Immunology Practice Questions

Q: Which cells are known to cause rosette formation with sheep red blood cells?

T cells. ***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

Q: Which complement proteins are formed in the liver?

C2, C4. ***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.

Q: Which component is considered the central part of the complement pathway?

C3 (complement component 3). ***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.

Q: Which of the following substances is toxic to parasites?

Peroxidase. ***Peroxidase*** - **Peroxidase** enzymes, especially those produced by **eosinophils**, generate toxic oxygen metabolites and hypohalous acids that are highly effective at damaging and killing parasites. - This enzyme plays a crucial role in the host's defense against larger parasites, such as **helminths (worms)**. *Interferon-alpha* - **Interferon-alpha** is an important cytokine primarily known for its **antiviral effects** and its role in activating natural killer (NK) cells. - While it modulates immune responses, it does not directly act as a toxic substance to parasites. *IL-2 (Interleukin-2)* - **IL-2** is a growth factor that primarily promotes the **proliferation and differentiation of T cells**, enhancing adaptive immune responses. - It does not directly kill parasites but rather supports the immune cells involved in parasite clearance. *IL-6 (Interleukin-6)* - **IL-6** is a pleiotropic cytokine involved in **inflammation, acute phase responses**, and the differentiation of B cells and T cells. - While it contributes to overall immune regulation, it lacks direct parasiticidal activity.

Q: The idiotype of an antibody is determined by -

Amino end. ***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**.

Q: Which of the following is the most potent stimulator of Naive T-cells?

Mature dendritic cells. ***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.

Q: NK cells' activity is enhanced by?

IL-2. ***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.

Q: In utero infection leads to which immunoglobulin?

IgM. ***IgM*** - **IgM** is the first antibody produced by the fetus in response to an in utero infection, as it cannot cross the placenta. - Its presence in a newborn's blood indicates an **active fetal immune response** to an infection acquired before birth. *IgG* - **IgG** antibodies from the mother cross the placenta and provide passive immunity to the fetus, but their presence does not necessarily indicate an active fetal infection. - High IgG levels in a neonate are typically maternal and do not reflect the infant's own immune response to an in utero infection. *IgA* - **IgA** is primarily found in mucosal secretions and is not typically produced by the fetus in significant amounts in response to in utero infection. - Its presence in a neonate's blood might suggest contamination or specific unusual circumstances, rather than routine in utero infection. *IgD* - The function of **IgD** is not fully understood, but it is primarily found on the surface of B lymphocytes and is not a major effector antibody in the primary immune response to infection. - It does not play a significant role in diagnosing in utero infections.

Q: Which type of hypersensitivity is associated with cell-mediated immunity?

Type 4. ***Type 4*** - Cell-mediated immunity primarily involves **T-lymphocytes** [1], essential for targeting and eliminating **intracellular pathogens** like viruses. - It plays a crucial role in **delayed-type hypersensitivity reactions** [2], making it vital for the adaptive immune response. *Type 3* - Type 3 immune responses are primarily associated with **immune complex-mediated** diseases and not directly with cell-mediated immunity. - This type involves primarily **B-cells** and antibodies in the response against antigens. *Type 2* - Type 2 immunity mainly concerns the activation of **B-lymphocytes** and antibody production against **extracellular pathogens** like bacteria. - It is characterized by **IgE-mediated responses** [3], particularly in allergic reactions, rather than cell-mediated actions. *Type 1* - Type 1 responses are associated with **Th1 cells** [2] and are more specifically linked to **autoimmunity and cell-mediated pathways**, but represent only a part of the broader cell-mediated immunity. - This type mainly focuses on clearance of **intracellular pathogens** but is not synonymous with the entire process of cell-mediated immunity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 207-208. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Q: Which of the following is not a component of innate immunity?

Helper T lymphocytes. ***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 1

Which cells are known to cause rosette formation with sheep red blood cells?

Accepted Answer

T cells

Answer

Monocytes

Answer

NK cells

Answer

All types of T cells

Question 2

Which complement proteins are formed in the liver?

Accepted Answer

C2, C4

Answer

C3, C6

Answer

C5, C8

Answer

C1

Question 3

Which component is considered the central part of the complement pathway?

Accepted Answer

C3 (complement component 3)

Answer

C1 (complement component 1)

Answer

C2 (complement component 2)

Answer

C5 (complement component 5)

Question 4

Which of the following substances is toxic to parasites?

Accepted Answer

Peroxidase

Answer

Interferon-alpha

Answer

IL-2 (Interleukin-2)

Answer

IL-6 (Interleukin-6)

Question 5

The idiotype of an antibody is determined by -

Accepted Answer

Amino end

Answer

Fc region

Answer

Hinge region

Answer

Carboxy end

Question 6

Which of the following is the most potent stimulator of Naive T-cells?

Accepted Answer

Mature dendritic cells

Answer

Macrophages

Answer

B-cell

Answer

Follicular dendritic cells

Question 7

NK cells' activity is enhanced by?

Accepted Answer

IL-2

Answer

IL-1

Answer

TNF

Answer

TGF-β

Question 8

In utero infection leads to which immunoglobulin?

Accepted Answer

IgM

Answer

IgG

Answer

IgA

Answer

IgD

Question 9

Which type of hypersensitivity is associated with cell-mediated immunity?

Accepted Answer

Type 4

Answer

Type 2

Answer

Type 3

Answer

Type 1

Question 10

Which of the following is not a component of innate immunity?

Accepted Answer

Helper T lymphocytes

Answer

Epithelial barriers

Answer

NK cells

Answer

Dendritic cells

Immunology — MCQs

Immunology — MCQs

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