Adaptive Immunity — MCQs

10 questions

A researcher is studying the interactions between foreign antigens and human immune cells. She has isolated a line of lymphocytes that is known to bind antigen-presenting cells. From this cell line, she has isolated a cell surface protein that binds to class I major histocompatibility complex molecules. The continued activation, proliferation and survival of this specific cell line requires which of the following signaling molecules?

Choose the correct option regarding graft rejection.

CD 40 marker is absent in the person. Which of the following would be seen?

With the lack of CD40 in B cells, which immunological abnormality is seen?

Which interleukin is specifically secreted by Th17 cells?

Which of the following is a function of MHC class I and II?

What is the primary function of Langerhans' cells?

The immunoglobulins that can be transported across the placenta include:

The acute inflammatory response is predominantly mediated by which type of immune cells?

Q10

What are the characteristics of polymorphonuclear leukocytes (PMNs) in the oral cavity?

Adaptive Immunity Indian Medical PG Practice Questions and MCQs

Question 1: A researcher is studying the interactions between foreign antigens and human immune cells. She has isolated a line of lymphocytes that is known to bind antigen-presenting cells. From this cell line, she has isolated a cell surface protein that binds to class I major histocompatibility complex molecules. The continued activation, proliferation and survival of this specific cell line requires which of the following signaling molecules?

A. Interleukin 1
B. Interleukin 4
C. Interleukin 2 (Correct Answer)
D. Interleukin 8
E. Interleukin 6

Explanation: ***Interleukin 2*** - The description of the lymphocyte binding the **constant portion of MHC class I** and requiring a signaling molecule for activation, proliferation, and survival points to a **T cell**. - **Interleukin-2 (IL-2)** is a crucial cytokine for the proliferation, differentiation, and survival of T lymphocytes, acting in an autocrine or paracrine fashion after T cell activation. *Interleukin 1* - **Interleukin-1 (IL-1)** is primarily involved in inflammation and fever, produced by macrophages and other innate immune cells. - While it can act as a costimulator for T cells, it is not the primary cytokine required for their sustained proliferation and survival after initial activation. *Interleukin 4* - **Interleukin-4 (IL-4)** is a key cytokine in humoral immunity, promoting B cell proliferation and differentiation, and inducing IgE class switching. - It also plays a role in the differentiation of naive T cells into **Th2 cells**, but it is not the main cytokine for general T cell proliferation and survival. *Interleukin 8* - **Interleukin-8 (IL-8)**, also known as CXCL8, is a chemokine primarily responsible for attracting and activating neutrophils to sites of infection or inflammation. - It does not have a direct role in the sustained proliferation and survival of activated lymphocytes. *Interleukin 6* - **Interleukin-6 (IL-6)** is a pleiotropic cytokine involved in acute phase reactions, hematopoiesis, and the immune response, particularly B cell differentiation and antibody production. - Although it can influence T cell responses, it is not the primary growth factor for activated T lymphocytes as IL-2 is.

Question 2: Choose the correct option regarding graft rejection.

A. CD4 and CD8 both play a role in graft rejection (Correct Answer)
B. None of the options
C. CD8 only plays a role in graft rejection
D. CD4 only plays a role in graft rejection

Explanation: ***CD4 and CD8 both play a role in graft rejection*** - **CD4+ T cells** (helper T cells) recognize donor MHC class II molecules and differentiate into effector cells that produce cytokines, promoting inflammation and activating other immune cells involved in rejection - **CD8+ T cells** (cytotoxic T lymphocytes, CTLs) recognize donor MHC class I molecules and directly kill donor cells in the graft, leading to tissue destruction - Both T cell subsets are crucial for initiating and mediating different aspects of the immune response against transplanted organs *CD8 only plays a role in graft rejection* - This is incorrect because while **CD8+ T cells** are vital for direct cytotoxicity, **CD4+ T cells** are also essential for orchestrating the overall immune response - **CD4+ T cells** provide help to B cells and CD8+ T cells, and their cytokines can also directly injure graft tissue *CD4 only plays a role in graft rejection* - This is incorrect because although **CD4+ T cells** are critical for initiating and amplifying the immune response through cytokine production and activation of other cells, **CD8+ T cells** are directly responsible for killing graft cells - Both cell types contribute significantly to the complex pathophysiology of graft rejection

Question 3: CD 40 marker is absent in the person. Which of the following would be seen?

A. Impaired Macrophage function
B. Impaired NK cell function
C. Impaired B cell function (Correct Answer)
D. Impaired T cell function

Explanation: ***Impaired B cell function*** - The **CD40 receptor** on B cells is crucial for receiving co-stimulatory signals from **CD40 ligand (CD40L)**, primarily expressed on activated T cells. - Absence of CD40 on B cells prevents proper **T-cell dependent antibody class switching** and germinal center formation, leading to impaired B cell activation, immunoglobulin production, and immune responses. - This condition is seen in **Hyper-IgM Syndrome Type 3** (very rare autosomal recessive disorder). *Impaired Macrophage function* - While macrophages express CD40, its absence would primarily affect their ability to be fully activated by T cells and present antigens, but the most direct and profound impact of absent CD40 is on B cells themselves. - Macrophages have other activation pathways not directly dependent on CD40. *Impaired NK cell function* - **Natural killer (NK) cells** primarily recognize and kill target cells lacking MHC class I molecules or those expressing activating ligands, independent of CD40 signaling. - NK cell function is not directly regulated by the CD40-CD40L interaction. *Impaired T cell function* - While **T cells express CD40L** (the ligand for CD40), the question specifies the absence of the **CD40 marker** itself, which is expressed on B cells, not T cells. - T cell function involves antigen recognition, activation, and cytokine production, which are not directly mediated by CD40 expression on T cells. - T-cell function would be indirectly affected due to the lack of proper B cell help and antigen presentation, but the direct impact of absent CD40 is on the cell expressing it (B cells).

Question 4: With the lack of CD40 in B cells, which immunological abnormality is seen?

A. Total lack of NK cells
B. Lack of CD8 mediated cytotoxicity
C. Inability of neutrophil against infections
D. Decreased IgG and increase in IgM (Correct Answer)

Explanation: ***Decreased IgG and increase in IgM*** - The interaction between **CD40 on B cells** and **CD40L (CD154) on T helper cells** is crucial for **B cell activation**, proliferation, and **class switch recombination** (CSR). - Without this interaction, B cells cannot undergo CSR, leading to a failure to produce **IgG, IgA, or IgE**, while **IgM levels remain high** because IgM production is the initial default. *Total lack of NK cells* - **Natural Killer (NK) cells** are part of the innate immune system and their development is largely independent of CD40-CD40L signaling. - The absence of CD40 on B cells primarily affects adaptive humoral immunity, not NK cell numbers or function. *Lack of CD8 mediated cytotoxicity* - **CD8+ T cells** mediate cytotoxicity against infected or cancerous cells and their activation is primarily dependent on antigen presentation by **MHC class I molecules** and costimulation, not directly on B cell CD40. - While B cells can act as APCs, their CD40 interaction is more critical for T helper cell help for humoral responses. *Inability of neutrophil against infections* - **Neutrophils** are phagocytic cells important in innate immunity, and their function is largely independent of CD40 on B cells. - Neutrophil activity relies on pathogen recognition, phagocytosis, and degranulation, which are not directly regulated by the B cell CD40-CD40L pathway.

Question 5: Which interleukin is specifically secreted by Th17 cells?

A. IFN Gamma
B. IL6
C. IL-17 (Correct Answer)
D. IL-22

Explanation: ***IL22*** - Th17 cells predominantly secrete **IL-17** and also produce **IL-22**, which is significant in mucosal immunity and inflammation [1]. - **IL-22** plays a crucial role in the response to infections and in the pathogenesis of inflammatory diseases. *IL16* - IL-16 is primarily associated with **chemoattractant and regulatory functions** for lymphocytes and not directly secreted by Th17 cells. - It is involved in **eosinophil and T cell activation**, which is not characteristic of the Th17 response. *IFN Gamma* - IFN-gamma is mainly produced by **Th1 cells** and is critical for **cell-mediated immunity**, which is distinct from the function of Th17 cells. - It plays a role in activating **macrophages**, unlike Th17 cells which focus on **neutrophil recruitment** and inflammation. *IL6* - While IL-6 is a pro-inflammatory cytokine that can be involved in various immune responses, it is not primarily secreted by Th17 cells. - It is produced by a variety of cell types including fibroblasts and macrophages, acting as a mediator in the **acute phase response**. **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. 158-160.

Question 6: Which of the following is a function of MHC class I and II?

A. Antibody class switching
B. Signal transduction in T cell
C. Antigen presentation to T cell (Correct Answer)
D. Increase the secretion of cytokine

Explanation: ***Antigen presentation to T cell*** - **MHC class I** molecules present **endogenous antigens** to **CD8+ cytotoxic T cells**, leading to the destruction of infected or cancerous cells. - **MHC class II** molecules present **exogenous antigens** to **CD4+ helper T cells**, which then coordinate the immune response. *Antibody class switching* - This process is primarily influenced by **cytokines** secreted by helper T cells, rather than direct MHC function. - While T cells interact with B cells to facilitate class switching, the direct role is not performed by the MHC molecules themselves. *Signal transduction in T cell* - **T cell receptor (TCR)** and associated co-receptors (like **CD3 complex**) are responsible for signal transduction upon antigen recognition. - MHC molecules present the antigen, but they do not directly mediate the intracellular signaling cascades within the T cell. *Increase the secretion of cytokine* - Cytokine secretion is a downstream effect of T cell activation, which occurs after successful antigen presentation by MHC molecules. - MHC molecules' direct function is presentation, not the direct increase in cytokine secretion.

Question 7: What is the primary function of Langerhans' cells?

A. Antigen presenting cells (Correct Answer)
B. Involved in immune responses
C. Phagocytosis of pathogens
D. Keratinocyte production and maintenance

Explanation: ***Antigen presenting cells*** - Langerhans' cells play a critical role as **antigen presenting cells** (APCs) in the immune system, facilitating the activation of T-cells [1][2]. - They are found in the **epidermis** and are essential in initiating immune responses against pathogens [1][3]. *Seen in auto immune conditions* - While Langerhans' cells may be involved in autoimmune responses, they are not exclusively seen in these conditions. - Their primary function isn't linked to autoimmunity but rather to **immunological surveillance** and **antigen presentation** [1]. *Phagocytic cells* - Langerhans' cells are not primarily **phagocytic**, as their main role focuses on presenting antigens rather than directly engulfing pathogens [1]. - Phagocytic cells include macrophages and neutrophils, which are more involved in **directly consuming foreign particles**. *Seen in chronic infection* - Although Langerhans' cells can participate in the immune response during infections, they are not specifically characterized as being prominent in **chronic infections**. - Chronic infections are typically associated with different immune cell dynamics, involving other cells such as **plasma cells** and **T-cells**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 200. [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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, p. 1144.

Question 8: The immunoglobulins that can be transported across the placenta include:

A. IgA only
B. Neither IgG nor IgA
C. IgG only (Correct Answer)
D. Both IgG and IgA

Explanation: ***IgG only*** - **IgG** is the only class of immunoglobulin that can actively be transported across the **placental barrier** from mother to fetus, providing passive immunity. - This transport is mediated by specialized receptors (FcRn) on placental cells, ensuring the fetus receives protection against pathogens. *IgA only* - **IgA** is primarily found in **mucosal secretions** (e.g., breast milk, tears, saliva) and plays a crucial role in mucosal immunity. - It does not significantly cross the placenta and therefore does not contribute to fetal immunity in utero. *Neither IgG nor IgA* - This statement is incorrect because **IgG** is well-established as being transported across the placenta. - Such an absence of maternal antibodies would leave the fetus highly vulnerable to infections during development and early life. *Both IgG and IgA* - While **IgG** readily crosses the placenta, **IgA** does not, making this option incorrect. - The primary route for IgA transfer to the infant is through **breast milk** after birth, providing crucial immunity for the newborn's gastrointestinal tract.

Question 9: The acute inflammatory response is predominantly mediated by which type of immune cells?

A. T lymphocytes
B. Neutrophils (Correct Answer)
C. Both B and T lymphocytes
D. B lymphocytes

Explanation: ***Neutrophils*** - **Neutrophils** are the **primary mediators** of the **acute inflammatory response**, being the first immune cells recruited to sites of injury or infection (usually within minutes to hours) [1], [3]. - They are **innate immune cells** that perform phagocytosis, release antimicrobial substances, and form neutrophil extracellular traps (NETs) to combat pathogens [1]. - Neutrophils constitute **50-70% of circulating leukocytes** and are the hallmark cells found in acute inflammation [3]. *T lymphocytes* - **T lymphocytes** are central to **cell-mediated immunity** in the adaptive immune response, requiring several days for activation and clonal expansion [2]. - They recognize specific antigens through TCRs and are not involved in the immediate, non-specific phase of acute inflammation. - T cells play roles in **chronic inflammation** and coordinating adaptive immunity, not acute responses. *B lymphocytes* - **B lymphocytes** mediate **humoral immunity** by producing antibodies during the adaptive immune response [1]. - Their activation, differentiation into plasma cells, and antibody production take days to weeks, making them irrelevant to the rapid acute inflammatory response. - B cells are not recruited to acute inflammatory sites in the initial phase. *Both B and T lymphocytes* - While both are critical for **adaptive immunity** and host defense, neither B nor T lymphocytes are primary mediators of acute inflammation [4]. - The acute inflammatory response relies on **innate immune cells** (neutrophils, macrophages, mast cells) for immediate, non-specific protection before adaptive immunity develops [4].

Question 10: What are the characteristics of polymorphonuclear leukocytes (PMNs) in the oral cavity?

A. PMNs function mainly as antigen-presenting cells in oral tissues.
B. Granulocytes found in the gingival connective tissue.
C. PMNs actively migrate to the gingival crevicular fluid as part of the immune response. (Correct Answer)
D. None of the options.

Explanation: **PMNs actively migrate to the gingival crevicular fluid as part of the immune response.** - **Polymorphonuclear leukocytes (PMNs)**, primarily neutrophils, are highly motile phagocytes that play a crucial role in the innate immune response to oral microbes. - Their active migration into the **gingival crevicular fluid (GCF)** is a hallmark of the body's defense against bacterial plaque, forming a crucial first line of defense against periodontal pathogens. *Granulocytes found in the gingival connective tissue.* - While PMNs are granulocytes that reside in the **gingival connective tissue**, this statement alone does not fully encompass their dynamic role and key characteristics in the oral cavity. - Their most significant characteristic in the context of oral health is their **active migration** to the epithelial surface and into the GCF, not just their presence in the connective tissue. *PMNs function mainly as antigen-presenting cells in oral tissues.* - **PMNs** are primarily involved in **phagocytosis** and intracellular destruction of pathogens, not as primary antigen-presenting cells (APCs). - **Dendritic cells** and **macrophages** are the main APCs that bridge innate and adaptive immunity by presenting antigens. *None of the options.* - This option is incorrect because the statement regarding **PMNs** actively migrating to the **gingival crevicular fluid** accurately describes a major characteristic and function of these cells in oral immunity.

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