Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 111: What are the most important cells in Type I hypersensitivity?

A. Macrophages
B. Mast cells (Correct Answer)
C. Neutrophils
D. Lymphocytes

Explanation: **Explanation:** **Type I Hypersensitivity (Immediate Hypersensitivity)** is an IgE-mediated immune response occurring within minutes of exposure to an antigen in a previously sensitized individual [1]. **Why Mast Cells are the Correct Answer:** Mast cells are the primary effector cells in Type I reactions [2]. Upon first exposure to an allergen, IgE antibodies are produced and bind to high-affinity **FcεRI receptors** on the surface of mast cells (sensitization) [1]. Upon re-exposure, the allergen cross-links these IgE molecules, triggering **degranulation** [1]. This releases potent preformed mediators like **histamine** and newly synthesized mediators like leukotrienes and prostaglandins, which cause vasodilation, edema, and bronchospasm [1]. **Why Other Options are Incorrect:** * **A. Macrophages:** These are primarily involved in Type IV (delayed-type) hypersensitivity as antigen-presenting cells and effector cells (forming granulomas). * **C. Neutrophils:** These are the hallmark of acute inflammation and are prominent in Type III hypersensitivity (Arthus reaction), where they are recruited by immune complexes to cause tissue damage. * **D. Lymphocytes:** While Th2-lymphocytes are necessary to induce the class switching to IgE, they are the "orchestrators" rather than the immediate effector cells that define the clinical manifestation of Type I reactions [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Key Cytokines:** IL-4 (stimulates IgE production) and IL-5 (activates eosinophils) are crucial [1]. * **Late-Phase Reaction:** While mast cells initiate the response, **eosinophils** are the most important cells in the late-phase reaction (2–24 hours later) [1]. * **Biochemical Marker:** Serum **tryptase** levels are used clinically to confirm mast cell degranulation following anaphylaxis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-212. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 171-172.

Question 112: All of the following are categorized as secondary lymphoid organs except?

A. Lymph nodes
B. Spleen
C. Thymus (Correct Answer)
D. Subepithelial collections of lymphocytes

Explanation: Explanation: Lymphoid organs are classified into two categories based on their functional role in lymphocyte development: 1. Primary (Central) Lymphoid Organs: These are the sites where lymphocytes are produced and undergo antigen-independent maturation [1]. * Bone Marrow: Site of B-cell maturation and origin of all hematopoietic cells [1]. * Thymus: Site of T-cell maturation and selection [1], [2]. Since the Thymus (Option C) is a primary lymphoid organ, it is the correct "except" answer. 2. Secondary (Peripheral) Lymphoid Organs: These are the sites where mature lymphocytes are stationed to encounter antigens and undergo antigen-dependent activation and proliferation [1]. * Lymph Nodes (Option A): Filter lymph and trap local tissue antigens [1]. * Spleen (Option B): Filters blood-borne antigens [1]. * MALT/Subepithelial collections (Option D): Includes Tonsils, Peyer’s patches, and Appendix. These protect mucosal surfaces [1]. Why other options are incorrect: Options A, B, and D are all secondary lymphoid organs because they provide the microenvironment for the initiation of the adaptive immune response. High-Yield Clinical Pearls for NEET-PG: * Hassall’s Corpuscles: Epithelial cell whorls found specifically in the Thymic medulla; their presence is a key histological marker [2]. * DiGeorge Syndrome: Results from the failure of the 3rd and 4th pharyngeal pouches to develop, leading to Thymic hypoplasia and T-cell deficiency. * B-cell vs. T-cell Zones: In secondary lymphoid organs, B-cells reside in follicles (germinal centers), while T-cells reside in the paracortex (lymph nodes) or PALS (periarteriolar lymphoid sheaths in the spleen). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 158-160. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 634.

Question 113: Which of the following is NOT true regarding subacute combined immunodeficiency?

A. Due to deficiency of adenosine deaminase
B. Toxicity of leucocytes due to accumulation of cAMP (Correct Answer)
C. Both cellular and humoral immunity affected
D. Bone marrow transplantation is the treatment

Explanation: **Explanation:** Severe Combined Immunodeficiency (SCID) is a group of genetic disorders characterized by the failure of both B-cell and T-cell maturation. The question refers to the **Adenosine Deaminase (ADA) deficiency** variant, which accounts for about 50% of autosomal recessive SCID cases. **Why Option B is the correct (False) statement:** The toxicity in ADA deficiency is **not** due to the accumulation of cAMP. In the absence of the ADA enzyme, there is an accumulation of **deoxyadenosine** and its metabolites, specifically **deoxy-ATP (dATP)**. High levels of dATP are toxic to immature lymphocytes because they inhibit **ribonucleotide reductase**, the enzyme required for DNA synthesis. This leads to a failure of lymphocyte proliferation and widespread apoptosis. **Analysis of other options:** * **Option A:** ADA deficiency is indeed the second most common cause of SCID (after X-linked SCID). * **Option C:** Since the defect occurs at the level of common lymphoid progenitors or early lymphocyte maturation, both **Cellular (T-cell)** and **Humoral (B-cell)** immunity are severely impaired, leading to recurrent infections. * **Option D:** **Hematopoietic Stem Cell Transplantation (HSCT)** is the definitive treatment [1]. Other options include Gene Therapy (ADA was the first disease treated with gene therapy) and Enzyme Replacement Therapy (PEG-ADA) [1]. **NEET-PG High-Yield Pearls:** * **Most common cause of SCID:** X-linked (mutation in the γ-chain of cytokine receptors, e.g., IL-7). * **Radiological sign:** Absence of thymic shadow on chest X-ray. * **Clinical presentation:** Failure to thrive, chronic diarrhea, and opportunistic infections (e.g., *Pneumocystis jirovecii*, *Candida*). * **Pathology:** Hypoplastic thymus lacking Hassall’s corpuscles. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 167-168.

Question 114: Thymic hypoplasia is seen in which of the following conditions?

A. Wiskott-Aldrich syndrome
B. DiGeorge syndrome (Correct Answer)
C. IgA deficiency
D. Agammaglobulinemia

Explanation: **Explanation:** **DiGeorge Syndrome (Correct Answer):** DiGeorge syndrome is a T-cell immunodeficiency caused by the **maldevelopment of the 3rd and 4th pharyngeal pouches** [1]. This results in **thymic hypoplasia or aplasia**, leading to a deficiency in mature T-cells and impaired cell-mediated immunity [1]. It is typically associated with a **22q11.2 deletion** [1], [2]. The classic clinical triad includes: 1. **Thymic hypoplasia** (T-cell deficiency/infections). 2. **Parathyroid hypoplasia** (Hypocalcemia and tetany) [1]. 3. **Congenital heart defects** (e.g., Tetralogy of Fallot, Truncus arteriosus) [1]. **Analysis of Incorrect Options:** * **Wiskott-Aldrich Syndrome:** An X-linked recessive disorder characterized by the triad of **thrombocytopenia (small platelets), eczema, and recurrent infections** [3]. It involves a defect in the WASP protein affecting the actin cytoskeleton, not primary thymic development [3]. * **IgA Deficiency:** The most common primary immunodeficiency [5]. It is characterized by a failure of B-cells to differentiate into IgA-secreting plasma cells. Thymic structure remains normal. * **Agammaglobulinemia (Bruton’s):** An X-linked defect in **Bruton Tyrosine Kinase (BTK)**, leading to a failure of pre-B cells to differentiate into mature B-cells [4]. While B-cell areas in lymph nodes are depleted, the thymus develops normally [4]. **High-Yield Clinical Pearls for NEET-PG:** * **CATCH-22 Mnemonic:** **C**ardiac defects, **A**bnormal facies, **T**hymic hypoplasia, **C**left palate, **H**ypocalcemia, **22**q11 deletion [1]. * **Chest X-ray:** Look for the **absence of a thymic shadow** in a neonate (also seen in SCID). * **Nezelof Syndrome:** Often described as "DiGeorge without the cardiac/parathyroid defects"—it features thymic dysplasia but normal calcium levels. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 167-168. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 173. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 250-251. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 248-249. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 249-250.

Question 115: Myasthenia gravis is which type of hypersensitivity?

A. Type I
B. Type II (Correct Answer)
C. Type III
D. Type IV

Explanation: **Explanation:** **Myasthenia Gravis (MG)** is a classic example of **Type II Hypersensitivity** (Antibody-mediated) [1]. In MG, the body produces autoantibodies (IgG) specifically directed against the **post-synaptic Nicotinic Acetylcholine Receptors (AChR)** at the neuromuscular junction [2]. These antibodies act via three mechanisms: blocking the receptor, increasing receptor internalization (downregulation), and activating the complement system to cause focal lysis of the post-synaptic membrane [3]. This results in impaired neuromuscular transmission, leading to muscle weakness and fatigability. **Why other options are incorrect:** * **Type I (Immediate):** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis, Asthma). * **Type III (Immune-complex):** Caused by the deposition of antigen-antibody complexes in tissues (e.g., SLE, Post-streptococcal glomerulonephritis) [4]. * **Type IV (Delayed-type):** Cell-mediated immunity involving T-lymphocytes, not antibodies (e.g., Mantoux test, Contact dermatitis). **High-Yield Clinical Pearls for NEET-PG:** * **Subtype:** MG is specifically a **Type II-b (Stimulatory/Inhibitory)** hypersensitivity because the antibody interferes with cell function without necessarily causing cell death [1]. * **Associated Pathology:** 75% of MG patients have **Thymic abnormalities** (65% Thymic Hyperplasia, 10% Thymoma). * **Antibody Variants:** While anti-AChR is most common, some patients are positive for **anti-MuSK** (Muscle-Specific Kinase) antibodies [2]. * **Clinical Sign:** Ptosis and diplopia are often the earliest symptoms; weakness worsens with repetitive use (fatigability). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 213-214. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1237-1238. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215.

Question 116: Serum sickness syndrome is an example of:

A. Anaphylactic shock
B. Angioneurotic edema
C. Cell-mediated immunity
D. Systemic Arthus reaction (Correct Answer)

Explanation: **Explanation:** **Serum Sickness** is the classic clinical prototype of a **Type III Hypersensitivity Reaction** (Immune-complex mediated) [1]. It occurs when an excess of antigen leads to the formation of small, soluble antigen-antibody complexes that circulate in the blood and deposit in various tissues, such as blood vessels, joints, and kidneys [2]. 1. **Why Option D is Correct:** The **Arthus reaction** is a localized area of tissue necrosis resulting from acute immune complex vasculitis. While the standard Arthus reaction is typically localized (e.g., skin), **Serum Sickness** is essentially a **Systemic Arthus reaction** [2]. In both cases, the underlying mechanism is the same: immune complex deposition, activation of the complement system (C5a, C3a), and subsequent neutrophilic infiltration leading to tissue damage. 2. **Why Other Options are Incorrect:** * **Option A & B:** Anaphylactic shock and Angioneurotic edema are examples of **Type I Hypersensitivity** (Immediate), mediated by IgE and mast cell degranulation. * **Option C:** Cell-mediated immunity refers to **Type IV Hypersensitivity**, which involves T-lymphocytes and macrophages (e.g., Mantoux test, contact dermatitis), not circulating immune complexes. **NEET-PG High-Yield Pearls:** * **Triad of Serum Sickness:** Fever, Rash (urticaria), and Arthralgia [2]. * **Morphology:** The characteristic vascular lesion is **Fibrinoid Necrosis**. * **Complement levels:** During the active phase, serum complement levels (C3, C4) are **decreased** due to consumption. * **Timeline:** Typically occurs 1–2 weeks after exposure to a foreign protein (e.g., anti-thymocyte globulin or certain antibiotics like penicillin) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 172-173. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 215-216.

Question 117: A lymph node biopsy of a 6-year-old boy shows markedly decreased numbers of lymphocytes in the paracortical areas. Analysis of his peripheral blood leukocytes is likely to show normal to elevated numbers of which of the following CD cells?

A. CD4
B. CD19 (Correct Answer)
C. CD3
D. CD2

Explanation: ### **Explanation** The correct answer is **CD19 (Option B)**. **1. Understanding the Concept** The lymph node is divided into specific functional zones: * **Cortex (Follicles):** Primarily contains **B-lymphocytes**. * **Paracortex:** Primarily contains **T-lymphocytes**. * **Medulla:** Contains cords (B-cells/plasma cells) and sinuses. In this clinical scenario, the 6-year-old boy has a **depletion of the paracortical area**, which signifies a **T-cell deficiency** (e.g., DiGeorge Syndrome). When T-cells are absent or markedly decreased, the body often compensates, or the underlying defect spares the B-cell lineage [1]. Therefore, the peripheral blood will show normal or even elevated levels of **B-cells**. **CD19** is a definitive marker for B-lymphocytes [2]. **2. Analysis of Incorrect Options** * **CD3 (Option C):** This is a pan-T-cell marker. Since the paracortex (T-cell zone) is depleted, CD3+ cells will be significantly decreased [1]. * **CD4 (Option A):** This marker represents T-helper cells. As a subset of T-cells, these would be decreased in a patient with paracortical atrophy [3]. * **CD2 (Option D):** This is an adhesion molecule found on all T-cells and Natural Killer (NK) cells. It would be decreased alongside the general T-cell population [1]. **3. NEET-PG High-Yield Pearls** * **DiGeorge Syndrome:** Classic cause of paracortical depletion due to thymic hypoplasia (3rd/4th pharyngeal pouch defect). * **Agammaglobulinemia (Bruton’s):** Shows the opposite pattern—absent germinal centers/follicles (B-cell zone) but a **preserved paracortex** [2]. * **T-cell Markers:** CD1, CD2, CD3, CD4, CD5, CD7, CD8. * **B-cell Markers:** CD19, CD20, CD21 (receptor for EBV), CD22. * **Paracortex Expansion:** Seen during cellular immune responses, such as viral infections (e.g., Infectious Mononucleosis). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 246-248. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 248-249. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 555-556.

Question 118: Antigen-antibody complex mediated hypersensitivity is which type?

A. Type I hypersensitivity
B. Type II hypersensitivity
C. Type IV hypersensitivity
D. Type III hypersensitivity (Correct Answer)

Explanation: **Explanation:** **Type III hypersensitivity** is characterized by the formation of **immune complexes** (antigen-antibody complexes) [1]. These complexes circulate in the blood and deposit in various tissues, such as blood vessel walls, synovial joints, and glomerular basements [2]. Once deposited, they trigger the **classical complement pathway**, leading to the recruitment of neutrophils and the release of lysosomal enzymes, which cause tissue damage and inflammation (vasculitis) [3]. **Analysis of Incorrect Options:** * **Type I (Immediate):** Mediated by **IgE antibodies** binding to mast cells. Upon re-exposure, the allergen causes mast cell degranulation and release of histamine (e.g., Anaphylaxis, Asthma). * **Type II (Antibody-mediated):** Caused by antibodies (IgG/IgM) binding directly to **antigens on specific cell surfaces** or tissues, leading to cell lysis or phagocytosis (e.g., Myasthenia gravis, Rheumatic fever). * **Type IV (Delayed-type):** This is **cell-mediated**, involving T-lymphocytes (CD4+ or CD8+) rather than antibodies [4]. It typically takes 48–72 hours to manifest (e.g., Mantoux test, Contact dermatitis) [4]. **NEET-PG High-Yield Pearls:** * **Classic Examples of Type III:** Systemic Lupus Erythematosus (SLE), Post-streptococcal glomerulonephritis (PSGN), Serum Sickness, and Arthus Reaction [2, 3]. * **Key Mediator:** Complement components **C3a and C5a** (anaphylatoxins) are crucial for neutrophil recruitment in Type III reactions [3]. * **Mnemonic (ACID):** * **A** - **A**naphylactic (Type I) * **C** - **C**ytotoxic (Type II) * **I** - **I**mmune Complex (Type III) * **D** - **D**elayed (Type IV) **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 215-216. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 172-173. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 173-174.

Question 119: Long-acting thyroid stimulator (LATS) in Graves' disease is an example of which type of hypersensitivity reaction?

A. Type 1 hypersensitivity
B. Type 2 hypersensitivity (Correct Answer)
C. Type 3 hypersensitivity
D. Type 4 hypersensitivity

Explanation: **Graves’ Disease and Type 2 Hypersensitivity** The correct answer is **Type 2 hypersensitivity**. This reaction is mediated by antibodies directed against specific cell surface receptors [1]. In Graves' disease, B-cells produce autoantibodies known as **Long-Acting Thyroid Stimulator (LATS)** or Thyroid Stimulating Immunoglobulins (TSI). These antibodies bind to the **TSH receptors** on thyroid follicular cells [2]. Unlike typical Type 2 reactions that cause cell destruction, these antibodies mimic the action of TSH, leading to continuous stimulation of adenylate cyclase and overproduction of thyroid hormones (T3 and T4). This specific subtype is often referred to as **Type 2 V (Quinary)** or "Stimulatory Hypersensitivity." **Analysis of Incorrect Options:** * **Type 1 (Immediate):** Mediated by IgE antibodies and mast cell degranulation (e.g., Anaphylaxis, Asthma) [3]. * **Type 3 (Immune Complex):** Caused by the deposition of antigen-antibody complexes in tissues, leading to complement activation (e.g., SLE, Post-streptococcal glomerulonephritis). * **Type 4 (Delayed):** Cell-mediated immunity involving T-lymphocytes and macrophages, not antibodies (e.g., Mantoux test, Contact dermatitis). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Antibody-mediated cellular dysfunction (Stimulatory) [1]. * **Contrast with Myasthenia Gravis:** Both are Type 2 hypersensitivity, but while Graves' involves *stimulation* of a receptor, Myasthenia Gravis involves *blocking/destruction* of the Acetylcholine receptor [2]. * **Triad of Graves':** Hyperthyroidism, Exophthalmos (due to retro-orbital inflammation), and Pretibial Myxedema. * **LATS** is specifically an IgG antibody that can cross the placenta, potentially causing neonatal thyrotoxicosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 213-214. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Question 120: Which of the following cells is instrumental in transmitting human immunodeficiency virus (HIV) to CD4+ T lymphocytes?

A. Neutrophils
B. Dendritic cells (Correct Answer)
C. CD8+ cells
D. NK cells

Explanation: ### Explanation **Correct Answer: B. Dendritic cells** Dendritic cells (DCs), specifically **Follicular Dendritic Cells (FDCs)** in lymph nodes and **Langerhans cells** in mucosal surfaces, play a critical role in the early pathogenesis of HIV [1]. Dendritic cells are located under epithelia at common sites of entry for microbes and are ideally located to present antigens to T cells [2]. The underlying mechanism involves a lectin-like receptor on the dendritic cell surface called **DC-SIGN**. When HIV enters the body through mucosal surfaces, dendritic cells capture the virus. Instead of being efficiently degraded, the virus is internalized into endosomes or remains attached to the cell surface. These DCs then migrate to regional lymph nodes, where they "present" the live virus to **CD4+ T lymphocytes**. This process, often called **"trans-infection,"** is instrumental in establishing the initial reservoir of infection in lymphoid tissues [1]. **Why the other options are incorrect:** * **A. Neutrophils:** These are the first responders to bacterial and fungal infections. While they are part of the innate immune response, they do not possess the specific receptors (like CD4 or DC-SIGN) required to capture and transmit HIV to T cells. * **C. CD8+ cells:** Also known as Cytotoxic T Lymphocytes (CTLs), these cells are responsible for killing HIV-infected cells [1]. They do not transmit the virus; rather, their decline in the later stages of AIDS contributes to immune failure. * **D. NK cells:** Natural Killer cells provide innate immunity against virally infected cells and tumors by inducing apoptosis. They are not involved in the transport or transmission of HIV. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Receptor:** CD4 molecule (found on T cells, macrophages, and DCs) [4]. * **Co-receptors:** **CCR5** (found on macrophages/T cells; important for initial infection/M-tropic strains) and **CXCR4** (found on T cells; important for late-stage/T-tropic strains) [3]. * **Homozygous mutation of CCR5 (Δ32)** provides resistance to HIV infection [3]. * **Major Reservoir:** Macrophages and Follicular Dendritic Cells serve as the primary reservoirs of HIV in the late stages of the disease. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 258-259. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 200. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 170-171. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 253-254.

Practice by Chapter

Cells and Tissues of the Immune System

Practice Questions

Innate Immunity

Practice Questions

Adaptive Immunity

Practice Questions

Hypersensitivity Reactions

Practice Questions

Autoimmune Diseases

Practice Questions

Immunodeficiency Disorders

Practice Questions

Transplantation Immunopathology

Practice Questions

Immune Response to Infections

Practice Questions

Immunologic Laboratory Techniques

Practice Questions

Tumor Immunology

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free