With the lack of CD40 in B cells, which immunological abnormality is seen?
Q932
CD 40 marker is absent in the person. Which of the following would be seen?
Q933
CD40 deficiency in a person signifies?
Q934
A 23-year-old woman presents with vulvar ulcers and lymphadenopathy. Testing confirms primary HSV infection. Which of the following statements about HSV antibody development is correct?
Q935
Multiple sclerosis is an autoimmune disease in which T-lymphocytes initiate an immune system response targeting the myelin sheaths of the central nervous system. What stage of T-lymphocyte development is the most likely to be defective in this disorder?
Q936
A 34-year-old female medical professional who works for a non-governmental organization visits her primary care provider for a routine health check-up. She made a recent trip to Sub-Saharan Africa where she participated in a humanitarian medical project. Her medical history and physical examination are unremarkable. A chest radiograph and a tuberculin skin test (PPD) are ordered. The chest radiograph is performed at the side and the PPD reaction measures 12 mm after 72 hours. Which of the following mechanisms is involved in the skin test reaction?
Q937
A 24-year-old man, an information technology professional, gets himself tested for serum immunoglobulin M (IgM) levels because he wants to know more about his immunity. He knows that IgM levels reflect the status of his immunity, based on the internet. Although the laboratory report is normal, he consults a physician. The physician discusses human immunity and its important components. He also tells him that most circulating IgM antibodies in the blood of normal persons are produced by a specific type of B cell, which is present mostly in the peritoneal cavity and in mucosal tissues. He also mentions that these cells are components of innate immunity. Which of the following types of B cells is the physician referring to?
Q938
Which antibody is seen in recent infection?
Q939
Which one of the following is a major component in activation of the complement alternative pathway?
Q940
Classical complement is activated by:
Immunology Indian Medical PG Practice Questions and MCQs
Question 931: 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 932: 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 933: CD40 deficiency in a person signifies?
A. IgG increase
B. T cell absent
C. IgM increase (Correct Answer)
D. B cell absent
Explanation: ***IgM increase***
- A deficiency in **CD40**, or its ligand **CD40L** (found on T helper cells), disrupts **T-cell-dependent B cell activation** and **class switching**.
- Without proper signaling through CD40/CD40L, B cells cannot undergo **isotype switching** from **IgM** to IgG, IgA, or IgE, leading to elevated IgM levels and deficiencies in other antibody classes.
*IgG increase*
- **IgG levels** would likely be **decreased** in CD40 deficiency due to the impaired ability of B cells to undergo **class switching** from IgM to other antibody isotypes.
- The primary role of CD40/CD40L interaction is to facilitate this class switching process.
*T cell absent*
- **CD40 deficiency** does not directly cause the absence of **T cells**; rather, it affects the ability of T cells to adequately activate B cells.
- T-cell absence or severe dysfunction would be indicative of a different primary immunodeficiency, such as **SCID (Severe Combined Immunodeficiency)**.
*B cell absent*
- **CD40 deficiency** does not result in the absence of **B cells**; B cells are present but are dysfunctional in terms of antibody class switching.
- Conditions like **X-linked agammaglobulinemia (XLA)** are characterized by the absence or severe deficiency of B cells.
Question 934: A 23-year-old woman presents with vulvar ulcers and lymphadenopathy. Testing confirms primary HSV infection. Which of the following statements about HSV antibody development is correct?
A. IgG appears immediately after infection
B. IgG antibodies appear 2-3 weeks after infection and persist (Correct Answer)
C. No antibody response occurs
D. IgM and IgG appear simultaneously at 6 weeks
Explanation: ***IgG antibodies appear 2-3 weeks after infection and persist***
- Following primary HSV infection, the body mounts an immune response, with **IgG antibodies** typically becoming detectable approximately **2-3 weeks post-infection**. [1]
- These **IgG antibodies** persist for life, providing long-term immunity and serving as a marker of past or latent infection. [1]
*IgG appears immediately after infection*
- The immune system requires time to generate a robust antibody response, so **IgG antibodies** do not appear immediately following infection. [2]
- The initial immune response involves innate immunity and the production of **IgM antibodies** before IgG. [1], [2]
*No antibody response occurs*
- The body's immune system recognizes the viral antigens and mounts an antibody response to combat the infection.
- Absence of an antibody response would imply a complete failure of the adaptive immune system, which is not the case in immunocompetent individuals with primary HSV. [1]
*IgM and IgG appear simultaneously at 6 weeks*
- **IgM antibodies** are produced earlier in the immune response compared to **IgG**. [2]
- While both may be present at 6 weeks, their appearance is not simultaneous, with IgM preceding IgG, and IgG often detectable by 2-3 weeks, not waiting until 6 weeks. [1]
Question 935: Multiple sclerosis is an autoimmune disease in which T-lymphocytes initiate an immune system response targeting the myelin sheaths of the central nervous system. What stage of T-lymphocyte development is the most likely to be defective in this disorder?
A. Negative selection (Correct Answer)
B. V-DJ rearrangement
C. Positive selection
D. D-J rearrangement
Explanation: ***Negative selection***
- **Negative selection** is the process by which T-cells that bind too strongly to **self-antigens** are eliminated in the **thymus** to prevent **autoimmunity**.
- A defect in negative selection would allow **autoreactive T-cells** to mature and exit the thymus, leading to diseases like **multiple sclerosis** where these cells attack self-components (myelin).
*V-DJ rearrangement*
- **V-DJ rearrangement** is crucial for generating diversity in the **T-cell receptor (TCR)** and **B-cell receptor (BCR)** genes, occurring early in lymphocyte development.
- While essential for a functional immune system, a defect in this process would likely result in an inability to recognize a wide range of antigens, rather than specifically causing autoimmunity due to self-reactivity.
*Positive selection*
- **Positive selection** occurs in the **thymus** and ensures that T-cells can recognize **MHC molecules** (either MHC I or MHC II), a necessary step for them to perform their function.
- A defect in positive selection would lead to a lack of functional T-cells capable of interacting with antigen-presenting cells, resulting in **immunodeficiency**, not autoimmunity.
*D-J rearrangement*
- **D-J rearrangement** is an early step in the formation of the **T-cell receptor (TCR)** beta chain (and immunoglobulin heavy chain in B-cells), occurring before V-DJ rearrangement.
- Like V-DJ rearrangement, a defect at this stage would impair the generation of a diverse T-cell repertoire, potentially leading to **immunodeficiency** rather than the specific failure to tolerize against self-antigens.
Question 936: A 34-year-old female medical professional who works for a non-governmental organization visits her primary care provider for a routine health check-up. She made a recent trip to Sub-Saharan Africa where she participated in a humanitarian medical project. Her medical history and physical examination are unremarkable. A chest radiograph and a tuberculin skin test (PPD) are ordered. The chest radiograph is performed at the side and the PPD reaction measures 12 mm after 72 hours. Which of the following mechanisms is involved in the skin test reaction?
A. Complement activation
B. Formation of immune complexes
C. Th1-mediated delayed-type hypersensitivity (Correct Answer)
D. IgE cross-linking
Explanation: ***Th1-mediated delayed-type hypersensitivity***
- The **tuberculin skin test (PPD)** is a classic example of a **Type IV hypersensitivity reaction**, which is mediated by **T-helper 1 (Th1) cells** [3].
- Upon re-exposure to mycobacterial antigens (tuberculin), previously sensitized Th1 cells release **cytokines** that recruit and activate **macrophages**, leading to the characteristic induration and erythema [3].
*Complement activation*
- This mechanism is primarily involved in host defense against microbial infections and in **Type II** and **Type III hypersensitivity reactions**, not Delayed-Type Hypersensitivity [2].
- Activation of the complement system leads to cell lysis, opsonization, and inflammation, but it does not directly drive the PPD skin test response [2].
*Formation of immune complexes*
- This describes a **Type III hypersensitivity reaction**, where **antigen-antibody complexes** deposit in tissues, leading to inflammation and tissue damage [1].
- Examples include serum sickness and Arthus reaction, which are distinct from the cell-mediated PPD response [1].
*IgE cross-linking*
- This mechanism is characteristic of **Type I (immediate) hypersensitivity reactions**, commonly known as allergies [4].
- **IgE antibodies** bind to mast cells and basophils; subsequent cross-linking by antigens triggers the release of mediators like histamine, leading to rapid allergic symptoms [4].
Question 937: A 24-year-old man, an information technology professional, gets himself tested for serum immunoglobulin M (IgM) levels because he wants to know more about his immunity. He knows that IgM levels reflect the status of his immunity, based on the internet. Although the laboratory report is normal, he consults a physician. The physician discusses human immunity and its important components. He also tells him that most circulating IgM antibodies in the blood of normal persons are produced by a specific type of B cell, which is present mostly in the peritoneal cavity and in mucosal tissues. He also mentions that these cells are components of innate immunity. Which of the following types of B cells is the physician referring to?
A. Naïve B cells
B. Marginal zone B cells
C. Follicular B cells
D. B-1 B cells (Correct Answer)
Explanation: ***B-1 B cells***
- **B-1 B cells** are a distinct lymphocyte population found primarily in the **peritoneal and pleural cavities**, and mucosal tissues. They spontaneously secrete **IgM antibodies** without T cell help, which are important for initial defense against common pathogens.
- They are considered a component of the **innate immune system** due to their rapid, T-cell-independent response and limited receptor diversity, providing immediate protection.
*Naïve B cells*
- **Naïve B cells** circulate in the blood and secondary lymphoid organs, express both **IgM and IgD** on their surface, and have not yet encountered their specific antigen.
- They require activation by antigen and often **T cell help** to differentiate into plasma cells and produce antibodies.
*Marginal zone B cells*
- **Marginal zone (MZ) B cells** are located in the marginal zone of the spleen and respond rapidly to **blood-borne polysaccharide antigens**.
- While they can produce **IgM without T-cell help**, they are primarily found in the spleen, not predominantly the peritoneal cavity or mucosal tissues.
*Follicular B cells*
- **Follicular B cells** are the most abundant B cell population in secondary lymphoid organs, residing in **B cell follicles**.
- They require **T cell help** to mount robust immune responses, undergo class-switching, and affinity maturation, and are not primarily known for spontaneous IgM production in the peritoneal cavity.
Question 938: Which antibody is seen in recent infection?
A. IgE
B. IgM (Correct Answer)
C. IgD
D. IgG
Explanation: ***IgM***
- **IgM** is the first antibody produced during a **primary immune response** to a new infection.
- Its presence indicates a **recent or ongoing acute infection**.
*IgE*
- **IgE** is primarily associated with **allergic reactions** and defense against parasites.
- It is not typically an indicator of a recent bacterial or viral infection.
*IgD*
- **IgD** is mostly found on the surface of **B cells** and plays a role in B cell activation.
- Its function in circulating blood is not well understood, and it is not used to diagnose recent infection.
*IgG*
- **IgG** is the most abundant antibody in serum and represents a **secondary, more delayed immune response**.
- Its presence indicates **past exposure or chronic infection**, as it provides long-term immunity.
Question 939: Which one of the following is a major component in activation of the complement alternative pathway?
A. C2
B. C3 (Correct Answer)
C. C4
D. C1
Explanation: ***C3***
- **C3** is a central component in all complement pathways. In the alternative pathway, spontaneous hydrolysis of **C3** leads to C3(H2O), initiating the formation of the **C3 convertase**.
- This **C3 convertase** (C3bBb) further cleaves more **C3** into C3a and C3b, amplifying the pathway and leading to downstream complement activation.
*C2*
- **C2** is a crucial component of the **classical** and **lectin pathways**, where it is cleaved by C1s or MASP-2, respectively, to form C2b and C2a.
- **C2a** then combines with C4b to form the **C3 convertase** (C4b2a) of these pathways; it does not play a direct role in initiating the alternative pathway.
*C4*
- **C4** is primarily involved in the **classical** and **lectin pathways**, where it is cleaved by C1s or MASP-2 to form C4a and C4b.
- **C4b** binds to pathogens or immune complexes and then associates with C2a to form the **C3 convertase** (C4b2a), which is not part of the alternative pathway initiation.
*C1*
- **C1** is the initiating complex of the **classical complement pathway** and is composed of C1q, C1r, and C1s.
- It recognizes and binds to antibody-antigen complexes or pathogen surfaces, but it has no direct role in the **alternative pathway activation**.
Question 940: Classical complement is activated by:
A. C3 Convertase
B. C1
C. Ag-Ab complex (Correct Answer)
D. IgA
Explanation: ***Ag-Ab complex***
- The **classical complement pathway** is initiated by the binding of **C1q** to an antigen-antibody complex, specifically involving **IgM** or certain subclasses of **IgG**.
- This binding triggers a cascade of events leading to the activation of the complement system, ultimately resulting in the **lysis of target cells**, **opsonization**, and **inflammation**.
*C3 Convertase*
- **C3 convertase** is an enzyme complex formed later in the complement cascade, responsible for cleaving C3 into C3a and C3b.
- While essential for all complement pathways, it is a **downstream effector** and not the initial activator of the classical pathway.
*C1*
- **C1** is a complex protein that includes C1q, C1r, and C1s. While C1 plays a crucial role in the classical pathway, it is **activated by** the antigen-antibody complex, not an independent activator.
- The activation sequence is: **Ag-Ab complex → C1q binding → C1 activation → cascade initiation**. Thus, the Ag-Ab complex is the primary trigger, and C1 is the responder.
*IgA*
- **IgA** primarily functions in mucosal immunity and is generally **not an activator** of the classical complement pathway.
- Instead, IgA can activate the **alternative complement pathway** under specific circumstances, but not the classical pathway through direct binding to C1q.
