Immunology Practice Questions

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

Decreased IgG and increase in IgM. ***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.

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

Impaired B cell function. ***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).

Q: CD40 deficiency in a person signifies?

IgM increase. ***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.

Q: 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?

Negative selection. ***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.

Q: 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?

B-1 B cells. ***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.

Q: Which antibody is seen in recent infection?

IgM. ***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.

Q: Which one of the following is a major component in activation of the complement alternative pathway?

C3. ***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**.

Q: Classical complement is activated by:

Ag-Ab complex. ***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.

Q: Increased susceptibility to N. meningitidis infections is associated with deficiency of which complement component:

C5-C9 deficiency. ***C5-C9 deficiency*** - Deficiencies in late complement components (C5-C9) prevent the formation of the **Membrane Attack Complex (MAC)**, which is essential for the lysis of **Neisseria species**. - This specific deficiency leads to an increased risk of recurrent, invasive infections with **Neisseria meningitidis** and **Neisseria gonorrhoeae**. *C1-C4 deficiency* - Deficiencies in early classical pathway components (C1, C2, C4) are most strongly associated with **systemic lupus erythematosus (SLE)** and other **immune complex disorders**. - While they increase the risk of pyogenic infections, they do not carry the same specific predilection for **Neisseria** as terminal pathway defects. *C3 deficiency* - **C3** is the central converging point for all complement pathways; its deficiency results in severe, recurrent infections with **encapsulated bacteria** (e.g., S. pneumoniae). - Deficiency impairs **opsonization** and recruitment of inflammatory cells, leading to a much broader spectrum of infectious susceptibility than MAC deficiency. *C2 deficiency* - **C2 deficiency** is the most common human complement deficiency and is frequently linked to **autoimmune diseases** like SLE due to poor immune complex clearance. - Although it can predispose individuals to infections by **encapsulated organisms**, it is not the classic association for isolated **meningococcal** susceptibility.

Q: Raji cell assays are used to quantitate

Immune complexes. ***Immune complexes*** - The Raji cell assay is a laboratory technique specifically designed to detect and quantify **circulating immune complexes** in serum. - Raji cells are a human lymphoblastoid cell line that expresses receptors for the Fc portion of IgG (FcγR) and complement components, allowing them to bind to and facilitate the detection of antigen-antibody complexes. *T cells* - **T cells** are a type of lymphocyte involved in cell-mediated immunity; their quantity is typically assessed using techniques like flow cytometry with specific cell markers (e.g., CD3, CD4, CD8). - Raji cell assays do not directly measure the absolute number or function of T cells. *Interferon level* - **Interferons** are cytokines with antiviral and immunomodulatory properties; their levels are usually measured using immunoassays such as ELISA (Enzyme-Linked Immunosorbent Assay). - The Raji cell assay is not designed to quantify interferon levels. *Complement level* - **Complement levels** (e.g., C3, C4, CH50) are typically assessed using immunoturbidimetric assays, nephelometry, or functional assays that measure complement activity. - While Raji cells express complement receptors, the assay primarily focuses on binding immune complexes, not direct quantification of complement proteins themselves.

Question 1

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

Accepted Answer

Decreased IgG and increase in IgM

Answer

Total lack of NK cells

Answer

Lack of CD8 mediated cytotoxicity

Answer

Inability of neutrophil against infections

Question 2

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

Accepted Answer

Impaired B cell function

Answer

Impaired Macrophage function

Answer

Impaired NK cell function

Answer

Impaired T cell function

Question 3

CD40 deficiency in a person signifies?

Accepted Answer

IgM increase

Answer

IgG increase

Answer

T cell absent

Answer

B cell absent

Question 4

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?

Accepted Answer

Negative selection

Answer

V-DJ rearrangement

Answer

Positive selection

Answer

D-J rearrangement

Question 5

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?

Accepted Answer

B-1 B cells

Answer

Naïve B cells

Answer

Marginal zone B cells

Answer

Follicular B cells

Question 6

Which antibody is seen in recent infection?

Accepted Answer

IgM

Answer

IgE

Answer

IgD

Answer

IgG

Question 7

Which one of the following is a major component in activation of the complement alternative pathway?

Accepted Answer

C3

Answer

C2

Answer

C4

Answer

C1

Question 8

Classical complement is activated by:

Accepted Answer

Ag-Ab complex

Answer

C3 Convertase

Answer

C1

Answer

IgA

Question 9

Increased susceptibility to N. meningitidis infections is associated with deficiency of which complement component:

Accepted Answer

C5-C9 deficiency

Answer

C1-C4 deficiency

Answer

C3 deficiency

Answer

C2 deficiency

Question 10

Raji cell assays are used to quantitate

Accepted Answer

Immune complexes

Answer

T cells

Answer

Interferon level

Answer

Complement level

Immunology — MCQs

Immunology — MCQs

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