Development of Immune System — MCQs
In ABO blood grouping, which is False?
Common site of haematopoiesis in the fetus is -
Which of the following is not a component of innate immunity?
In utero infection leads to which immunoglobulin?
A 6-month-old male infant presents with recurrent severe bacterial infections with encapsulated organisms (Streptococcus pneumoniae and Haemophilus influenzae). Laboratory findings reveal profound deficiency of all immunoglobulin classes (IgG, IgA, IgM) with absent mature B cells in peripheral blood. The most likely diagnosis is:
A 5-year-old male child presents to the clinic with a history of recurrent infections. On examination, he was found to have rashes. On routine blood investigation, a low platelet count was found. What will be the diagnosis?
Which condition is characterized by wire loop lesions in the glomeruli?
Which antibody is not transmitted from mother to baby?
At what age does clinically significant IgG production begin?
Which of the following statements about Wiskott-Aldrich syndrome is false?
Development of Immune System Indian Medical PG Practice Questions and MCQs
Question 1: In ABO blood grouping, which is False?
- A. IgM is most common antibody in ABO
- B. ABO are carbohydrate Ag
- C. ABO antibodies are natural and present since birth (Correct Answer)
- D. Ab are present only if Ag is absent
Explanation: ***ABO antibodies are natural and present since birth*** - **ABO antibodies** are naturally occurring, but they are typically **not present at birth** [1]. - They develop within the **first 3 to 6 months of life** as a response to exposure to similar antigens in the environment (e.g., bacteria). *IgM is most common antibody in ABO* - The primary **ABO antibodies** (anti-A, anti-B) are indeed predominantly **IgM antibodies** [1]. - IgM antibodies are large pentameric structures, and their size prevents them from crossing the placenta [2]. *ABO are carbohydrate Ag* - The **ABO blood group antigens** (A, B, H) are **carbohydrate structures** (glycans) found on the surface of red blood cells and other tissues. - These carbohydrate chains are attached to proteins or lipids. *Ab are present only if Ag is absent* - This statement is a fundamental principle of ABO blood grouping: individuals naturally produce antibodies against the **ABO antigens** they **lack** [1]. - For example, a person with **Type A blood** (A antigen present) will have **anti-B antibodies** (B antigen absent). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 469-470.
Question 2: Common site of haematopoiesis in the fetus is -
- A. Liver (Correct Answer)
- B. Spleen
- C. Bone marrow
- D. Gut
Explanation: ***Liver*** - The **liver** is the **primary and most common site of hematopoiesis** during the fetal period, taking over from the yolk sac around the **second month of gestation**. - It remains the **dominant hematopoietic organ from the second to the seventh month of gestation**, making it the longest-serving primary site during fetal development. - This is why the liver is the correct answer to this question about the "common site" of fetal hematopoiesis. *Spleen* - The spleen contributes to hematopoiesis during the fetal period but is **not the primary or most common site**. - Its role is **secondary to the liver** and diminishes significantly as bone marrow becomes more active. *Bone marrow* - While it eventually becomes the **primary site of hematopoiesis in adults**, the bone marrow's role in fetal hematopoiesis becomes prominent **only in the late second and third trimesters** (after 5 months). - It gradually overtakes the liver as the main hematopoietic organ near term and postnatally. *Gut* - The **gut** is **not a site of hematopoiesis** at any stage of development. - Its primary function is digestion and absorption. **Note:** The yolk sac is the earliest site of hematopoiesis (0-2 months), but the liver serves as the primary site for the longest duration during fetal life.
Question 3: Which of the following is not a component of innate immunity?
- A. Epithelial barriers
- B. NK cells
- C. Dendritic cells
- D. Helper T lymphocytes (Correct Answer)
Explanation: ***Helper T lymphocyte*** - Helper T lymphocytes are a crucial part of **adaptive immunity** [4], facilitating responses against pathogens. - They specifically activate B cells and cytotoxic T cells [2], unlike components of innate immunity, which respond nonspecifically. *NK cells* - Natural Killer (NK) cells are integral to **innate immunity** [1], targeting infected or tumor cells without prior sensitization. - They play a role in the initial response to viral infections and can produce **cytokines** [2]. *Epithelial barriers* - Epithelial barriers act as the first line of defense in **innate immunity** [1], preventing pathogen entry. - They include physical and chemical barriers like skin and mucous membranes [3]. *Dendritic cells* - Dendritic cells are key antigen-presenting cells involved in **innate immunity** [1] and link to adaptive immunity. - They capture and present antigens [2], activating T cells to mount an immune response. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 194-196. [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] 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. 152-153. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 196-198.
Question 4: In utero infection leads to which immunoglobulin?
- A. IgG
- B. IgA
- C. IgM (Correct Answer)
- D. IgD
Explanation: ***IgM*** - **IgM** is the first antibody produced by the fetus in response to an in utero infection, as it cannot cross the placenta. - Its presence in a newborn's blood indicates an **active fetal immune response** to an infection acquired before birth. *IgG* - **IgG** antibodies from the mother cross the placenta and provide passive immunity to the fetus, but their presence does not necessarily indicate an active fetal infection. - High IgG levels in a neonate are typically maternal and do not reflect the infant's own immune response to an in utero infection. *IgA* - **IgA** is primarily found in mucosal secretions and is not typically produced by the fetus in significant amounts in response to in utero infection. - Its presence in a neonate's blood might suggest contamination or specific unusual circumstances, rather than routine in utero infection. *IgD* - The function of **IgD** is not fully understood, but it is primarily found on the surface of B lymphocytes and is not a major effector antibody in the primary immune response to infection. - It does not play a significant role in diagnosing in utero infections.
Question 5: A 6-month-old male infant presents with recurrent severe bacterial infections with encapsulated organisms (Streptococcus pneumoniae and Haemophilus influenzae). Laboratory findings reveal profound deficiency of all immunoglobulin classes (IgG, IgA, IgM) with absent mature B cells in peripheral blood. The most likely diagnosis is:
- A. X-linked agammaglobulinemia of Bruton (Correct Answer)
- B. DiGeorge's syndrome
- C. Isolated IgA deficiency
- D. Chronic granulomatous disease
Explanation: ***X-linked agammaglobulinemia of Bruton*** - Characterized by a **severe deficiency of immunoglobulins**, leading to frequent bacterial infections in infants [1][2]. - The absence of mature B cells in the peripheral blood is a hallmark [1], along with a positive family history due to its **X-linked recessive inheritance** [2]. *Chronic granulomatous disease* - Presents with recurrent **bacterial and fungal infections** due to a defect in **immune response**, but not primarily characterized by low immunoglobulin levels. - Typically involves **catalase-positive organisms**, which differs from the broad antibody deficiency seen in the correct diagnosis. *Isolated IgA deficiency* - Commonly manifests with **sinus and respiratory infections**, but patients often have normal **IgG and IgM levels**. - It does not usually cause severe or recurrent infections in infants, differentiating it from the severe immunodeficiency seen in X-linked agammaglobulinemia. *DiGeorge's syndrome* - Associated with **congenital heart defects** and **thyroid issues**, along with T-cell deficiency, but typically presents with **low T-cell counts rather than low B cells or immunoglobulins**. - The immunological profile is distinct from that of X-linked agammaglobulinemia, where B cells are severely affected [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 248-249. [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. 165-166.
Question 6: A 5-year-old male child presents to the clinic with a history of recurrent infections. On examination, he was found to have rashes. On routine blood investigation, a low platelet count was found. What will be the diagnosis?
- A. Wiskott-Aldrich syndrome (Correct Answer)
- B. Hyper-IgE syndrome
- C. Chediak-Higashi syndrome
- D. None of the options
Explanation: ***Wiskott-Aldrich syndrome*** - This syndrome is characterized by the classic triad of **recurrent infections** (due to immunodeficiency), **eczema-like rashes**, and **thrombocytopenia** (low platelet count), which perfectly matches the clinical presentation. - The underlying defect involves the WAS protein, crucial for **hematopoietic cell function**, leading to severe combined immunodeficiency. *Hyper-IgE syndrome* - While it features **recurrent infections** and **eczema**, it is primarily associated with **elevated IgE levels** and typically presents with a hallmark finding of **"cold" abscesses**. - **Low platelet count** is not a defining characteristic of Hyper-IgE syndrome. *Chediak-Higashi syndrome* - This syndrome involves **recurrent infections** and findings like **partial oculocutaneous albinism** and neurologic abnormalities. - While it can manifest with bleeding tendencies due to **platelet dysfunction**, the defining features of **eczema** and a consistently **low platelet count** as seen here are less prominent compared to Wiskott-Aldrich. *None of the options* - The presenting symptoms of **recurrent infections, rashes, and low platelet count** are highly specific for Wiskott-Aldrich syndrome, making this option incorrect.
Question 7: Which condition is characterized by wire loop lesions in the glomeruli?
- A. IgA nephropathy
- B. Systemic Lupus Erythematosus (SLE) (Correct Answer)
- C. Amyloidosis
- D. Membranous nephropathy
Explanation: ***SLE*** - Wire loop lesions in glomeruli are a classic histological finding in **Systemic Lupus Erythematosus (SLE)**, indicating severe glomerulonephritis. - These lesions result from **subendothelial immune complex deposits**, leading to a distinctive appearance on renal biopsy [1]. *Amyloidosis* - Characterized by **polarized light appearance** of apple-green birefringence due to amyloid deposits, not wire loop lesions. - Renal involvement occurs with **nodular glomerulosclerosis**, shown by different histological patterns. *Nephrotic* - Refers to a syndrome characterized by **heavy proteinuria**, **hypoalbuminemia**, and **edema**, but not specifically wire loop lesions. - The histopathology typically reveals **minimal change disease** or **focal segmental glomerulosclerosis**, not wire loops. *IgA nephropathy* - Generally presents with **IgA deposits** in mesangial regions causing **hematuria** and mild proteinuria. - It does not exhibit wire loop lesions, which are characteristic of **lupus nephritis** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 232.
Question 8: Which antibody is not transmitted from mother to baby?
- A. Tetanus IgG antibodies
- B. IgA antibodies (Correct Answer)
- C. Diphtheria IgG antibodies
- D. Measles IgG antibodies
Explanation: ***IgA antibodies*** - While IgA is found in breast milk and provides **passive immunity** to the infant's gastrointestinal tract, it is **not transferred across the placenta** to the fetus. - This antibody has a larger molecular structure and is primarily involved in **mucosal immunity**, making it unsuitable for transplacental transfer. *Diphtheria IgG antibodies* - **IgG antibodies**, including those for diphtheria, are actively transported across the **placenta** from mother to fetus during the third trimester. - This transfer provides the newborn with **passive immunity** against diphtheria during the first few months of life. *Tetanus IgG antibodies* - Similar to diphtheria IgG, **tetanus IgG antibodies** are efficiently transported across the **placenta** from mother to baby. - This offers crucial **passive protection** against tetanus, particularly important after birth. *Measles IgG antibodies* - **Measles IgG antibodies** from a vaccinated or previously infected mother cross the **placenta** to the fetus. - This maternal transfer provides temporary **passive immunity** to the newborn against measles.
Question 9: At what age does clinically significant IgG production begin?
- A. Around 6 months (Correct Answer)
- B. Around 1 year
- C. Around 2 years
- D. Around 3 years
Explanation: ***Around 6 months*** - Maternal IgG levels, which provide **passive immunity**, decrease significantly by 3-6 months of age. - Infants begin to produce their own **clinically significant** levels of IgG around this time, coinciding with the "physiologic nadir" of IgG. *Around 1 year* - While IgG production continues to mature, significant production has already begun by 6 months to replace declining maternal antibodies. - By 1 year, the immune system is more robust, but the initial critical transition occurs earlier. *Around 2 years* - By this age, children generally have a robust adaptive immune response, and the period of vulnerability due to low IgG has passed. - This option is too late for the beginning of clinically significant IgG production. *Around 3 years* - This age is far past the point where children start producing their own significant levels of IgG. - The immune system is well-developed by 3 years, and initial IgG production started much earlier.
Question 10: Which of the following statements about Wiskott-Aldrich syndrome is false?
- A. Autosomal Recessive disorder (Correct Answer)
- B. Impaired platelet aggregation in response to agonist
- C. Thrombocytopenia
- D. Eczematous Rash
Explanation: ***Autosomal Recessive disorder*** - **Wiskott-Aldrich Syndrome (WAS)** is an **X-linked recessive disorder**, not autosomal recessive. This statement is therefore false, making it the correct answer to the question. - It is caused by mutations in the WAS gene, which encodes the Wiskott-Aldrich syndrome protein (WASp) and is located on the X chromosome. *Eczematous Rash* - Patients with Wiskott-Aldrich syndrome frequently present with severe and persistent **eczematous rash**, which is a key component of the clinical triad. - This rash is often recalcitrant to standard treatments and can be widespread. *Impaired platelet aggregation in response to agonist* - Patients with WAS exhibit **abnormal platelet function**, specifically **impaired aggregation** in response to various agonists. - This functional defect contributes to the bleeding diathesis seen in the syndrome, alongside reduced platelet count. *Thrombocytopenia* - **Thrombocytopenia**, characterized by a low platelet count, is a hallmark feature of Wiskott-Aldrich syndrome. - The platelets are also typically very small in size (**microthrombocytopenia**), which is a distinctive finding.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free