Cells and Tissues of the Immune System — MCQs
Which of the following is not considered an antigen-presenting cell?
All of the following are features of Lymph node histology except:
Cell surface molecules involved in peripheral tolerance induction are
t(2,8) is associated with:
All are true regarding the development of T-cells, except?
What type of hypersensitivity reaction is primarily associated with allergic rhinitis?
Histamine in anaphylaxis is secreted by which of the following cells?
In chronic allergy, which immunoglobulin is predominantly elevated?
Amyloidosis shown in cardiac muscle is mainly due to which fibril?
Which of the following components are involved in non-IgE mediated anaphylactic reactions?
Cells and Tissues of the Immune System Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following is not considered an antigen-presenting cell?
- A. Macrophages
- B. Langerhans cells
- C. Thymocytes (Correct Answer)
- D. B lymphocytes
Explanation: ***Thymocytes*** - Thymocytes are **developing T cells** found in the thymus and do not function as antigen-presenting cells (APCs) [1]. - Unlike APCs, thymocytes are primarily involved in the **maturation** and selection of T lymphocytes. *Langerhans cells* - Langerhans cells are a type of **dendritic cell** found in the skin and are effective antigen-presenting cells to T cells [1]. - They play a crucial role in **immune surveillance** and response to skin infections. *Macrophages* - Macrophages are well-known antigen-presenting cells that engulf pathogens and present antigens to T cells [1]. - They are also involved in **phagocytosis** and secrete various cytokines to modulate immune responses. *M-cells* - M-cells (microfold cells) are specialized epithelial cells that transport antigens from the intestinal lumen to underlying immune cells. - Although not traditional APCs, they play a role in immune surveillance and stimulating **mucosal immunity**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 200, 207-208.
Question 2: All of the following are features of Lymph node histology except:
- A. Both Efferent and Afferent are present
- B. Subcapsular sinus present
- C. Cortex and Medulla are present
- D. Red pulp and White pulp are present (Correct Answer)
Explanation: ***Red pulp and White pulp are present*** - **Red pulp** and **white pulp** are characteristic histological features of the **spleen**, not lymph nodes [1]. - The white pulp contains lymphoid follicles (PALS - periarteriolar lymphoid sheaths), while the red pulp is involved in filtering blood and destroying old red blood cells [1]. - This is the feature that does NOT belong to lymph node histology. *Both Efferent and Afferent are present* - Lymph nodes have multiple **afferent lymphatic vessels** that bring lymph into the node and usually one or two **efferent lymphatic vessels** that carry lymph away [2]. - This arrangement allows for efficient filtering of lymph and immune surveillance [2]. - This IS a feature of lymph nodes. *Subcapsular sinus present* - The **subcapsular sinus** is a space located directly beneath the capsule of the lymph node, which receives lymph from the afferent lymphatic vessels. - It contains a network of reticular fibers and macrophages, acting as the initial filtering area. - This IS a feature of lymph nodes. *Cortex and Medulla are present* - Lymph nodes are histologically divided into an outer **cortex** and an inner **medulla**. - The cortex contains lymphoid follicles (B-cell areas) and paracortical areas (T-cell areas), while the medulla consists of medullary cords and sinuses. - This IS a feature of lymph nodes.
Question 3: Cell surface molecules involved in peripheral tolerance induction are
- A. CD40 and CD40L
- B. CD34 and CD51
- C. B7 and CD28 (Correct Answer)
- D. B7 and CD3
Explanation: ***B7 and CD28*** - B7 is crucial for providing a **costimulatory signal** to T cells via interaction with CD28, promoting **T cell activation** and peripheral tolerance [1][2]. - This interaction is essential in preventing autoimmune responses by ensuring T cells require both antigen and costimulatory signals for full activation [1][3]. *B7 and CD3* - CD3 is a part of the T cell receptor (TCR) complex, primarily involved in **T cell activation**, not specifically in peripheral tolerance. - The interaction of B7 with **CD3** does not provide the costimulatory signal necessary for peripheral tolerance [3]. *CD34 and CD51* - CD34 is primarily involved in **hematopoietic stem cell trafficking** and does not play a role in T cell tolerance mechanisms. - CD51 is associated with **integrins** and plays a role in adhesion rather than in peripheral tolerance induction. *CD40 and CD40L* - While CD40-CD40L interactions are important for **B cell activation** and other immune responses, they are not directly involved in the inductive mechanisms of **peripheral tolerance** in T cells. - They primarily mediate costimulatory signals in **adaptive immunity**, not specifically for tolerance purposes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 204-206. [2] 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. 157-158. [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. 176-177.
Question 4: t(2,8) is associated with:
- A. T cell ALL
- B. CML
- C. B cell ALL (Correct Answer)
- D. CLL
Explanation: ***B cell ALL*** - The translocation **t(2;8)(p11;q24)** is a **variant cytogenetic abnormality** specifically associated with **Burkitt lymphoma/leukemia**, a highly aggressive form of mature B-cell neoplasm, which can present as B-cell ALL. [1] - This variant translocation (occurring in ~15% of Burkitt lymphoma cases) leads to the **dysregulation of the MYC oncogene** on chromosome 8q24 due to its juxtaposition with the **kappa (κ) immunoglobulin light chain gene (IGK)** on chromosome 2p11. [1] - The most common translocation in Burkitt lymphoma is **t(8;14)(q24;q32)** involving MYC and the immunoglobulin heavy chain gene IGH (~80% of cases), while **t(8;22)** involving the lambda light chain occurs in ~5% of cases. [1] *T cell ALL* - T-cell ALL is primarily associated with translocations involving **T-cell receptor genes (e.g., TCRα/δ on 14q11, TCRβ on 7q34)** and various oncogenes like *TAL1*, *LMO1*, *LMO2*, *HOXA*, and *NKX2-5*. - It does not typically involve the **t(2;8) translocation**. *CML* - **Chronic Myeloid Leukemia (CML)** is classically defined by the presence of the **Philadelphia chromosome**, an acquired reciprocal translocation **t(9;22)(q34;q11)**. - This translocation results in the formation of the **BCR-ABL1 fusion gene**, which encodes a constitutively active tyrosine kinase. *CLL* - **Chronic Lymphocytic Leukemia (CLL)** is most frequently associated with cytogenetic abnormalities such as **deletions of 13q14, 11q22-23 (ATM gene), and 17p13 (TP53 gene)**, and **trisomy 12**. - The **t(2;8) translocation** is not characteristic of CLL. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325.
Question 5: All are true regarding the development of T-cells, except?
- A. T-cells are formed in bone marrow
- B. In lymph nodes, T-cells are found in paracortical area
- C. Maturation of T-cells take place in thymus
- D. T-cells are located in mantle layer of spleen (Correct Answer)
Explanation: ***T-cells are located in mantle layer of spleen*** - The **mantle layer** (or marginal zone) of the spleen is primarily associated with **B-lymphocytes**, which are involved in antibody production. - While T-cells are present in the spleen, they are predominantly found in the **periarteriolar lymphoid sheath (PALS)**, which is part of the white pulp, rather than the mantle layer. *T-cells are formed in bone marrow* - **Hematopoietic stem cells** in the **bone marrow** are the progenitors of all blood cells, including lymphocytes. - These stem cells differentiate into **lymphoid stem cells**, which then travel to the thymus to become T-cells. *Maturation of T-cells take place in thymus* - **T-cell precursors** migrate from the bone marrow to the **thymus**, where they undergo a complex process of differentiation and selection. - In the thymus, T-cells acquire their **T-cell receptors (TCRs)** and undergo positive and negative selection to ensure they are self-MHC restricted and tolerant to self-antigens. *In lymph nodes, T-cells are found in paracortical area* - The **paracortical area** (or paracortex) of the lymph node is the **T-cell zone**, rich in T-lymphocytes and dendritic cells. - This region is crucial for the interaction between T-cells and antigen-presenting cells, initiating adaptive immune responses.
Question 6: What type of hypersensitivity reaction is primarily associated with allergic rhinitis?
- A. Type I hypersensitivity reaction (Correct Answer)
- B. Type IV hypersensitivity reaction
- C. Type II hypersensitivity reaction
- D. Type III hypersensitivity reaction
Explanation: ***Type I hypersensitivity reaction*** - Allergic rhinitis is a classic example of a **Type I hypersensitivity reaction**, mediated primarily by **IgE antibodies** [1]. - Exposure to allergens triggers mast cell degranulation, releasing **histamine** and other mediators that cause symptoms like sneezing, rhinorrhea, and nasal congestion [2]. *Type II* - **Type II hypersensitivity reactions** involve **IgG or IgM antibodies** targeting antigens on cell surfaces or extracellular matrix, leading to cell lysis or dysfunction [4]. - Examples include **hemolytic anemia** and **Goodpasture syndrome**, which are distinct from allergic rhinitis. *Type III* - **Type III hypersensitivity reactions** involve the formation of **immune complexes** (antigen-antibody complexes) that deposit in tissues, leading to inflammation [4]. - Conditions like **serum sickness** and **lupus nephritis** are examples, not allergic rhinitis. *Type IV* - **Type IV hypersensitivity reactions** are **delayed-type hypersensitivity** reactions mediated by **T lymphocytes**, not antibodies. - Examples include **contact dermatitis** and the **tuberculin skin test**, which manifest much later after antigen exposure [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 210. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212. [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. 171-172. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.
Question 7: Histamine in anaphylaxis is secreted by which of the following cells?
- A. Mast cells (Correct Answer)
- B. B-cells
- C. Basophils
- D. Macrophages
Explanation: ***Mast cells*** - Mast cells are the primary cells responsible for the secretion of **histamine** during anaphylaxis, leading to rapid allergic responses [2][4]. - They are located in **tissues** and are involved in **immediate hypersensitivity reactions** by releasing various mediators upon activation [1][2]. *Basophils* - While basophils do contain **histamine**, they play a lesser role in acute anaphylaxis as compared to mast cells [1]. - Basophils are more associated with chronic allergic reactions rather than the **immediate release** observed in anaphylaxis [1]. *Macrophages* - Macrophages are primarily involved in **phagocytosis** and immune response but do not secrete significant amounts of histamine. - They release cytokines and other mediators but are not key players in **histamine-dependent** anaphylactic reactions. *B-cells* - B-cells are crucial for the production of **antibodies** but do not secrete histamine at all. - They are involved in **adaptive immunity** and do not play a direct role in **anaphylaxis** mechanisms [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 212-213. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94.
Question 8: In chronic allergy, which immunoglobulin is predominantly elevated?
- A. Ig A
- B. Ig E (Correct Answer)
- C. Ig M
- D. Ig G
Explanation: ***Ig E*** - **IgE** antibodies are primarily responsible for mediating **allergic reactions** [1] and play a key role in the pathogenesis of allergic diseases such as asthma, allergic rhinitis, and atopic dermatitis [2]. - In chronic allergy, there is a persistent overproduction of **IgE** in response to allergens, leading to chronic symptoms and inflammation [1]. *Ig A* - **IgA** is predominantly found in mucous secretions (e.g., saliva, tears, breast milk) and protects against mucosal infections. - While it plays a role in immune responses, it is not the primary mediator of chronic allergic reactions. *Ig M* - **IgM** is the first antibody produced in a primary immune response and is crucial for immediate defense against new infections. - It does not typically persist at high levels in chronic conditions like allergies [3]. *Ig G* - **IgG** is the most abundant antibody in serum and provides long-term immunity against pathogens. - While some **IgG** antibodies might be involved in allergic responses (e.g., IgG4 in blocking responses), **IgE** remains the predominant antibody in chronic allergic conditions [3]. **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. 171-172. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 686-687. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-211.
Question 9: Amyloidosis shown in cardiac muscle is mainly due to which fibril?
- A. AA (Amyloid A Protein Amyloidosis)
- B. AL (Immunoglobulin Light Chain Amyloidosis) (Correct Answer)
- C. ATTR (Transthyretin Amyloidosis)
- D. Atrial Natriuretic Peptide Amyloidosis (Theoretical Form)
Explanation: ***ATTR*** - Cardiac amyloidosis is mainly associated with **transthyretin amyloidosis** (ATTR), which is related to the deposition of **transthyretin fibrils** in the heart tissue [1]. - This type of amyloidosis often presents in patients with **senile systemic amyloidosis** or familial cases linked to mutations in the transthyretin gene [1]. *AA* - **AA amyloidosis** is usually secondary to chronic inflammatory conditions and does not primarily affect the cardiac muscle. - It is derived from **serum amyloid A protein**, differing from the fibrils associated with cardiac involvement. *AL* - **AL amyloidosis** results from the deposition of **light chain immunoglobulins**, typically related to plasma cell dyscrasias rather than the transthyretin fibrils affecting the heart. - This form of amyloidosis is distinguished by its systemic effects primarily in the kidneys and nervous system. *AANF* - **AANF amyloidosis** is not a recognized type of amyloidosis in medical literature related to cardiac involvement. - The primary fibrils associated with cardiac amyloidosis are either **transthyretin (ATTR)** or **light chain (AL)**, making this option misleading [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 266. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 580-581.
Question 10: Which of the following components are involved in non-IgE mediated anaphylactic reactions?
- A. Complement
- B. Ig G
- C. Ig M
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - **Non-IgE mediated anaphylactic reactions** can involve various immune components beyond IgE, including **IgG**, **IgM**, and the **complement system**. - For instance, **IgG antibodies** can bind to mast cells or basophils and trigger degranulation, while **complement activation** can directly release anaphylatoxins, both leading to anaphylactoid symptoms. *Ig G* - While many anaphylactic reactions are **IgE-mediated**, **IgG antibodies** can also contribute to anaphylaxis, particularly in drug reactions or reactions to biologics. - **IgG-mediated anaphylaxis** often involves immune complexes that activate mast cells or basophils through Fcγ receptors. *Ig M* - **IgM antibodies** are less commonly implicated in direct anaphylactic reactions compared to IgE or IgG. - However, **IgM** can play a role in complex formation that activates the complement system, indirectly contributing to **anaphylactoid responses**. *Complement* - The **complement system** can be directly activated by certain drugs, physical stimuli, or immune complexes without the involvement of immunoglobulins. - This activation releases **anaphylatoxins (C3a, C4a, C5a)**, which can directly degranulate mast cells and basophils, leading to symptoms mimicking true anaphylaxis.
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