Immunology Practice Questions

Q: Which cell type lacks HLA antigens?

Red blood cell. **Explanation:** The Human Leukocyte Antigen (HLA) system is the human version of the **Major Histocompatibility Complex (MHC)**. HLA Class I antigens (HLA-A, B, and C) are expressed on the surface of almost all **nucleated cells** in the body. **1. Why Red Blood Cells (RBCs) are the correct answer:** Mature Red Blood Cells are **non-nucleated** cells. Because they lack a nucleus and the necessary protein-synthesizing machinery, they do not express HLA Class I or Class II antigens on their surface. Instead, RBCs express blood group antigens (ABO and Rh systems). This is why HLA matching is not required for simple blood transfusions, whereas it is critical for organ and bone marrow transplants. **2. Why the other options are incorrect:** * **Monocytes (A) & Neutrophils (C):** These are nucleated white blood cells. As nucleated cells, they express high levels of HLA Class I antigens. Monocytes, being professional antigen-presenting cells (APCs), also express HLA Class II antigens. * **Thrombocytes/Platelets (B):** Although platelets are anucleated fragments of megakaryocytes, they are a notable **exception** to the "nucleated cell" rule. Platelets **do express HLA Class I antigens** on their surface (inherited from the megakaryocyte). This is clinically significant as patients can develop "HLA alloimmunization" after multiple platelet transfusions. **High-Yield NEET-PG Pearls:** * **HLA Class I:** Found on all nucleated cells + Platelets. (Mnemonic: 1 x 8 = 8; interacts with CD8+ T cells). * **HLA Class II:** Found only on professional Antigen Presenting Cells (B-cells, Macrophages, Dendritic cells, and Thymic epithelial cells). (Mnemonic: 2 x 4 = 8; interacts with CD4+ T cells). * **Trophoblasts:** These are another important cell type that lacks classical HLA-A and HLA-B to avoid maternal immune rejection.

Q: The binding of complement to a bacterial cell surface is termed as:

Opsonization. **Explanation:** The correct answer is **Opsonization**. **1. Why Opsonization is correct:** Opsonization is the process by which a pathogen is marked for ingestion and destruction by a phagocyte. In the complement system, **C3b** (and to a lesser extent C4b) acts as a potent **opsonin**. When these complement proteins bind to the bacterial cell surface, they act as "tags." Phagocytic cells, such as macrophages and neutrophils, possess specific receptors (CR1) for C3b. This binding significantly enhances the efficiency of phagocytosis, acting like a "handle" that allows the immune cell to grip and engulf the bacteria. **2. Why other options are incorrect:** * **Complement activation:** This refers to the entire biochemical cascade (Classical, Alternative, or Lectin pathways) that leads to the generation of effector molecules. While binding is a *step* in activation, the specific term for "coating" a cell to enhance phagocytosis is opsonization. * **Complement stabilization:** This is not a standard immunological term for surface binding. In immunology, "stabilization" usually refers to the role of **Properdin**, which stabilizes the C3 convertase (C3bBb) in the alternative pathway, rather than the binding of complement to the bacteria itself. **Clinical Pearls for NEET-PG:** * **Most potent opsonins:** IgG and C3b are the two most important opsonins in the body. * **C3b function:** Remember the mnemonic "C3**b** **B**inds **B**acteria" (Opsonization). * **C5a function:** Primarily involved in **chemotaxis** and inflammation. * **Membrane Attack Complex (MAC):** Formed by C5b-C9; its primary role is the osmotic lysis of Gram-negative bacteria (especially *Neisseria*). * **Deficiency:** Patients with C3 deficiency suffer from recurrent pyogenic infections due to impaired opsonization.

Q: The class of antibodies that plays an important role in type I hypersensitivity reactions is _____,

IgE. **Explanation:** **Correct Answer: C. IgE** Type I hypersensitivity (Immediate Hypersensitivity) is mediated by **IgE antibodies**. Upon initial exposure to an allergen, IgE is produced and binds to high-affinity receptors (**FcεRI**) on the surface of **mast cells and basophils**. On subsequent exposure, the allergen cross-links these membrane-bound IgE molecules, triggering degranulation and the release of pharmacological mediators like **histamine**, leukotrienes, and prostaglandins. This leads to clinical manifestations such as anaphylaxis, asthma, and urticaria. **Why other options are incorrect:** * **IgA:** Primarily found in secretions (tears, saliva, colostrum) and provides mucosal immunity. It does not mediate Type I hypersensitivity. * **IgD:** Acts mainly as a surface receptor on B-cells for antigen recognition; its systemic effector function is minimal. * **IgG:** The most abundant serum antibody, involved in Type II (cytotoxic) and Type III (immune-complex) hypersensitivity. It provides long-term immunity and crosses the placenta. **High-Yield NEET-PG Pearls:** * **Mnemonic for Hypersensitivity:** **ACID** (Type **A**naphyalctic/IgE, Type **C**ytotoxic/IgG, Type **I**mmune-Complex, Type **D**elayed/T-cells). * **Prausnitz-Küstner (PK) Reaction:** A classic test used to demonstrate the presence of IgE (reaginic antibodies) in serum. * **Eosinophilia:** Type I reactions are often associated with an increase in eosinophil count, stimulated by IL-5. * **Casoni’s Test:** A skin test for Hydatid disease that relies on a Type I hypersensitivity mechanism.

Q: Which of the following is NOT an example of delayed type hypersensitivity?

Arthus phenomenon. ### Explanation **1. Why Arthus Phenomenon is the Correct Answer:** The **Arthus phenomenon** is a localized **Type III Hypersensitivity** reaction (Immune-complex mediated). It occurs when an antigen is injected into the skin of an individual with high levels of pre-existing circulating IgG antibodies. This leads to the formation of antigen-antibody complexes that deposit in small blood vessel walls, activating the complement system and causing inflammatory vasculitis and tissue necrosis. Unlike delayed-type reactions, it is mediated by antibodies, not T-cells. **2. Analysis of Incorrect Options (Type IV Hypersensitivity):** * **Contact Dermatitis (Option B):** A classic example of Type IV hypersensitivity. It is mediated by CD4+ and CD8+ T-cells reacting to haptens (like nickel or poison ivy) upon re-exposure. * **Tuberculin Test (Option C):** The prototype of Delayed-Type Hypersensitivity (DTH). It involves the recruitment of macrophages by Th1 cells in response to PPD (Purified Protein Derivative), peaking at 48–72 hours. * **Graft versus Host Reaction (Option D):** This involves donor T-cells recognizing and attacking the recipient’s (host) tissues. It is a cell-mediated immune response, falling under the spectrum of Type IV reactions. **3. High-Yield Clinical Pearls for NEET-PG:** * **Coombs and Gell Classification:** * **Type I:** Immediate (IgE) * **Type II:** Cytotoxic (IgG/IgM) * **Type III:** Immune Complex (Arthus, Serum Sickness) * **Type IV:** Delayed/Cell-mediated (T-cells) * **Memory Aid:** **"ACID"** (Anaphylactic, Cytotoxic, Immune-complex, Delayed). * **Arthus vs. Serum Sickness:** Arthus is **localized** (e.g., post-vaccination swelling), while Serum Sickness is **systemic** (e.g., fever, rash, arthralgia after antitoxin administration). Both are Type III.

Q: Killer cells are associated with which type of immunologic response?

None of the above. **Explanation:** The correct answer is **None of the above** because "Killer cells" (specifically Natural Killer or NK cells) are primary mediators of **Type IV Hypersensitivity** (Cell-mediated immunity), which is not listed among the options. **1. Why "None of the above" is correct:** Killer cells, including **Natural Killer (NK) cells** and **Cytotoxic T-lymphocytes (CD8+ T cells)**, are the hallmark of cell-mediated immune responses. In the Gell and Coombs classification, Type IV hypersensitivity is the only "delayed-type" response that does not involve antibodies; instead, it relies on T-cells and NK cells to induce direct cytotoxicity or cytokine-mediated inflammation. **2. Why other options are incorrect:** * **Type I (Immediate):** Mediated by **IgE antibodies** and mast cell degranulation (e.g., Anaphylaxis, Asthma). * **Type II (Cytotoxic):** Mediated by **IgG or IgM antibodies** directed against antigens on specific cell surfaces (e.g., ABO incompatibility, Myasthenia Gravis). While NK cells can participate here via Antibody-Dependent Cellular Cytotoxicity (ADCC), the primary mechanism is antibody-driven. * **Type III (Immune-complex):** Mediated by the deposition of **antigen-antibody complexes** in tissues, leading to complement activation (e.g., SLE, Serum sickness). **High-Yield Clinical Pearls for NEET-PG:** * **NK Cells:** Large granular lymphocytes that do not require prior sensitization. They recognize cells lacking **MHC Class I** molecules ("Missing Self" hypothesis). * **ADCC:** A bridge between humoral and innate immunity where NK cells kill target cells coated with IgG via the **CD16 receptor** (FcγRIII). * **Type IV Subtypes:** Remember that Type IV is subdivided (IVa to IVd) based on the specific cell type involved (Th1, Th2, Cytotoxic T-cells, or Neutrophils).

Q: Which of the following is NOT a component of innate immunity?

Antibody. **Explanation:** Innate immunity is the body's first line of defense, providing a non-specific, rapid response that is present from birth. It lacks memory and does not improve with repeated exposure. **Why Antibody is the Correct Answer:** Antibodies (Immunoglobulins) are components of **Adaptive (Acquired) Immunity**. They are produced by B-lymphocytes (plasma cells) in response to specific antigens. Unlike innate components, antibodies are highly specific, involve a lag period for initial production, and generate immunological memory. **Why the other options are part of Innate Immunity:** * **Epithelial surfaces (Option A):** These act as **physical/mechanical barriers**. The skin and mucous membranes prevent the entry of pathogens through shedding (desquamation) and ciliary movement. * **Lysozyme (Option C):** This is a **chemical/physiological barrier**. It is an enzyme found in tears, saliva, and nasal secretions that kills bacteria by hydrolyzing the peptidoglycan layer of the cell wall. * **Sebum (Option D):** Produced by sebaceous glands, sebum contains long-chain fatty acids that create an acidic pH (3-5) on the skin, inhibiting the growth of many pathogenic bacteria and fungi. **High-Yield Clinical Pearls for NEET-PG:** * **Components of Innate Immunity:** Physical barriers (Skin/Mucosa), Chemical barriers (pH, Lysozyme, Complement), Cellular barriers (Phagocytes, NK cells), and Cytokines (Interferons). * **NK Cells:** These are the only lymphocytes that are part of the **innate** immune system. * **Complement System:** While it bridges both systems, the **Alternative and Lectin pathways** are considered part of innate immunity, whereas the Classical pathway (antibody-dependent) is part of adaptive immunity. * **TLRs (Toll-Like Receptors):** These are key PRRs (Pattern Recognition Receptors) in innate immunity that recognize PAMPs on pathogens.

Q: CD4 cells are involved in all of the following processes, EXCEPT:

Processing and presenting antigens. ### Explanation The correct answer is **B. Processing and presenting antigens.** **1. Why Option B is correct:** CD4+ T cells (Helper T cells) are the **recipients** of antigen presentation, not the presenters. Antigen processing and presentation is the function of **Antigen-Presenting Cells (APCs)** such as Dendritic cells, Macrophages, and B cells. These APCs process exogenous antigens and present them via **MHC Class II** molecules to the T-cell receptor (TCR) on CD4 cells. CD4 cells then become activated to coordinate the immune response. **2. Why the other options are incorrect:** * **Option A:** CD4 cells (specifically Th2 subset) provide "help" to B cells by releasing cytokines (like IL-4, IL-5) and through CD40-CD40L interaction, which is essential for B cell activation, isotype switching, and memory cell formation. * **Option C:** Upon activation, CD4 cells (specifically Th1 subset) produce **Interleukin-2 (IL-2)**, which acts as an autocrine growth factor to stimulate T-cell proliferation (clonal expansion). * **Option D:** Activated Th1 cells produce **Interferon-gamma (IFN-γ)**, which is the primary cytokine responsible for activating macrophages and enhancing their microbicidal activity. **3. High-Yield Clinical Pearls for NEET-PG:** * **MHC Restriction:** CD4 cells recognize antigens only in association with **MHC Class II** (Rule of 8: 4 × 2 = 8), while CD8 cells recognize **MHC Class I** (8 × 1 = 8). * **Th1 vs. Th2:** Th1 cells primarily mediate **Cell-Mediated Immunity** (IFN-γ, IL-2, TNF-β), while Th2 cells mediate **Humoral Immunity** (IL-4, IL-5, IL-10, IL-13). * **HIV Pathogenesis:** HIV selectively infects and depletes CD4+ T cells by binding to the CD4 molecule and CCR5/CXCR4 co-receptors, leading to profound immunodeficiency.

Q: Which of the following interleukins is NOT primarily produced by T cells?

Interleukin 1. **Explanation:** The correct answer is **Interleukin 1 (IL-1)**. The fundamental concept here is distinguishing between cytokines produced by innate immune cells (monocytes/macrophages) and those produced by adaptive immune cells (T-lymphocytes). * **Interleukin 1 (IL-1):** This is a pro-inflammatory cytokine primarily produced by **activated macrophages**, monocytes, and dendritic cells. It acts as an endogenous pyrogen (inducing fever) and stimulates T-cell activation. It is a hallmark of the innate immune response rather than a T-cell product. * **Interleukin 2 (IL-2):** Produced primarily by **Th1 cells**. It is known as the "T-cell growth factor," essential for the proliferation and clonal expansion of T and B lymphocytes. * **Interleukin 4 (IL-4):** Produced by **Th2 cells**. It promotes B-cell differentiation into plasma cells and mediates the "class switching" of antibodies to IgE. * **Interleukin 5 (IL-5):** Also produced by **Th2 cells**. Its primary role is the recruitment and activation of eosinophils, making it crucial in parasitic infections and allergic reactions. **High-Yield NEET-PG Pearls:** * **Hot T-BONE Steak:** A classic mnemonic for IL functions: * **IL-1:** **Hot** (Fever) * **IL-2:** Stimulates **T** cells * **IL-3:** Stimulates **B**one marrow * **IL-4:** Stimulates Ig**E** production * **IL-5:** Stimulates Ig**A** production * **IL-8:** The primary chemotactic factor for **neutrophils** ("Clean up on aisle 8"). * **IL-10 & TGF-β:** The major "anti-inflammatory" cytokines that downregulate the immune response.

Question 1

Which cell type lacks HLA antigens?

Accepted Answer

Red blood cell

Answer

Monocyte

Answer

Thrombocytes

Answer

Neutrophil

Question 2

The binding of complement to a bacterial cell surface is termed as:

Accepted Answer

Opsonization

Answer

Complement activation

Answer

Complement stabilization

Answer

None of the above

Question 3

Prozone phenomenon is a feature of which of the following diseases?

Accepted Answer

Brucellosis

Answer

Tularemia

Answer

Legionnaire's disease

Answer

Plague

Question 4

ASLO titres are used in the diagnosis of which condition?

Accepted Answer

Acute rheumatic fever

Answer

Acute rheumatoid arthritis

Answer

Ankylosing spondylitis

Answer

Osteoarthritis

Question 5

The class of antibodies that plays an important role in type I hypersensitivity reactions is _____,

Accepted Answer

IgE

Answer

IgA

Answer

IgD

Answer

IgG

Question 6

Which of the following is NOT an example of delayed type hypersensitivity?

Accepted Answer

Arthus phenomenon

Answer

Contact dermatitis

Answer

Tuberculin test

Answer

Graft versus host reaction

Question 7

Killer cells are associated with which type of immunologic response?

Accepted Answer

None of the above

Answer

Type I

Answer

Type II

Answer

Type III

Question 8

Which of the following is NOT a component of innate immunity?

Accepted Answer

Antibody

Answer

Epithelial surfaces

Answer

Lysozyme

Answer

Sebum

Question 9

CD4 cells are involved in all of the following processes, EXCEPT:

Accepted Answer

Processing and presenting antigens

Answer

Acting as a helper function for B cells

Answer

Producing and releasing interleukin-2

Answer

Producing and releasing interferon-gamma

Question 10

Which of the following interleukins is NOT primarily produced by T cells?

Accepted Answer

Interleukin 1

Answer

Interleukin 2

Answer

Interleukin 4

Answer

Interleukin 5

Immunology — MCQs

Immunology — MCQs

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