Transplantation Immunology — MCQs
HLA typing is useful in:
Which of the following drugs shows nephrotoxicity during administration?
Which of the following statements regarding rejection of solid organ transplants is true?
Hyperacute rejection occurs within:-
Most strongly associated with rheumatoid arthritis among the following is?
Which antigen is most critical in initiating graft rejection?
What is the most common immunosuppressant regimen used in renal transplant for maintenance?
Cell surface molecules involved in peripheral tolerance induction are
What is the most common type of graft rejection?
Which of the following is a cause of post-transplantation hypertension? I. Rejection II. Cyclosporine nephrotoxicity III. Renal transplant artery stenosis (RTAS) IV. Recurrent disease in the allograft. Select the correct option.
Transplantation Immunology Indian Medical PG Practice Questions and MCQs
Question 1: HLA typing is useful in:
- A. Disputed paternity
- B. Dactylography
- C. Organ transplant (Correct Answer)
- D. Thanatology
Explanation: ***Organ transplant*** - **HLA typing** is crucial for **matching donors and recipients** in organ transplantation to minimize the risk of transplant rejection [1]. - A better **HLA match** between donor and recipient reduces the likelihood of the recipient's immune system attacking the transplanted organ [1]. *Disputed paternity* - While **HLA typing** was historically used, **DNA fingerprinting** (using STR markers) is now the primary and more accurate method for determining paternity [2]. - **DNA analysis** provides a higher probability of inclusion or exclusion and is less complex to interpret than HLA typing for paternity [2]. *Dactylography* - **Dactylography** refers to the study of fingerprints for **identification purposes**, a field entirely unrelated to genetic markers. - It involves analyzing the unique patterns of **ridges and valleys** on fingertips, not genetic typing. *Thanatology* - **Thanatology** is the scientific study of **death and dying**, including the psychological, social, and cultural aspects. - It does not involve genetic testing like **HLA typing** but rather focuses on end-of-life care, grief, and the processes surrounding death.
Question 2: Which of the following drugs shows nephrotoxicity during administration?
- A. Azathioprine
- B. Tacrolimus (Correct Answer)
- C. Mycophenolate mofetil
- D. Leflunomide
Explanation: ***Tacrolimus*** - **Tacrolimus** is a calcineurin inhibitor and a well-known cause of **nephrotoxicity**, which can manifest as acute kidney injury or chronic renal dysfunction [1], [4]. - Its mechanism involves vasoconstriction of afferent arterioles and direct tubular toxicity, leading to reduced glomerular filtration. *Azathioprine* - **Azathioprine** is an immunosuppressant primarily associated with **bone marrow suppression** (leukopenia, thrombocytopenia) and **hepatotoxicity**, not typically nephrotoxicity [2]. - While it can cause renal impairment in rare cases, it is not a primary mechanism of action. *Mycophenolate mofetil* - **Mycophenolate mofetil (MMF)** is an immunosuppressant that primarily causes **gastrointestinal side effects** (diarrhea, nausea) and **myelosuppression**. - It is generally considered **renal-sparing** and is often used in situations where calcineurin inhibitors are contraindicated due to nephrotoxicity. *Leflunomide* - **Leflunomide** is an immunosuppressant used in rheumatoid arthritis, known for causing **hepatotoxicity**, **hypertension**, and **teratogenicity** [3]. - While it can affect various organ systems, direct and significant nephrotoxicity is not a prominent adverse effect.
Question 3: Which of the following statements regarding rejection of solid organ transplants is true?
- A. Most immunosuppressive medications are used to prevent chronic rejection
- B. The major cause of graft failure is acute rejection
- C. Liver transplants are especially susceptible to hyperacute rejection
- D. Hyperacute rejection begins in the operating room with reperfusion of the transplanted organ (Correct Answer)
Explanation: ***Hyperacute rejection begins in the operating room with reperfusion of the transplanted organ*** - **Hyperacute rejection** is a rapidly-occurring immune response that starts almost immediately after the transplanted organ is re-vascularized, often while the patient is still in the operating room [1]. - This type of rejection is mediated by **pre-formed antibodies** (e.g., ABO blood group antibodies or anti-HLA antibodies) in the recipient's circulation that bind to antigens on the donor organ's endothelium, leading to massive thrombosis and organ destruction [1]. *Most immunosuppressive medications are used to prevent chronic rejection* - While immunosuppressants play a role in mitigating **chronic rejection**, their primary and most effective targets are **acute rejection episodes** and the initial prevention of organ rejection [2]. - **Chronic rejection** is often a more complex process involving both immune and non-immune factors, and current immunosuppressive regimens are less effective at completely preventing or reversing it compared to acute rejection. *The major cause of graft failure is acute rejection* - In the long term, **chronic rejection** (or chronic allograft dysfunction) is the leading cause of late graft loss, rather than acute rejection. - With advancements in immunosuppression, **acute rejection rates** have significantly decreased, making chronic issues and non-immune factors more prominent in overall graft failure. *Liver transplants are especially susceptible to hyperacute rejection* - **Liver transplants** are notably more tolerant to ABO and HLA mismatches compared to other solid organ transplants (like kidney or heart). - This relative immunotolerance means that **hyperacute rejection** is far less common in liver transplantation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242. [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. 180-181.
Question 4: Hyperacute rejection occurs within:-
- A. 12 hours
- B. 24 hours
- C. 6 hours
- D. Minutes to hours (Correct Answer)
Explanation: ***Minutes to hours*** - **Hyperacute rejection** is a rapidly occurring complication post-transplant, characterized by its onset within minutes to hours after **organ reperfusion** [1]. - This type of rejection is mediated by pre-formed **recipient antibodies** that recognize donor antigens, leading to immediate graft damage [1]. *12 hours* - While plausible, 12 hours is a bit too broad as **hyperacute rejection** primarily begins much sooner, typically within the first few hours [1]. - This timeframe might overlap with the initial stages of **acute cellular rejection**, which typically occurs days to weeks later [1]. *24 hours* - **Hyperacute rejection** is almost always observed and causes graft failure well before the 24-hour mark, if it is going to happen. - Rejection occurring within this extended period is more indicative of **accelerated acute rejection** rather than true hyperacute rejection. *6 hours* - While hyperacute rejection certainly can occur within 6 hours, "minutes to hours" better captures the immediate onset, often within seconds or minutes [1]. - Some cases of **hyperacute rejection** can be so rapid that the 6-hour mark would be considered a late presentation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242.
Question 5: Most strongly associated with rheumatoid arthritis among the following is?
- A. HLA B27
- B. HLA DR4 (Correct Answer)
- C. HLA DQ1
- D. HLA DR8
Explanation: ***HLA DR4*** - **HLA-DR4** is the **MHC Class II allele** most strongly associated with an increased risk and severity of **rheumatoid arthritis (RA)**. - It is thought to contribute to RA pathogenesis by presenting specific peptides that activate **auto-reactive T cells**, initiating the autoimmune response. *HLA B27* - **HLA-B27** is primarily associated with **seronegative spondyloarthropathies**, such as **ankylosing spondylitis** and **reactive arthritis**. - It has no significant association with **rheumatoid arthritis**. *HLA DQ1* - While a variety of **HLA-DQ alleles** are involved in autoimmune diseases, **HLA-DQ1** is not among the primary genetic associations for **rheumatoid arthritis**. - Its pathogenic role is more commonly studied in other conditions, such as **coeliac disease**, though various subtypes exist. *HLA DR8* - **HLA-DR8** has some associations with certain autoimmune conditions, such as **primary biliary cholangitis** and **Crohn's disease**. - It is not considered a primary or strong genetic risk factor for **rheumatoid arthritis**.
Question 6: Which antigen is most critical in initiating graft rejection?
- A. DHA
- B. Polysaccharide
- C. HLA - Antigen (Correct Answer)
- D. MHC - molecule
Explanation: ***MHC - molecule*** - The **Major Histocompatibility Complex (MHC)** molecules are critical in presenting **antigens** to T-cells, which initiates the graft rejection process [1]. - MHC molecules play a central role in the **immune response** by determining the compatibility of tissue transplanted between individuals [1]. *HLA - Antigen* - HLA is a part of the **MHC** and represents a group of genes, but it is not the most crucial factor for initiating graft rejection on its own. - HLA typing is significant for compatibility [2], but the overall process of rejection is driven by **MHC** interactions with T-cells [1]. *DHA* - **DHA** does not relate to graft rejection as it is an **omega-3 fatty acid** rather than an immune antigen. - It has no direct involvement in **immune response** or tissue compatibility processes. *Polysaccharide* - Polysaccharides are primarily components of **cell walls** in bacteria and fungi, and are not involved in the rejection of grafts. - They do not activate **T-cells** or engage in the typical mechanisms of **graft rejection** mediated by MHC. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-241. [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. 179-180.
Question 7: What is the most common immunosuppressant regimen used in renal transplant for maintenance?
- A. Calcineurin inhibitors + Purine antagonists + Basliximab
- B. Glucocorticoids + Cyclophosphamide
- C. Cyclophosphamide + Purine antagonists + Glucocorticoids
- D. Calcineurin inhibitors + Purine antagonists + Glucocorticoids (Correct Answer)
Explanation: ***Calcineurin inhibitors + Purine antagonists + Glucocorticoids*** - This triple therapy regimen is the **most common and effective** approach for long-term maintenance immunosuppression in renal transplant recipients [1]. - **Calcineurin inhibitors** (e.g., tacrolimus, cyclosporine) are the cornerstone for preventing T-cell activation, **purine antagonists** (e.g., mycophenolate mofetil, azathioprine) inhibit lymphocyte proliferation, and **glucocorticoids** provide broad anti-inflammatory effects [1]. *Calcineurin inhibitors + Purine antagonists + Basliximab* - **Basiliximab** is typically used for **induction therapy** (immediately post-transplant) to prevent acute rejection by blocking the IL-2 receptor, not as a long-term maintenance component. - The standard maintenance regimen *replaces* induction agents like basiliximab with a long-term steroid or calcineurin inhibitor alongside a purine antagonist. *Glucocorticoids + Cyclophosphamide* - **Cyclophosphamide** is a potent alkylating agent primarily used in specific autoimmune diseases or certain cancers, and its use in transplant is generally limited to cases of organ rejection resistant to standard therapy due to its significant toxicity. - This combination is **not a standard maintenance regimen** for renal transplant due to the high toxicity and side effects of cyclophosphamide. *Cyclophosphamide + Purine antagonists + Glucocorticoids* - As mentioned, **cyclophosphamide** is not a first-line agent for maintenance immunosuppression in renal transplant due to its severe side effect profile, including myelosuppression and hemorrhagic cystitis. - While purine antagonists and glucocorticoids are components of maintenance therapy, the inclusion of cyclophosphamide makes this an **uncommon and usually unfavorable regimen** for long-term use.
Question 8: 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 9: What is the most common type of graft rejection?
- A. Hyperacute
- B. Acute (Correct Answer)
- C. Chronic
- D. Acute on chronic
Explanation: ***Acute*** - **Acute rejection** is the most common type of graft rejection, occurring in **10-40% of transplant recipients**. [1] - It typically occurs **days to weeks to months** after transplantation (most commonly within the first 6 months). [1] - Mediated primarily by **T-lymphocytes** (cellular rejection) or **antibodies** (antibody-mediated rejection) reacting against donor antigens. [1] - Usually **responsive to immunosuppressive therapy** when detected early. *Hyperacute* - **Hyperacute rejection** is rare (occurs in <1% of cases) due to routine **pre-transplant cross-matching**. - Occurs within **minutes to hours** after transplantation due to **pre-existing circulating antibodies** against donor antigens. [1] - Results in immediate thrombosis and graft necrosis, requiring **immediate graft removal**. [1] *Chronic* - **Chronic rejection** (chronic allograft dysfunction) develops **months to years** after transplantation. - It is the **most common cause of late graft failure**, but not the most common type of rejection episode. - Characterized by **gradual, progressive loss of graft function** with vascular and fibrotic changes. - **Largely irreversible** and poorly responsive to treatment. *Acute on chronic* - This is **not a primary category** of graft rejection but represents an **acute rejection episode superimposed** on a graft already undergoing chronic changes. - Reflects exacerbation in a chronically rejecting graft. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-242.
Question 10: Which of the following is a cause of post-transplantation hypertension? I. Rejection II. Cyclosporine nephrotoxicity III. Renal transplant artery stenosis (RTAS) IV. Recurrent disease in the allograft. Select the correct option.
- A. None of the above are correct causes.
- B. I, II, and IV are correct causes.
- C. I and III are correct causes.
- D. All of the options are correct causes of post-transplantation hypertension. (Correct Answer)
Explanation: ***All of the options are correct causes of post-transplantation hypertension.*** - Post-transplantation hypertension often has a multifactorial etiology, with **rejection**, **cyclosporine nephrotoxicity**, **renal transplant artery stenosis (RTAS)**, and **recurrent disease in the allograft** all being significant contributors. - Each of these conditions can lead to mechanisms that elevate blood pressure, such as **renal ischemia**, activation of the **renin-angiotensin system**, and inflammatory responses affecting renal function. *I, II, and IV are correct causes.* - This option is incorrect because it excludes **renal transplant artery stenosis (RTAS)** (III), which is a well-established cause of secondary hypertension in transplant recipients due to reduced blood flow to the allograft. - **RTAS** activates the renin-angiotensin-aldosterone system (RAAS), leading to **vasoconstriction** and **sodium retention**, contributing to hypertension. *I and III are correct causes.* - This option is incorrect as it omits other crucial causes like **cyclosporine nephrotoxicity** (II) and **recurrent disease in the allograft** (IV), both of which are documented contributors to post-transplantation hypertension. - **Cyclosporine nephrotoxicity** causes afferent arteriolar vasoconstriction and glomerulosclerosis, directly increasing blood pressure. *None of the above are correct causes.* - This option is incorrect because **rejection**, **cyclosporine nephrotoxicity**, **renal transplant artery stenosis (RTAS)**, and **recurrent disease in the allograft** are all recognized and significant causes of post-transplantation hypertension. - Each condition has distinct pathological mechanisms that contribute to **elevated blood pressure** in transplant recipients.
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