Immunopathology Practice Questions

Q: Interleukin-5 (IL-5) is released in which type of hypersensitivity reaction?

Type I. **Explanation:** **Why Type I is Correct:** Type I Hypersensitivity (Immediate/Anaphylactic) is mediated by **IgE antibodies** and **Th2 cells**. Upon exposure to an allergen, Th2 cells secrete a specific profile of cytokines: * **IL-4:** Stimulates B-cell class switching to IgE. * **IL-5:** Crucial for the **recruitment, activation, and survival of eosinophils**, which are hallmark effector cells in late-phase Type I reactions (e.g., bronchial asthma). * **IL-13:** Stimulates mucus secretion. Since IL-5 is the primary driver for eosinophilia in allergic responses, it is fundamentally linked to Type I reactions. **Why Other Options are Incorrect:** * **Type II (Antibody-mediated):** Involves IgG or IgM binding to cell surface antigens, leading to complement activation or ADCC (e.g., Autoimmune Hemolytic Anemia). It does not primarily involve Th2-derived IL-5. * **Type III (Immune-complex):** Caused by the deposition of antigen-antibody complexes in tissues (e.g., SLE, Arthus reaction). The primary mediators are complement (C5a) and neutrophils. * **Type IV (Delayed-type):** Cell-mediated immunity involving Th1 cells (secreting IFN-γ) or CD8+ T cells. While some subtypes (Type IVb) involve IL-5 and eosinophils (e.g., DRESS syndrome), for NEET-PG purposes, IL-5 is classically associated with the Th2 response of Type I Hypersensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **Mepolizumab/Reslizumab:** Monoclonal antibodies against **IL-5** used in severe eosinophilic asthma. * **Benralizumab:** Acts against the **IL-5 receptor**. * **Key Cytokine "Rule of Thumb":** Th1 = IFN-γ, IL-2 (Type IV); Th2 = IL-4, IL-5, IL-13 (Type I). * **Eosinophils** are the characteristic cells of the **late-phase** response in Type I hypersensitivity.

Q: IgE receptors are present on which of the following cells?

Mast cells. The correct answer is **Mast cells**. **1. Why Mast Cells are Correct:** Mast cells (and basophils) express high-affinity receptors for the Fc region of IgE, known as **FcεRI** [1]. When an allergen binds to the IgE already attached to these receptors, it causes "cross-linking," leading to degranulation [1]. This releases inflammatory mediators like histamine, leukotrienes, and prostaglandins, which mediate Type I Hypersensitivity reactions (e.g., anaphylaxis, asthma). **2. Why the Other Options are Incorrect:** * **NK cells (Natural Killer cells):** These cells primarily express **CD16** (an Fcγ receptor for IgG), which allows them to perform Antibody-Dependent Cellular Cytotoxicity (ADCC). They do not typically express IgE receptors. * **B cells:** While B cells produce IgE after class-switching, they primarily express **CD23** (a low-affinity IgE receptor) only during specific activation stages. However, in the context of classical IgE-mediated immunity and NEET-PG patterns, Mast cells/Basophils are the primary functional targets. * **Histiocytes:** These are tissue-resident macrophages. Their primary role is phagocytosis and antigen presentation; they typically express receptors for IgG (FcγR) and Complement (C3b), not IgE. **3. NEET-PG Clinical Pearls:** * **High-Affinity Receptor:** FcεRI (Found on Mast cells and Basophils) [1]. * **Low-Affinity Receptor:** FcεRII or CD23 (Found on B cells and activated Macrophages). * **Location:** Mast cells are found in connective tissue (especially near blood vessels) and mucosal surfaces [1]. * **Staining:** Mast cells show **metachromasia** (stain purple with Toluidine blue) due to the presence of heparin in their granules. * **Biochemical Marker:** **Tryptase** levels are measured clinically to confirm mast cell degranulation during an anaphylactic event.

Q: Which cells are typically positive for CD16 and CD56 markers?

NK cells. **Explanation:** **NK (Natural Killer) cells** are large granular lymphocytes that form a critical part of the innate immune system [1]. They are characterized by the expression of two primary surface markers: 1. **CD16:** Also known as Fc̹RIII, it acts as a low-affinity receptor for the Fc portion of IgG, mediating **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. 2. **CD56:** Also known as Neural Cell Adhesion Molecule (NCAM), it is the definitive marker used to identify NK cells in clinical pathology. **Analysis of Incorrect Options:** * **B Lymphocytes:** Characterized by markers **CD19, CD20, and CD21**. They also express MHC Class II and surface Immunoglobulins (sIg) [1]. * **Helper T Lymphocytes (Th):** These are defined by the presence of **CD3** (pan-T cell marker) and **CD4** [1]. * **Cytotoxic T Lymphocytes (Tc):** These are defined by **CD3** and **CD8** [1]. While some activated CD8+ T cells may occasionally express CD16, the combination of CD16 and CD56 is the classic signature for NK cells. **High-Yield Clinical Pearls for NEET-PG:** * **NK Cell Function:** They do not require prior sensitization and kill cells that show "missing self" (downregulation of MHC-I), a common tactic used by viruses and tumor cells [1]. * **CD56 Bright vs. Dim:** CD56^bright cells are primarily cytokine producers (IFN-̳), while CD56^dim cells (which are CD16+) are more potently cytotoxic. * **Chediak-Higashi Syndrome:** A high-yield association where NK cell function is impaired due to defective vesicle trafficking. * **Marker Tip:** If a question mentions **CD16, CD56, and CD3 negative**, it is definitively an NK cell. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 200-201.

Q: Which category of hypersensitivity involves complement activation?

Type II and Type III. **Explanation** Hypersensitivity reactions are classified by the Gell and Coombs system based on the underlying immune mechanism. Complement activation is a hallmark of both **Type II** and **Type III** hypersensitivity. * **Type II (Cytotoxic):** Antibodies (IgG or IgM) bind to antigens on the surface of specific cells or tissues. This antigen-antibody complex activates the **classical complement pathway**, leading to the formation of the Membrane Attack Complex (MAC) and cell lysis (e.g., Autoimmune Hemolytic Anemia). * **Type III (Immune-Complex):** Soluble antigens bind to antibodies, forming circulating immune complexes. These complexes deposit in tissues (like blood vessel walls or glomeruli) and trigger **complement activation**. This recruits neutrophils, leading to tissue damage (e.g., SLE, Post-streptococcal Glomerulonephritis). **Why other options are incorrect:** * **Type I:** Mediated by IgE binding to mast cells; involves histamine release, not complement. * **Type IV:** A delayed-type hypersensitivity mediated by T-cells (Th1, Th17, and CD8+), not antibodies or complement. **NEET-PG High-Yield Pearls:** * **Type II** is "Tissue-specific" (Antigen is fixed). * **Type III** is "Systemic" (Antigen is soluble/circulating). * **Complement levels (C3, C4):** Often decreased in Type III reactions (like SLE flares) due to massive consumption during the inflammatory process. * **Mnemonic (ACID):** **A**naphylactic (I), **C**ytotoxic (II), **I**mmune-Complex (III), **D**elayed (IV).

Question 1

Interleukin-5 (IL-5) is released in which type of hypersensitivity reaction?

Accepted Answer

Type I

Answer

Type II

Answer

Type III

Answer

Type IV

Question 2

In the immunofluorescence method to detect antinuclear antibodies, which of the following rat tissues is commonly used?

Accepted Answer

Liver

Answer

Kidney

Answer

Brain

Answer

Stomach

Question 3

Severe Combined Immunodeficiency (SCID) is due to deficiency of which of the following?

Accepted Answer

Any of the above

Answer

Adenosine deaminase

Answer

JAK 3

Answer

Recombinase - activating genes (RAG)

Question 4

A 9-month-old girl with a history of recurrent pulmonary infections is found to have a congenital deficiency of adenosine deaminase, which is associated with a virtual absence of lymphocytes in her peripheral lymphoid organs. What is the appropriate diagnosis?

Accepted Answer

Severe combined immunodeficiency

Answer

Bruton X-linked agammaglobulinemia

Answer

DiGeorge syndrome

Answer

Isolated IgA deficiency

Question 5

Deficiency of late complement factors is associated with which of the following?

Accepted Answer

Recurrent infections, particularly with Neisseria species

Answer

Hereditary angioneurotic edema

Answer

Systemic lupus erythematosus

Answer

Hemolytic uremic syndrome

Question 6

IgE receptors are present on which of the following cells?

Accepted Answer

Mast cells

Answer

NK cells

Answer

B cells

Answer

Histiocytes

Question 7

Which cells are typically positive for CD16 and CD56 markers?

Accepted Answer

NK cells

Answer

B Lymphocytes

Answer

Helper T lymphocyte

Answer

Cytotoxic T lymphocyte

Question 8

Which of the following is an immune privilege site?

Accepted Answer

Seminiferous tubule

Answer

Optic nerve

Answer

Area postrema

Answer

Spinal canal

Question 9

Which category of hypersensitivity involves complement activation?

Accepted Answer

Type II and Type III

Answer

Type II

Answer

Type III

Answer

Type IV and Type II

Question 10

A 30-year-old man presents with fever, chills, and neck stiffness. Cerebrospinal fluid analysis reveals gram-negative diplococci. The patient has a history of sepsis with meningococcemia. Which immunologic deficiency is most likely responsible?

Accepted Answer

Complement deficiency C5-C9

Answer

Post-splenectomy status

Answer

Drug-induced agranulocytosis

Answer

Interleukin-12 receptor deficit

Immunopathology — MCQs

Immunopathology — MCQs

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