Immunology — MCQs
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Which cells are known to cause rosette formation with sheep red blood cells?
Which immunoglobulin is known as the pentameric immunoglobulin?
Which of the following statements about interferons is true?
Which complement proteins are formed in the liver?
Which component is considered the central part of the complement pathway?
The idiotype of an antibody is determined by -
Which of the following statements is true regarding T cell independent antigens?
Which of the following is the most potent stimulator of Naive T-cells?
HIV window period indicates:
NK cells' activity is enhanced by?
Immunology Indian Medical PG Practice Questions and MCQs
Question 1021: Which cells are known to cause rosette formation with sheep red blood cells?
- A. Monocytes
- B. T cells (Correct Answer)
- C. NK cells
- D. All types of T cells
Explanation: ***T cells*** - **T cells** are the classic cells known to form rosettes with sheep red blood cells, a phenomenon called **E-rosette formation** - This interaction is mediated by the **CD2 receptor** on human T cells binding to **CD58 (LFA-3)** on sheep red blood cells - E-rosette formation was historically used as a diagnostic test to identify and enumerate T cells before the advent of flow cytometry - This is a characteristic feature of **mature T cells** and was widely used in immunology laboratories *NK cells* - **NK cells** do NOT typically form rosettes with sheep red blood cells - NK cells lack the specific CD2-mediated interaction required for classical E-rosette formation - NK cells are identified by other markers such as CD16 and CD56, and by their ability to kill target cells without prior sensitization *Monocytes* - **Monocytes** do not form rosettes with sheep red blood cells - Their primary functions include phagocytosis, antigen presentation, and cytokine production - They are identified by surface markers like **CD14** and their characteristic morphology (large size, kidney-shaped nucleus) *All types of T cells* - While this option is technically correct since all mature T cells express CD2 and can form E-rosettes, the more conventional answer is simply **"T cells"** - Both CD4+ helper T cells and CD8+ cytotoxic T cells possess the CD2 receptor and can participate in rosette formation - The distinction between "T cells" and "All types of T cells" is subtle, but "T cells" is the standard textbook answer
Question 1022: Which immunoglobulin is known as the pentameric immunoglobulin?
- A. IgA
- B. IgG
- C. IgM (Correct Answer)
- D. IgE
Explanation: ***IgM*** - **IgM** is found as a **pentamer** in its secreted form, meaning it is composed of five immunoglobulin monomer units joined together. - This pentameric structure gives IgM a high valency, making it very effective at **binding multiple antigens** simultaneously and activating the **complement system**. *IgA* - **IgA** primarily exists as a **monomer** in serum and as a **dimer** in secretions like mucus, tears, and saliva. - Its main function is to provide **mucosal immunity**, protecting epithelial surfaces from pathogens. *IgG* - **IgG** is the most abundant immunoglobulin in serum and exists as a **monomer**. - It crosses the **placenta** to provide passive immunity to the fetus and is crucial for **opsonization** and neutralizing toxins and viruses. *IgE* - **IgE** is present in very low concentrations in serum and exists as a **monomer**. - It plays a critical role in **allergic reactions** and defense against **parasites** by binding to mast cells and basophils.
Question 1023: Which of the following statements about interferons is true?
- A. Interferons inhibit viral replication in host cells. (Correct Answer)
- B. Interferons are specific for particular viruses.
- C. Interferons have no effect on viral infections.
- D. Interferons are synthetic antiviral agents.
Explanation: **Interferons inhibit viral replication in host cells.** - Interferons are a crucial part of the **innate immune response** against viral infections. - They work by inducing an **antiviral state** in neighboring uninfected cells, preventing viral replication. - Interferons are **non-specific** antiviral cytokines with broad-spectrum activity. *Interferons are specific for particular viruses.* - This is incorrect. Interferons are **virus-non-specific** in their antiviral action. - While their production is triggered by viral infection, they can inhibit replication of various different viruses. - This broad-spectrum activity is a key feature distinguishing them from antibodies (which are specific). *Interferons have no effect on viral infections.* - This is false. Interferons are potent **antiviral cytokines** essential for host defense against viruses. - They activate immune cells (NK cells, macrophages) and induce expression of genes that inhibit viral processes. *Interferons are synthetic antiviral agents.* - This is incorrect. Interferons are **naturally produced proteins** by the body's cells (leukocytes, fibroblasts, dendritic cells) in response to viral infections. - While recombinant interferons are used therapeutically, interferons are biological molecules, not synthetic drugs.
Question 1024: Which complement proteins are formed in the liver?
- A. C3, C6
- B. C2, C4 (Correct Answer)
- C. C5, C8
- D. C1
Explanation: ***C2, C4*** - While **all complement proteins (C1-C9) are primarily synthesized in the liver**, this question (NEET PG 2012) expects this as the answer based on the context of **classical pathway activation**. - **C2** and **C4** are essential components of the **C3 convertase (C4b2a)** in both the classical and lectin pathways. - These proteins work together in the early activation steps of complement-mediated immunity. - **Clinical relevance:** Deficiencies in C2 or C4 lead to increased susceptibility to **autoimmune diseases** (especially SLE) and **recurrent infections**. *C3, C6* - **C3** is the most abundant complement protein and central to all three pathways (classical, alternative, lectin). - **C6** is part of the membrane attack complex (MAC: C5b-C6-C7-C8-C9). - Both are indeed synthesized in the liver, but this was not the expected answer for this examination question. *C5, C8* - Both **C5** and **C8** are synthesized in the liver and are crucial components of the **membrane attack complex (MAC)**. - C5 is cleaved into C5a (potent anaphylatoxin) and C5b (initiates MAC formation). - C8 binds to the C5b-C7 complex and recruits C9 for membrane pore formation. *C1* - The **C1 complex** (C1q, C1r, C1s) is synthesized in the liver and initiates the classical complement pathway. - C1q recognizes antibody-antigen complexes (IgG or IgM bound to antigen). - **C1 deficiency** is associated with severe **SLE-like syndromes** and recurrent infections. **Note:** From a purely biochemical standpoint, all major complement components are produced primarily by hepatocytes in the liver, though some can also be synthesized by macrophages and other cells. This question reflects the specific context of the original examination.
Question 1025: Which component is considered the central part of the complement pathway?
- A. C1 (complement component 1)
- B. C3 (complement component 3) (Correct Answer)
- C. C2 (complement component 2)
- D. C5 (complement component 5)
Explanation: ***C3*** - **C3** is considered the central component because all three major pathways of complement activation (classical, alternative, and lectin) converge at the point of **C3 activation**. - Its cleavage product, **C3b**, is crucial for opsonization, formation of the C5 convertase, and initiating the assembly of the **membrane attack complex (MAC)**. *C1 (complement component 1)* - **C1** is the initial component of the **classical complement pathway** but does not play a direct role in the alternative or lectin pathways. - Its primary function is to bind to **antibody-antigen complexes** or directly to pathogens to activate C4 and C2. *C2 (complement component 2)* - **C2** is a component of the **classical** and **lectin pathways**, acting as a substrate for C1s and MASP to form the C3 convertase. - It is not involved in the initial activation of the **alternative pathway**. *C5 (complement component 5)* - **C5** is activated downstream of C3 and is a key component in the formation of the **membrane attack complex (MAC)**. - While critical for pathogen lysis, its activation is dependent on the prior cleavage of **C3** into C3b.
Question 1026: The idiotype of an antibody is determined by -
- A. Fc region
- B. Hinge region
- C. Carboxy end
- D. Amino end (Correct Answer)
Explanation: ***Amino end*** - The **idiotypic class** of an antibody is determined by the unique amino acid sequences within the **variable regions** of both the heavy and light chains, located at the **amino-terminal end** of the antibody. - These variable regions form the **antigen-binding sites**, giving each antibody its specific binding capabilities and thus its idiotype. *Fc region* - The **Fc (fragment crystallizable) region** is the tail region of an antibody that interacts with cell surface receptors and other immune system molecules. - It determines the **isotype (class)** of the antibody (e.g., IgG, IgM) and mediates effector functions but does not define the idiotype. *Hinge region* - The **hinge region** is a flexible segment in the middle of the heavy chains of IgG, IgA, and IgD antibodies. - It allows flexibility between the antigen-binding (Fab) arms, facilitating bivalent binding, but does not determine the idiotype. *Carboxy end* - The **carboxy end** (C-terminus) of the heavy and light chains typically corresponds to the constant regions of the antibody. - While it contributes to the antibody's overall structure and effector functions (especially the Fc region), it does not contain the unique sequences that define the **idiotype**.
Question 1027: Which of the following statements is true regarding T cell independent antigens?
- A. They primarily activate T-cells.
- B. They primarily activate B-cells. (Correct Answer)
- C. They primarily activate macrophages.
- D. They primarily activate CD8+ T cells.
Explanation: ***Correct: They primarily activate B-cells*** - T-cell independent antigens are typically **polysaccharides** (TI-2) or **lipopolysaccharides** (TI-1) with repeating epitopes that can directly cross-link B cell receptors (BCRs) - This direct binding and cross-linking provide a strong enough signal to activate B cells and induce **antibody production** (mainly IgM) without the need for T cell help - They induce a rapid but limited immune response with minimal memory formation *Incorrect: They primarily activate T-cells* - T-cell independent antigens do not require processing and presentation by **MHC molecules**, which is essential for T cell activation - T cells recognize processed peptides presented by MHC, a mechanism not utilized by T-cell independent antigens - By definition, these antigens activate B cells **without** T cell involvement *Incorrect: They primarily activate macrophages* - While macrophages are antigen-presenting cells, their primary role in adaptive immunity is to process and present antigens to T cells - Macrophages are involved in **phagocytosis** and antigen processing, but are not the primary target cells for T-independent antigens - The key feature of TI antigens is direct B cell activation, not macrophage activation *Incorrect: They primarily activate CD8+ T cells* - **CD8+ T cells** are activated by processed antigens presented on **MHC class I molecules**, typically derived from intracellular pathogens - T-cell independent antigens do not utilize this pathway and are primarily involved in **humoral immunity** through direct B cell activation - TI antigens cannot activate CD8+ T cells as they bypass the T cell-dependent pathway entirely
Question 1028: Which of the following is the most potent stimulator of Naive T-cells?
- A. Macrophages
- B. B-cell
- C. Mature dendritic cells (Correct Answer)
- D. Follicular dendritic cells
Explanation: ***Mature dendritic cells*** - **Mature dendritic cells** are the most potent professional antigen-presenting cells (APCs) for activating **naive T cells** due to their efficient antigen processing, presentation abilities, and high expression of costimulatory molecules (e.g., CD80, CD86) and MHC-peptide complexes. - Activated by pathogens or inflammatory signals, they migrate to secondary lymphoid organs where they initiate primary immune responses by presenting antigens to and activating naive T cells. *Follicular dendritic cells* - **Follicular dendritic cells** primarily present intact antigens to **B cells** in germinal centers of secondary lymphoid organs, playing a crucial role in B cell maturation, selection, and antibody production. - They lack MHC class II molecules and thus cannot directly present antigens to naive T cells. *Macrophages* - While **macrophages** are professional APCs, they are generally less efficient than mature dendritic cells at activating **naive T cells**, especially in the initiation of primary immune responses. - They are more involved in presenting antigens to already activated T cells and clearing pathogens, often acting as secondary APCs. *B-cell* - **B cells** can act as APCs, but they are generally less efficient than **dendritic cells** in activating **naive T cells**, especially for the primary immune response. - Their primary role in antigen presentation is to present processed antigens to **helper T cells** to receive costimulation for their own activation and differentiation into plasma cells, often after being activated themselves.
Question 1029: HIV window period indicates:
- A. time period between infection and onset of first symptoms
- B. time period between infection and minimum viral load
- C. time period between infection and maximum viral load
- D. time period between infection and detection of antibodies (Correct Answer)
Explanation: ***time period between infection and detection antibodies*** - The **HIV window period** refers specifically to the time frame after initial infection during which **HIV antibodies** have not yet reached detectable levels in routine serological tests. - During this period, an infected individual can still transmit the virus, even if their test results would appear **negative** for antibodies. *time period between infection and onset of first symptoms* - The onset of **first symptoms**, such as acute retroviral syndrome, can occur before or after antibodies are detectable, and is not the defining characteristic of the window period. - Symptoms are a **clinical manifestation**, whereas the window period is a **diagnostic concept** related to test detectability. *time period between infection and minimum viral load* - **Viral load** (the amount of virus in the blood) is typically **high** shortly after infection, then decreases somewhat before rising again, and its minimum point is not directly related to the antibody window period. - The window period focuses on the host's **immune response** to the virus, specifically antibody production. *time period between infection and maximum viral load* - The **maximum viral load** usually occurs during the acute (early) phase of infection, often before the development of detectable antibodies. - This represents a peak in viral replication, not the interval until the **immune system's antibody response** becomes detectable.
Question 1030: NK cells' activity is enhanced by?
- A. IL-1
- B. TNF
- C. IL-2 (Correct Answer)
- D. TGF-β
Explanation: ***IL-2*** - **Interleukin-2** is a crucial cytokine that stimulates the proliferation and differentiation of T cells and **NK cells**, thus enhancing their cytotoxic activity. - It plays a vital role in both **adaptive and innate immune responses** by promoting NK cell maturation and increasing their ability to recognize and kill infected or cancerous cells. *IL-1* - **Interleukin-1** primarily functions as a **pro-inflammatory cytokine**, mediating systemic inflammatory responses and activating macrophages and endothelial cells. - While it modulates immune responses, its direct effect on **enhancing NK cell cytotoxicity** is not as prominent as that of IL-2. *TNF* - **Tumor Necrosis Factor (TNF)** is a cytokine involved in **systemic inflammation** and acute phase responses, also inducing apoptosis in tumor cells. - Though TNF can influence various immune cells, it is not primarily known for directly stimulating and **enhancing NK cells' activity** in the same manner as IL-2. *TGF-β* - **Transforming Growth Factor-beta (TGF-β)** is a cytokine with predominantly **immunosuppressive functions**, inhibiting the proliferation and differentiation of many immune cells, including NK cells. - It generally **downregulates immune responses** and promotes tolerance rather than enhancing NK cell activity.
Practice by Chapter
Cells and Organs of Immune System
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Innate Immunity
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Adaptive Immunity
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Antigens and Antibodies
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Major Histocompatibility Complex
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Complement System
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Cytokines and Chemokines
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Hypersensitivity Reactions
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Autoimmunity and Autoimmune Diseases
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Immunodeficiency Disorders
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Transplantation Immunology
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Tumor Immunology
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