Major Histocompatibility Complex — MCQs
In the context of immune response, which of the following cell types does not express MHC class II molecules?
Which of the following techniques can be used to detect single base pair substitutions?
Which of the following is not a component of innate immunity?
Increased frequency of HLA-B 27 is seen in all the following diseases except
Human leukocyte antigen (HLA) DR4 occurs in about 70% of patients with rheumatoid arthritis. HLA-DR4 is encoded in the major histocompatibility complex (MHC) region on:
Inactivated SA 14-14-2 vaccine is an example of which type of vaccine?
Antigen presented along with HLA-II stimulates
t(2,8) is associated with:
HLA B27 is associated with all except: a) Ankylosing spondylitis b) Pernicious anemia c) Behcet's syndrome d) Reiter's syndrome
Both antibody dependent and independent complement pathways converge on which complement component
Major Histocompatibility Complex Indian Medical PG Practice Questions and MCQs
Question 1: In the context of immune response, which of the following cell types does not express MHC class II molecules?
- A. Cortical macrophages
- B. Neutrophils
- C. Medullary macrophages
- D. NK cells (Correct Answer)
Explanation: ***NK cells*** - **Natural Killer (NK) cells)** are innate lymphocytes that do **NOT express MHC class II molecules** under any circumstances. - NK cells use alternative recognition mechanisms (KIRs, activating receptors) to detect target cells, primarily recognizing the **absence of MHC class I** or stress-induced ligands. - They function in innate immunity without antigen presentation capability. - **This is the best answer** as NK cells never express MHC class II, making them distinctly different from professional APCs. *Cortical macrophages* - **Cortical macrophages** in lymphoid organs are professional **antigen-presenting cells (APCs)** that constitutively express **MHC class II molecules**. - They present processed antigens to CD4+ T helper cells, playing a crucial role in initiating adaptive immune responses. *Medullary macrophages* - **Medullary macrophages** are also professional APCs that constitutively express **MHC class II molecules**. - They participate in antigen presentation and immune surveillance within the medullary regions of lymphoid tissues. *Neutrophils* - Neutrophils are granulocytes that **typically do not constitutively express MHC class II molecules** in their resting state. - However, under certain inflammatory conditions with prolonged stimulation (IFN-γ, GM-CSF), neutrophils can be induced to express low levels of MHC class II. - While neutrophils generally lack MHC class II, **NK cells are the more definitive answer** as they never express MHC class II under any physiological or pathological conditions.
Question 2: Which of the following techniques can be used to detect single base pair substitutions?
- A. FISH
- B. Southern blot
- C. PCR (Correct Answer)
- D. Restriction Fragment Length Polymorphism (RFLP)
Explanation: ***PCR (with sequencing or allele-specific methods)*** - **PCR-based techniques** are the most versatile methods for detecting single base pair substitutions (point mutations) - **Allele-specific PCR** can directly detect known point mutations by using primers specific to mutant or wild-type alleles - **PCR followed by Sanger sequencing** is the gold standard for identifying any single base pair substitution - **High-resolution melting (HRM) analysis** after PCR can detect mutations based on melting curve differences - PCR amplification is the foundation that enables these detection methods *FISH (Fluorescence in situ hybridization)* - FISH detects **large chromosomal abnormalities** such as aneuploidy, translocations, large deletions, and duplications - It visualizes chromosomal-level changes using fluorescent probes - **Not sensitive enough** to detect single base pair changes, as these are too small to visualize cytogenetically *Southern blot* - Southern blot detects **large DNA rearrangements**, insertions, deletions, or copy number variations - Analyzes restriction enzyme fragments separated by gel electrophoresis - **Generally cannot detect** single base pair substitutions unless they create or abolish a restriction enzyme recognition site - Even when applicable, PCR-based methods are more efficient and sensitive *Restriction Fragment Length Polymorphism (RFLP)* - RFLP can detect single base pair substitutions **only if** they create or abolish a **restriction enzyme recognition site** - Classic example: **Sickle cell mutation** (GAG→GTG in β-globin gene) abolishes an MstII restriction site - **Limited applicability** - can only detect the subset of point mutations that affect restriction sites - PCR-based methods are preferred as they can detect **any** single base pair substitution, not just those affecting restriction sites
Question 3: 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 4: Increased frequency of HLA-B 27 is seen in all the following diseases except
- A. Ankylosing spondylitis
- B. Reiters syndrome
- C. Acute anterior uveitis
- D. Myasthenia gravis (Correct Answer)
Explanation: ***Myasthenia gravis*** - **Myasthenia gravis** is an autoimmune disorder characterized by muscle weakness and fatigue due to antibodies against acetylcholine receptors at the neuromuscular junction; it is not associated with **HLA-B27**. - Its pathogenesis involves **antibodies** and T-cell mediated responses against muscle proteins, distinct from the **spondyloarthropathies**. *Ankylosing spondylitis* - **Ankylosing spondylitis** is a chronic inflammatory disease primarily affecting the spine and sacroiliac joints, showing a very strong association with **HLA-B27** (over 90% of cases) [1]. - The presence of **HLA-B27** is a key diagnostic and prognostic factor in this condition [1]. *Reiters syndrome* - **Reiter's syndrome**, now more commonly known as **Reactive arthritis**, is a seronegative spondyloarthropathy often triggered by an infection and strongly associated with **HLA-B27** [1]. - It classically presents with a triad of **arthritis**, **urethritis**, and **conjunctivitis**, linked to the **HLA-B27** allele [1]. *Acute anterior uveitis* - **Acute anterior uveitis** is an inflammation of the iris and ciliary body, and it commonly occurs in association with **HLA-B27** positive spondyloarthropathies, including ankylosing spondylitis and reactive arthritis [1]. - Approximately 50% of patients with **acute anterior uveitis** are **HLA-B27** positive, even in the absence of other systemic diseases [1].
Question 5: Human leukocyte antigen (HLA) DR4 occurs in about 70% of patients with rheumatoid arthritis. HLA-DR4 is encoded in the major histocompatibility complex (MHC) region on:
- A. Chromosome 22
- B. Chromosome 9
- C. Chromosome 18
- D. Chromosome 6 (Correct Answer)
Explanation: ***Chromosome 6*** - The HLA complex, an essential part of the **major histocompatibility complex (MHC)**, is located on the **short arm of chromosome 6**. - This region encodes proteins crucial for the immune system's ability to **distinguish self from non-self**, including class I, II, and III MHC molecules [1]. *Chromosome 22* - Chromosome 22 is known for containing genes associated with various conditions but is **not the location of the MHC complex** or HLA genes. - For example, the **BCR gene** involved in the Philadelphia chromosome translocation in chronic myeloid leukemia is found here. *Chromosome 9* - Chromosome 9 harbors genes linked to conditions like **Friedreich's ataxia** and **tuberous sclerosis**, but not the HLA locus. - It also contains genes related to **blood group determination** (ABO system), but not immune recognition via HLA [2]. *Chromosome 18* - Chromosome 18 is associated with several genetic disorders, such as **Edwards syndrome** (trisomy 18), but it is **not where the MHC genes are located**. - Its genes are primarily involved in development and cellular function rather than direct immune surveillance through HLA. **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. 49-50, 175-176. [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. 49-50.
Question 6: Inactivated SA 14-14-2 vaccine is an example of which type of vaccine?
- A. Toxoid vaccine
- B. Live attenuated vaccine (Correct Answer)
- C. Inactivated vaccine
- D. Subunit vaccine
Explanation: ***Live attenuated vaccine*** - The **SA 14-14-2 vaccine** is a **live attenuated Japanese Encephalitis (JE) vaccine** developed through serial passage and attenuation of the wild-type SA 14 strain. - The designation "14-14-2" refers to the specific **attenuated strain** after multiple passages, not to an inactivation process. - This vaccine uses **weakened (attenuated) virus** that can replicate minimally, providing robust and long-lasting immunity similar to natural infection. - It is widely used in **China, India, and other Asian countries** in national immunization programs. *Inactivated vaccine* - While there is also an **inactivated version** of the SA 14-14-2 strain (vero cell-derived inactivated JE vaccine), the term "SA 14-14-2 vaccine" by itself typically refers to the **live attenuated formulation**. - Inactivated vaccines contain killed viral particles that cannot replicate. *Toxoid vaccine* - **Toxoid vaccines** are based on inactivated bacterial toxins (toxoids), not viral antigens. - Examples include vaccines for **tetanus** and **diphtheria**, which target toxins produced by bacteria. - This type does not apply to viral vaccines like Japanese Encephalitis. *Subunit vaccine* - **Subunit vaccines** contain only specific purified antigenic components (proteins, polysaccharides) rather than whole organisms. - Examples include **Hepatitis B vaccine** (HBsAg) and **HPV vaccine**. - The SA 14-14-2 vaccine uses the whole attenuated virus, not subunits.
Question 7: Antigen presented along with HLA-II stimulates
- A. CD2 cells
- B. CD8 cells
- C. CD4 cells (Correct Answer)
- D. CD19 cells
Explanation: ***CD4 cells*** - Antigen presented with **MHC class II molecules** (formerly HLA-II) on antigen-presenting cells (APCs) is recognized by the **T-cell receptor (TCR)** on **CD4+ T helper cells**. - This interaction is crucial for the activation and differentiation of CD4+ T cells, leading to cytokine production and the coordination of the adaptive immune response. *CD2 cells* - **CD2** is a surface molecule found predominantly on T cells and NK cells, involved in cell adhesion and co-stimulation but not directly in the primary antigen recognition with MHC class II. - While CD2 plays a role in T cell activation, it does not directly recognize antigen presented via MHC class II. *CD8 cells* - **CD8+ T cells** (cytotoxic T lymphocytes) primarily recognize antigens presented by **MHC class I molecules**, which display intracellular (endogenous) antigens. - MHC class I presentation signals to CD8 cells to induce apoptosis in infected or cancerous cells. *CD19 cells* - **CD19** is a cell surface marker found on **B lymphocytes** and is involved in B cell activation and signaling. - B cells can act as APCs and present antigen, but their primary recognition of antigen is typically through their B-cell receptor (BCR), and they are not themselves stimulated by MHC class II in the same manner as T cells.
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: HLA B27 is associated with all except: a) Ankylosing spondylitis b) Pernicious anemia c) Behcet's syndrome d) Reiter's syndrome
- A. Ankylosing spondylitis
- B. Reiter's syndrome
- C. Behcet's syndrome (Correct Answer)
- D. Psoriatic arthritis
Explanation: ***Behcet's syndrome*** - While Behcet's syndrome is an inflammatory condition, it is **not typically associated with HLA-B27**. It is more commonly linked to **HLA-B51**. - Its clinical presentation involves recurrent oral and genital ulcers, uveitis, and skin lesions, which are distinct from the spondyloarthritis spectrum. *Ankylosing spondylitis* - This is a classic **HLA-B27 associated spondyloarthropathy**, characterized by chronic inflammation of the sacroiliac joints and spine [1]. - The presence of HLA-B27 significantly increases susceptibility to this condition. *Reiter's syndrome* - Now more commonly referred to as **Reactive Arthritis**, this condition is strongly associated with **HLA-B27** [1]. - It often presents with a triad of arthritis, urethritis, and conjunctivitis following a genitourinary or gastrointestinal infection. *Psoriatic arthritis* - While not as strongly linked as ankylosing spondylitis or reactive arthritis, about **30-50% of patients with psoriatic arthritis test positive for HLA-B27**, especially those with spinal involvement [1]. - It is an inflammatory arthritis associated with **psoriasis** and can affect peripheral joints, the spine, and entheses.
Question 10: 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.
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