Innate Immunity — MCQs
Which cytokine activates macrophages?
Most effective bactericidal system within phagocytes is-
Which is NOT a feature of chronic inflammation?
Which of the following is least associated with the mediation of inflammation?
All of the following are pattern recognition receptors for extracellular or ingested microbes, except:
Virus-infected cells are killed by
In which type of graft rejection is prior immunosuppression NOT helpful in prevention?
Which of the following best denotes classical complement pathway activation in immune inflammatory conditions?
In chronic allergy, which immunoglobulin is predominantly elevated?
Which of the following is the MOST COMMON cause of acute hypocomplementemia in children following an infection?
Innate Immunity Indian Medical PG Practice Questions and MCQs
Question 1: Which cytokine activates macrophages?
- A. Leukotriene B4
- B. IL-8
- C. IFN-γ (Correct Answer)
- D. PAF
Explanation: ***IFN-γ (Interferon-gamma)*** - **IFN-γ is the classic macrophage-activating cytokine**, enhancing phagocytic and antimicrobial functions - Promotes expression of **MHC class I and II molecules**, increasing antigen presentation capacity - Produced mainly by **Th1 cells and NK cells** during cell-mediated immunity - Key cytokine in defense against **intracellular pathogens** (mycobacteria, viruses) *IL-8* - **IL-8 is a chemokine** (cytokine subfamily) primarily involved in **neutrophil chemotaxis** - Recruits neutrophils to sites of infection or inflammation - Does not directly activate macrophages like IFN-γ - Important in acute inflammatory responses *PAF (Platelet-Activating Factor)* - **Not a cytokine** - it is a **phospholipid mediator** - Involved in allergic and inflammatory responses - Functions include **platelet aggregation**, **vasodilation**, and **bronchoconstriction** - While it affects immune responses, it doesn't function as a macrophage-activating cytokine *Leukotriene B4* - **Not a cytokine** - it is a **lipid mediator** (eicosanoid) derived from arachidonic acid - Primarily acts as a **chemoattractant for neutrophils** - Promotes neutrophil and monocyte adhesion and migration to inflammatory sites - Does not directly activate macrophages
Question 2: Most effective bactericidal system within phagocytes is-
- A. Cationic basic protein mediated
- B. Reactive oxygen metabolite mediated (Correct Answer)
- C. Lysozyme mediated
- D. Lactoferrin mediated
Explanation: ***Reactive oxygen metabolite mediated*** - The production of **reactive oxygen metabolites** (like superoxide, hydrogen peroxide, and hydroxyl radicals) through the **respiratory burst** is a highly potent mechanism for killing phagocytosed bacteria. - These highly reactive molecules cause **oxidative damage** to bacterial components, leading to their degradation and death. *Cationic basic protein mediated* - **Cationic proteins** (e.g., defensins) have antimicrobial properties by damaging bacterial membranes, but they are generally less potent than reactive oxygen species in overall bacterial killing within phagocytes. - While important, they contribute to a broader array of antimicrobial mechanisms but are not considered the *most effective* single system. *Lysozyme mediated* - **Lysozyme** primarily targets bacterial **peptidoglycan**, breaking down bacterial cell walls, especially in gram-positive bacteria. - It is an important antimicrobial enzyme, but its effectiveness is limited against many gram-negative bacteria with outer membranes and it is generally less destructive than the radical-forming reactive oxygen species. *Lactoferrin mediated* - **Lactoferrin** primarily acts by **chelating iron**, which is an essential nutrient for bacterial growth, thereby inhibiting bacterial proliferation. - While important for bacteriostasis, its direct bactericidal activity is often limited compared to the direct damaging effects of reactive oxygen species.
Question 3: Which is NOT a feature of chronic inflammation?
- A. Mononuclear cells
- B. Neutrophil predominance (Correct Answer)
- C. Fibrosis
- D. Granulation tissue
Explanation: ***Neutrophil predominance*** - **Neutrophil predominance** is characteristic of **acute inflammation**, where these cells are among the first responders to injury or infection [1]. - In chronic inflammation, neutrophils are typically present in much smaller numbers compared to mononuclear cells, or their presence indicates an acute exacerbation [3]. *Mononuclear cells* - **Mononuclear cells**, such as **macrophages**, **lymphocytes**, and **plasma cells**, are the hallmark cellular infiltrates of chronic inflammation [1]. - These cells are responsible for sustained immune responses, tissue destruction, and repair processes [2]. *Fibrosis* - **Fibrosis**, or the deposition of **collagen** by fibroblasts, is a common outcome of chronic inflammation as the body attempts to repair ongoing tissue damage [3]. - It leads to **scarring** and functional impairment of affected organs [4]. *Granulation tissue* - **Granulation tissue** is an early phase of **tissue repair** during chronic inflammation, characterized by the proliferation of **fibroblasts** and new **blood vessels (angiogenesis)** [5]. - It represents the body's effort to fill tissue defects and prepare for eventual fibrous scar formation [5]. **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. 195-196. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 107-109. [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. 196-197. [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. 200-202. [5] 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. 194-195.
Question 4: Which of the following is least associated with the mediation of inflammation?
- A. Prostaglandins/Interleukins
- B. Myeloperoxidase
- C. IFN (Correct Answer)
- D. TNF
Explanation: ***Myeloperoxidase*** - Myeloperoxidase is primarily an enzyme involved in the **oxidative burst** of neutrophils, not a classic mediator of inflammation. - It plays a role in **microbial killing** but does not directly participate in inflammation mechanisms like cytokines do. *IFN* - Interferons (IFNs) are cytokines crucial in immune responses and have roles in **inflammatory signaling** [1]. - They are produced in response to **viral infections** and activate immune cells, thus mediating inflammation. *Prostaglandins/Interleukins* - Prostaglandins are lipid compounds that promote **vasodilation** and **sensitize pain receptors**, key factors in the inflammatory process [1][2]. - Interleukins are a diverse group of cytokines that play significant roles in **cell signaling** during inflammation [1][3]. *TNF* - Tumor Necrosis Factor (TNF) is a major pro-inflammatory cytokine crucial in promoting systemic inflammation [1]. - It is involved in the activation of other inflammatory mediators and is significant in numerous inflammatory diseases [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100.
Question 5: All of the following are pattern recognition receptors for extracellular or ingested microbes, except:
- A. Toll-like receptors (TLRs) - Detect pathogen-associated molecular patterns (PAMPs).
- B. NOD-like receptors (NLRs) - Intracellular sensors for microbial components.
- C. Killer-cell immunoglobulin receptors (KIRs) - Recognize MHC class I molecules on host cells. (Correct Answer)
- D. C-type lectin receptors (CLRs) - Recognize carbohydrate structures on microbes.
Explanation: ***Killer-cell immunoglobulin receptors (KIRs)*** - KIRs are primarily involved in regulating **natural killer (NK) cells**, not in recognizing microbes [1]. - They primarily interact with **MHC class I molecules** and play a role in **immune surveillance**, rather than pattern recognition of pathogens [1]. *NOD-like receptors (NLRs)* - NLRs detect **intracellular pathogens** and damaged cells, playing a crucial role in **innate immunity** [2]. - They initiate responses to **bacterial peptidoglycans** and work in the recognition of microbial patterns [2]. *Toll-like receptors (TLRs)* - TLRs are well-known for recognizing **extracellular microbes** and activate the immune response upon pathogen detection [3]. - They are critical in detecting **lipopolysaccharides (LPS)** and **viral nucleic acids** to elicit immune responses. *C-type lectin receptors (CLRs)* - CLRs specifically recognize **carbohydrate structures** on pathogens, playing a key role in **innate immune responses** [3]. - They are important in identifying **fungi** and **bacteria**, enhancing phagocytosis and cytokine production. **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. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 196. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 200.
Question 6: Virus-infected cells are killed by
- A. Natural killer (NK) cells
- B. Macrophages
- C. Neutrophils
- D. Cytotoxic T lymphocytes (CTLs) (Correct Answer)
Explanation: ***Cytotoxic T lymphocytes (CTLs)*** - **CTLs are the primary adaptive immune cells** specifically designed to recognize and kill virus-infected cells - They recognize **viral antigens presented on MHC class I molecules** on the surface of infected cells - CTLs kill infected cells through **perforin and granzyme-mediated cytotoxicity** and **Fas-FasL pathway** - This is the **classic and most specific answer** for virus-infected cell killing in immunology *Natural killer (NK) cells* - NK cells provide **early innate defense** against viral infections before CTL response develops - They kill virus-infected cells by recognizing **downregulation of MHC class I** ("missing self") - While NK cells do kill virus-infected cells, CTLs are the **specific adaptive immune response** - NK cells act within hours, while CTLs take days to develop but provide targeted immunity *Macrophages* - Macrophages are **phagocytic cells** that primarily engulf pathogens and dead cells - They play a **supporting role** in viral immunity through antigen presentation and cytokine production - They do **NOT directly kill virus-infected cells** as their primary antiviral mechanism - Their main contribution is activating other immune cells, not direct cytotoxicity *Neutrophils* - Neutrophils are the **first responders to bacterial and fungal infections** - They have a **very limited role** in antiviral immunity - Not involved in direct killing of virus-infected cells - May be recruited to sites of inflammation but are not primary antiviral effectors
Question 7: In which type of graft rejection is prior immunosuppression NOT helpful in prevention?
- A. Hyperacute rejection (Correct Answer)
- B. Chronic rejection
- C. Acute rejection
- D. Graft-versus-host disease
Explanation: ***Hyperacute rejection*** - Occurs within minutes to hours after transplantation and is due to **pre-existing recipient antibodies** against the donor's **antigens** [1]. - Immune suppression is ineffective because it is a **humoral response** that happens almost immediately upon graft recognition [1]. *None of the above* - Misleading as it does not specify any type of rejection, making it an incorrect answer. - All other options provide distinct types of rejection, with characteristics that indicate the importance of immune suppression. *Chronic rejection* - Develops over months to years and is mediated mainly by **cell-mediated immunity** rather than immediate antibody-mediated response. - Immune suppression is critical in managing chronic rejection to prolong graft survival. *Acute rejection* - Typically occurs days to weeks post-transplant, caused by **T-cell mediated** responses and requires ongoing immune suppression [1]. - **Histological changes** and graft dysfunction are often observed, distinguishing it from hyperacute rejection. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242.
Question 8: Which of the following best denotes classical complement pathway activation in immune inflammatory conditions?
- A. C2, C4 and C3 decreased (Correct Answer)
- B. C2 and C4 normal, C3 is decreased
- C. C3 normal and C2, C4 decreased
- D. C2, C4, C3 all are elevated
Explanation: ***C2, C4 and C3 decreased*** - Activation of the **classical complement pathway** consumes upstream components C2 and C4, leading to their depletion [2]. - The activation also consumes C3 as all complement pathways converge at C3, thus its levels will also be decreased [1]. *C2 and C4 normal, C3 is decreased* - This pattern is more indicative of **alternate pathway activation** or a C3 deficiency, where classical pathway components (C2, C4) are not primarily involved [3]. - In classical pathway activation, C2 and C4 would be depressed due to their role early in the cascade. *C3 normal and C2, C4 decreased* - While C2 and C4 being decreased is consistent with **classical pathway activation**, the C3 component would also be decreased as it is consumed by the **C3 convertase** [1]. - A normal C3 level would imply either very early or ineffective classical pathway activation, which is unlikely given significant C2 and C4 consumption. *C2, C4, C3 all are elevated* - Elevated levels of complement components typically occur during the **acute phase response** in inflammatory conditions, but this indicates increased production, not consumption due to activation. - Active consumption in an immune inflammatory condition would lead to **decreased serum levels** of these components, not increased levels. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100. [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. 162-163. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 534-535.
Question 9: In chronic allergy, which immunoglobulin is predominantly elevated?
- A. Ig A
- B. Ig E (Correct Answer)
- C. Ig M
- D. Ig G
Explanation: ***Ig E*** - **IgE** antibodies are primarily responsible for mediating **allergic reactions** [1] and play a key role in the pathogenesis of allergic diseases such as asthma, allergic rhinitis, and atopic dermatitis [2]. - In chronic allergy, there is a persistent overproduction of **IgE** in response to allergens, leading to chronic symptoms and inflammation [1]. *Ig A* - **IgA** is predominantly found in mucous secretions (e.g., saliva, tears, breast milk) and protects against mucosal infections. - While it plays a role in immune responses, it is not the primary mediator of chronic allergic reactions. *Ig M* - **IgM** is the first antibody produced in a primary immune response and is crucial for immediate defense against new infections. - It does not typically persist at high levels in chronic conditions like allergies [3]. *Ig G* - **IgG** is the most abundant antibody in serum and provides long-term immunity against pathogens. - While some **IgG** antibodies might be involved in allergic responses (e.g., IgG4 in blocking responses), **IgE** remains the predominant antibody in chronic allergic conditions [3]. **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. 171-172. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 686-687. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-211.
Question 10: Which of the following is the MOST COMMON cause of acute hypocomplementemia in children following an infection?
- A. PSGN (Correct Answer)
- B. Membranous GN
- C. Focal Segmental Glomerulosclerosis (FSGS)
- D. Membranoproliferative GN (MPGN)
Explanation: ***PSGN*** - **Post-streptococcal glomerulonephritis (PSGN)** is the **most common cause of acute hypocomplementemia** in children following a streptococcal infection [1]. - Characterized by **immune complex deposition** in the glomeruli with activation of the complement system [2]. - Results in **transient hypocomplementemia** (both C3 and C4 decreased) that typically normalizes within 6-8 weeks. - Classic presentation: acute nephritic syndrome 1-3 weeks after pharyngitis or 3-6 weeks after skin infection [1]. *Membranous GN* - **Membranous glomerulonephritis** presents with **nephrotic syndrome** and immune complex deposition [2]. - Associated with **normal complement levels** in most cases. - Complement activation is not severe enough to cause significant consumption. *Focal Segmental Glomerulosclerosis (FSGS)* - **FSGS** causes nephrotic syndrome with **scarring of selected glomeruli** [3]. - **Not an immune complex-mediated disease**, hence no complement consumption [3]. - Complement levels remain **normal**. *Membranoproliferative GN (MPGN)* - **MPGN** can also cause hypocomplementemia, particularly Type II (dense deposit disease) with persistent C3 consumption due to C3 nephritic factor. - However, **MPGN is much less common** than PSGN in the pediatric population. - Type I MPGN may show low C3 with normal or low C4. - PSGN remains the **classic and most frequent** acute post-infectious cause [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 914-915. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.
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