Hypervariable region

Answer

Variable region

Answer

Constant region

Answer

Idiotype

Question 9

Which of the following is coded by the HLA III gene?

Accepted Answer

Complement

Answer

Immunological reaction in graft rejection

Answer

Graft versus host reaction

Answer

Immunoglobulins

Question 10

The peptide binding site on Class I MHC molecules is located in which region?

Accepted Answer

The distal domain of the alpha subunit

Answer

The proximal domain of the alpha subunit

Answer

The proximal domains of the alpha and beta subunits

Answer

The distal domains of the alpha and beta subunits

Immunology — MCQs

Immunology — MCQs

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