Adaptive Immunity — MCQs
Which of the following is not considered an antigen-presenting cell?
Which of the following statements about the secondary immune response is false?
What is the primary mechanism by which cytotoxic T lymphocytes (CTLs) recognize target cells in the immune response?
Which of the following is not a component of innate immunity?
MHC II is associated with:-
Both antibody dependent and independent complement pathways converge on which complement component
Which is the cell of origin of Chronic Lymphocytic Leukaemia / Small Lymphocytic Lymphoma?
t(2,8) is associated with:
Adoptive immunity is by what mechanism?
What are the changes in the variable region of immunoglobulins?
Adaptive Immunity Indian Medical PG Practice Questions and MCQs
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
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.
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)
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.
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
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**.
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)
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.
Question 5: MHC II is associated with:-
- A. Red blood cells
- B. Antigen presenting cells (Correct Answer)
- C. Platelets
- D. Epithelial cells
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.
Question 6: Both antibody dependent and independent complement pathways converge on which complement component
- A. C8
- B. C1q
- C. C3 (Correct Answer)
- D. C5
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.
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)
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.
Question 8: t(2,8) is associated with:
- A. T cell ALL
- B. CML
- C. B cell ALL (Correct Answer)
- D. CLL
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.
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
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.
Question 10: What are the changes in the variable region of immunoglobulins?
- A. Isotype
- B. Epitope
- C. Allotype
- D. Idiotype (Correct Answer)
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.
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