Adaptive Immunity Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Adaptive Immunity. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Adaptive Immunity Indian Medical PG Question 1: Which of the following is not considered an antigen-presenting cell?
- A. Macrophages
- B. Langerhans cells
- C. Thymocytes (Correct Answer)
- D. B lymphocytes
Adaptive Immunity Explanation: ***Thymocytes***
- Thymocytes are **developing T cells** found in the thymus and do not function as antigen-presenting cells (APCs) [1].
- Unlike APCs, thymocytes are primarily involved in the **maturation** and selection of T lymphocytes.
*Langerhans cells*
- Langerhans cells are a type of **dendritic cell** found in the skin and are effective antigen-presenting cells to T cells [1].
- They play a crucial role in **immune surveillance** and response to skin infections.
*Macrophages*
- Macrophages are well-known antigen-presenting cells that engulf pathogens and present antigens to T cells [1].
- They are also involved in **phagocytosis** and secrete various cytokines to modulate immune responses.
*M-cells*
- M-cells (microfold cells) are specialized epithelial cells that transport antigens from the intestinal lumen to underlying immune cells.
- Although not traditional APCs, they play a role in immune surveillance and stimulating **mucosal immunity**.
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 200, 207-208.
Adaptive Immunity Indian Medical PG Question 2: Which of the following statements about the secondary immune response is false?
- A. The lag period is absent or significantly shorter.
- B. There is a negative phase in the response.
- C. Only T-dependent antigens are recognized.
- D. Immune response against a subsequent antigenic challenge is absent. (Correct Answer)
Adaptive Immunity Explanation: ***Immune response against a subsequent antigenic challenge is absent.***
- This statement is **false** because the secondary immune response is characterized by a **much stronger and faster** immune response upon subsequent exposure to the same antigen.
- The presence of **memory cells** ensures that the immune system is highly prepared to combat the antigen more efficiently than during the primary response.
*The lag period is absent or significantly shorter.*
- This statement is **true** for the secondary immune response. The **memory B and T cells** can be rapidly activated, reducing the time needed to mount an effective response.
- Unlike primary responses that can take 5-10 days to produce antibodies, secondary responses typically produce antibodies within **1-3 days**.
*There is a negative phase in the response.*
- This statement is **false** for the secondary immune response. The **negative phase** is characteristic of the **primary immune response**, not the secondary response.
- The negative phase in primary response refers to a transient drop in antibody concentration after initial antigen exposure due to antigen-antibody complex formation. However, the **secondary response shows immediate and robust antibody production** without this negative phase due to pre-existing memory cells.
- While this statement is technically false, the question asks for THE false statement, and Option D is more obviously and fundamentally false.
*Only T-dependent antigens are recognized.*
- This statement is **partially false** but has some truth in context. While **T-dependent antigens** generate the most robust secondary responses with strong memory cell formation, the immune system doesn't ONLY recognize T-dependent antigens.
- **T-independent antigens** can elicit responses but typically generate weaker, shorter-lived immunity without strong memory formation. The classical, robust secondary immune response with anamnestic features is predominantly associated with T-dependent antigens.
Adaptive Immunity Indian Medical PG Question 3: What is the primary mechanism by which cytotoxic T lymphocytes (CTLs) recognize target cells in the immune response?
- A. Are important in the control of viral infections
- B. Recognize antigens presented by MHC class I molecules (Correct Answer)
- C. Secrete cytokines that stimulate the differentiation and proliferation of T cells
- D. Most often recognize antigens presented by MHC class II molecules
Adaptive Immunity Explanation: ***Recognize antigens presented by MHC class I molecules***
- **Cytotoxic T lymphocytes (CTLs)**, or CD8+ T cells, specifically recognize antigens presented by **MHC class I molecules** on the surface of target cells.
- This recognition is crucial for identifying and eliminating **virally infected** or **cancerous cells**.
*Secrete cytokines that stimulate the differentiation and proliferation of T cells*
- While CTLs do secrete some cytokines, their primary role is direct cytotoxicity rather than broadly stimulating T cell differentiation and proliferation.
- **Helper T cells (CD4+ T cells)** are primarily responsible for secreting cytokines that orchestrate the immune response and stimulate other immune cells.
*Are important in the control of viral infections*
- This statement is true, but it describes a *consequence* of CTL function, not their fundamental *role* in antigen recognition.
- CTLs eliminate virally infected cells, thereby controlling viral spread, but their initial role is antigen recognition via MHC class I.
*Most often recognize antigens presented by MHC class II molecules*
- **MHC class II molecules** are primarily recognized by **helper T cells (CD4+ T cells)**, which respond to extracellular antigens processed by professional antigen-presenting cells.
- CTLs (CD8+ T cells) are specific for antigens presented by **MHC class I molecules**.
Adaptive Immunity Indian Medical PG Question 4: Which of the following is not a component of innate immunity?
- A. Epithelial barriers
- B. NK cells
- C. Dendritic cells
- D. Helper T lymphocytes (Correct Answer)
Adaptive Immunity Explanation: ***Helper T lymphocyte***
- Helper T lymphocytes are a crucial part of **adaptive immunity** [4], facilitating responses against pathogens.
- They specifically activate B cells and cytotoxic T cells [2], unlike components of innate immunity, which respond nonspecifically.
*NK cells*
- Natural Killer (NK) cells are integral to **innate immunity** [1], targeting infected or tumor cells without prior sensitization.
- They play a role in the initial response to viral infections and can produce **cytokines** [2].
*Epithelial barriers*
- Epithelial barriers act as the first line of defense in **innate immunity** [1], preventing pathogen entry.
- They include physical and chemical barriers like skin and mucous membranes [3].
*Dendritic cells*
- Dendritic cells are key antigen-presenting cells involved in **innate immunity** [1] and link to adaptive immunity.
- They capture and present antigens [2], activating T cells to mount an immune response.
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 194-196.
[2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 207-208.
[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. 152-153.
[4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 196-198.
Adaptive Immunity Indian Medical PG Question 5: MHC II is associated with:-
- A. Red blood cells
- B. Antigen presenting cells (Correct Answer)
- C. Platelets
- D. Epithelial cells
Adaptive Immunity Explanation: ***Antigen presenting cells***
- **MHC II (Major Histocompatibility Complex class II)** molecules are primarily expressed on the surface of professional **antigen-presenting cells (APCs)**.
- APCs, such as **macrophages**, **dendritic cells**, and **B lymphocytes**, use MHC II to present **extracellularly derived antigens** to **CD4+ T helper cells**.
*Red blood cells*
- **Red blood cells (RBCs)** are anucleated and lack MHC molecules entirely.
- Their primary function is **oxygen transport**, not immune cell communication.
*Platelets*
- **Platelets** are cell fragments involved in **hemostasis** (blood clotting).
- They do not express MHC class II molecules as they are not involved in antigen presentation.
*Epithelial cells*
- Most **epithelial cells** primarily express **MHC class I** molecules to present **intracellular antigens** to **CD8+ cytotoxic T cells**.
- They do not typically express MHC class II unless under specific inflammatory conditions, and even then, not as their primary function.
Adaptive Immunity Indian Medical PG Question 6: Both antibody dependent and independent complement pathways converge on which complement component
- A. C8
- B. C1q
- C. C3 (Correct Answer)
- D. C5
Adaptive Immunity Explanation: ***Correct: C3***
- Both the **classical** (antibody-dependent) and **alternative** (antibody-independent) complement pathways lead to the activation and cleavage of **C3** into C3a and C3b.
- This convergence on C3 is critical as **C3b** acts as a central opsonin and initiator of the downstream common pathway (terminal pathway).
- The **lectin pathway** also converges at C3, making it the central hub of complement activation.
*Incorrect: C8*
- **C8** is a component of the **membrane attack complex (MAC)**, which forms much later in the complement cascade and is downstream from C3 activation.
- While essential for cell lysis, C8 does not represent the initial point of convergence between the antibody-dependent and independent pathways.
*Incorrect: C1q*
- **C1q** is specifically involved only in the **classical pathway**, where it binds to antibody-antigen complexes or directly to pathogen surfaces.
- It plays no direct role in the **alternative pathway**, thus not a point of convergence for both pathways.
*Incorrect: C5*
- **C5** is activated downstream of C3 and initiates the formation of the **membrane attack complex (MAC)**, similar to C8.
- While central to the lytic phase, its activation occurs after the convergence at C3 and is not the initial point where the classical and alternative pathways meet.
Adaptive Immunity Indian Medical PG Question 7: Which is the cell of origin of Chronic Lymphocytic Leukaemia / Small Lymphocytic Lymphoma?
- A. Mature B cells
- B. Progenitor T cells
- C. Mature T cells
- D. Naïve B cells (Correct Answer)
Adaptive Immunity Explanation: ***Naïve B cells***
- Chronic Lymphocytic Leukaemia (CLL) and Small Lymphocytic Lymphoma (SLL) originate from **CD5-positive B lymphocytes** arrested in a mature but **naïve differentiation stage** [1].
- These cells express both **B-cell markers (CD19, CD20, CD23)** and a T-cell marker (CD5), which is characteristic of the clone [4].
*Mature B cells*
- While CLL/SLL are derived from B cells, they are specifically from **naïve, not fully mature, B cells**.
- **Other B-cell lymphomas** like follicular lymphoma or mantle cell lymphoma originate from distinct stages of mature B-cell differentiation [2].
*Progenitor T cells*
- **Progenitor T cells** are the cells of origin for **T-cell acute lymphoblastic leukaemia (T-ALL)**, not CLL/SLL [3].
- T-ALL involves immature T lymphocytes and presents with different clinical and immunophenotypic features [3].
*Mature T cells*
- **Mature T cells** can give rise to various **peripheral T-cell lymphomas**, like peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS) or cutaneous T-cell lymphoma (Mycosis Fungoides).
- These are distinct from CLL/SLL, which is a B-cell neoplasm [4].
**References:**
[1] 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, pp. 596-598.
[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, pp. 610-612.
[3] 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, pp. 598-599.
[4] 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. 598.
Adaptive Immunity Indian Medical PG Question 8: t(2,8) is associated with:
- A. T cell ALL
- B. CML
- C. B cell ALL (Correct Answer)
- D. CLL
Adaptive Immunity Explanation: ***B cell ALL***
- The translocation **t(2;8)(p11;q24)** is a **variant cytogenetic abnormality** specifically associated with **Burkitt lymphoma/leukemia**, a highly aggressive form of mature B-cell neoplasm, which can present as B-cell ALL. [1]
- This variant translocation (occurring in ~15% of Burkitt lymphoma cases) leads to the **dysregulation of the MYC oncogene** on chromosome 8q24 due to its juxtaposition with the **kappa (κ) immunoglobulin light chain gene (IGK)** on chromosome 2p11. [1]
- The most common translocation in Burkitt lymphoma is **t(8;14)(q24;q32)** involving MYC and the immunoglobulin heavy chain gene IGH (~80% of cases), while **t(8;22)** involving the lambda light chain occurs in ~5% of cases. [1]
*T cell ALL*
- T-cell ALL is primarily associated with translocations involving **T-cell receptor genes (e.g., TCRα/δ on 14q11, TCRβ on 7q34)** and various oncogenes like *TAL1*, *LMO1*, *LMO2*, *HOXA*, and *NKX2-5*.
- It does not typically involve the **t(2;8) translocation**.
*CML*
- **Chronic Myeloid Leukemia (CML)** is classically defined by the presence of the **Philadelphia chromosome**, an acquired reciprocal translocation **t(9;22)(q34;q11)**.
- This translocation results in the formation of the **BCR-ABL1 fusion gene**, which encodes a constitutively active tyrosine kinase.
*CLL*
- **Chronic Lymphocytic Leukemia (CLL)** is most frequently associated with cytogenetic abnormalities such as **deletions of 13q14, 11q22-23 (ATM gene), and 17p13 (TP53 gene)**, and **trisomy 12**.
- The **t(2;8) translocation** is not characteristic of CLL.
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325.
Adaptive Immunity Indian Medical PG Question 9: Adoptive immunity is by what mechanism?
- A. Vaccination with killed pathogens
- B. Injection of lymphocytes (Correct Answer)
- C. Natural infection
- D. Passive transfer of antibodies
Adaptive Immunity Explanation: ***Injection of lymphocytes***
- **Adoptive immunity** refers to the transfer of immunity by transferring immune cells, specifically **lymphocytes**, from an immune individual to a non-immune individual.
- This method directly provides the recipient with pre-existing, functional immune cells capable of mediating an immune response.
*Natural infection*
- Natural infection leads to **active immunity**, where an individual's own immune system responds to a pathogen and generates memory cells and antibodies.
- This process involves the host's immune system actively recognizing and clearing the pathogen, not the transfer of pre-formed immune cells.
*Passive transfer of antibodies*
- This describes **passive immunity**, where pre-formed **antibodies** are transferred from one individual to another, providing immediate but temporary protection.
- While it confers immunity, it does not involve the transfer of whole immune cells (lymphocytes) that can mount a sustained cellular immune response.
*Vaccination with killed pathogens*
- Vaccination, even with killed pathogens, induces **active immunity** by stimulating the recipient's own immune system to produce antibodies and memory cells.
- This method aims to generate a primary immune response internally rather than directly providing effector immune cells.
Adaptive Immunity Indian Medical PG Question 10: What are the changes in the variable region of immunoglobulins?
- A. Isotype
- B. Epitope
- C. Allotype
- D. Idiotype (Correct Answer)
Adaptive Immunity Explanation: ***Idiotype***
- **Idiotype** refers to the unique set of antigenic determinants in the **variable region** of an antibody molecule, specifically within the **hypervariable regions (complementarity-determining regions, CDRs)**.
- These unique determinants allow antibodies to recognize specific antigens and are generated by the specific **V(D)J gene rearrangements** in B cells.
*Isotype*
- **Isotype** refers to the constant region of an antibody, determining its class (e.g., **IgG, IgM, IgA, IgD, IgE**).
- This region defines the antibody's effector functions and has nothing to do with the antigen-binding variability.
*Allotype*
- **Allotype** refers to minor genetic variations within the **constant region** of an antibody molecule within a species.
- These variations are due to different alleles inherited from parents and are not associated with the variable region that binds to antigens.
*Epitope*
- An **epitope** is the specific part of an **antigen** that an antibody or T-cell receptor recognizes and binds to.
- It is a feature of the antigen, not a change within the variable region of the immunoglobulin itself.
More Adaptive Immunity Indian Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
