Immunology Practice Questions

Q: ABO antibodies are primarily which immunoglobulin class?

IgM. **Explanation:** The correct answer is **IgM**. ABO blood group antibodies (Anti-A and Anti-B) are considered **"natural antibodies"** because they are produced without prior exposure to foreign red blood cells, likely as a cross-reaction to environmental antigens (gut flora). These antibodies are primarily of the **IgM class**. Due to their pentameric structure, they are highly efficient at fixing complement and causing intravascular hemolysis, which is why ABO incompatibility leads to severe immediate transfusion reactions. **Analysis of Options:** * **IgG (Option A):** While ABO antibodies are primarily IgM, **Rh antibodies** (Anti-D) are primarily IgG. Additionally, in individuals with **Type O blood**, the anti-A and anti-B antibodies can sometimes be of the IgG class, which is clinically significant as IgG can cross the placenta. * **IgA (Option B):** IgA is the primary immunoglobulin found in secretions (mucosal immunity). While trace amounts may be found in serum, it is not the primary class for ABO antibodies. * **IgD (Option D):** IgD functions mainly as an antigen receptor on the surface of B-cells; it does not circulate in significant quantities as a functional antibody in the ABO system. **High-Yield Clinical Pearls for NEET-PG:** * **Cold vs. Warm:** IgM antibodies (like ABO) are "Cold Agglutinins" (react best at 4°C), whereas IgG antibodies (like Rh) are "Warm Agglutinins" (react best at 37°C). * **Placental Transfer:** Only IgG crosses the placenta. This is why ABO incompatibility rarely causes severe Hemolytic Disease of the Newborn (HDN) in Type A or B mothers (who have IgM), but can occur in Type O mothers (who may have IgG anti-A/B). * **Size Matters:** IgM is a large pentamer and cannot cross the placental barrier, whereas IgG is a small monomer.

Q: Which immunoglobulin is predominantly found in Peyer's patches?

IgA. **Explanation:** **Correct Option: C (IgA)** Peyer’s patches are organized lymphoid tissues located in the lamina propria of the small intestine (ileum). They serve as the primary induction sites for the **Mucosal Immune System**. The predominant immunoglobulin produced here is **Secretory IgA (sIgA)**. B-cells in the Peyer’s patches undergo class-switching specifically to IgA in response to local cytokines (like TGF-β). This IgA is then transported across the intestinal epithelium to neutralize pathogens and toxins before they can penetrate the mucosal barrier. **Incorrect Options:** * **IgM (Option A):** While IgM is the first antibody produced during a primary immune response and is found on the surface of naive B-cells, it is not the dominant isotype associated with specialized mucosal lymphoid tissue like Peyer's patches. * **IgG (Option B):** IgG is the most abundant antibody in the **systemic circulation** (serum) and provides long-term immunity, but it is not the primary defender of the gut mucosa. * **IgD (Option D):** IgD is primarily found on the surface of mature B-lymphocytes as an antigen receptor; its secreted form has no significant role in mucosal immunity. **High-Yield NEET-PG Pearls:** * **M-Cells (Microfold cells):** These are specialized cells overlying Peyer’s patches that sample antigens from the intestinal lumen via transcytosis. * **J-Chain:** Secretory IgA is a **dimer** held together by a J-chain; this structure allows it to resist proteolysis by digestive enzymes. * **Selective IgA Deficiency:** The most common primary immunodeficiency; patients often present with recurrent sinopulmonary and gastrointestinal infections.

Q: All of the following statements are true regarding Bare lymphocyte syndrome, except?

MHC overexpression. **Bare Lymphocyte Syndrome (BLS)** is a rare form of Severe Combined Immunodeficiency (SCID) characterized by the failure of lymphocytes to express Major Histocompatibility Complex (MHC) molecules on their surface. ### Explanation of Options: * **MHC Overexpression (Correct Answer):** This statement is false. BLS is defined by the **absence or severe reduction** of MHC molecules. Without these molecules, T-cells cannot "see" antigens, leading to a profound failure of the adaptive immune system. * **Autosomal Recessive Inheritance:** Most forms of BLS (both Type I and Type II) follow an autosomal recessive pattern. * **Defect in $\beta_2$-Microglobulin:** This is a classic cause of **BLS Type I (MHC Class I deficiency)**. Mutations in the TAP1, TAP2, or TAPBP genes prevent the transport of peptides into the endoplasmic reticulum, or mutations in $\beta_2$-microglobulin prevent the stable assembly of the MHC Class I molecule. * **MHC Non-expression:** This is the hallmark of the disease. In **BLS Type II (MHC Class II deficiency)**, there is a defect in the transcription factors (like CIITA or RFX) required to turn on MHC II genes, leading to a lack of MHC II expression on Antigen Presenting Cells (APCs). ### High-Yield Clinical Pearls for NEET-PG: * **Type I BLS:** Deficiency of **MHC Class I**. Presents with recurrent bacterial respiratory infections and chronic lung disease. * **Type II BLS:** Deficiency of **MHC Class II**. More common and more severe. It leads to a lack of CD4+ T-cell activation, mimicking SCID. * **Diagnostic Clue:** Normal numbers of B and T cells, but they are non-functional due to the lack of "antigen presentation" machinery. * **Treatment:** Hematopoietic stem cell transplantation (HSCT) is the definitive treatment.

Q: Which immunoglobulin has the longest half-life?

IgG. **Explanation:** The correct answer is **IgG**. **Why IgG is correct:** IgG is the most abundant immunoglobulin in the serum (constituting about 75-80% of the total pool) and possesses the longest half-life, averaging **23 days**. This longevity is attributed to its interaction with the **neonatal Fc receptor (FcRn)**. Unlike other antibodies, IgG is salvaged from degradation within endothelial cells and monocytes by FcRn, which recycles it back into the circulation. This mechanism is also responsible for the passive transfer of IgG across the placenta, providing immunity to the newborn. **Why the other options are incorrect:** * **IgA:** Has a half-life of approximately **6–8 days**. It is the primary antibody in secretions (mucosal immunity) but does not benefit from the FcRn recycling mechanism. * **IgM:** Has a half-life of approximately **5 days**. It is the first antibody produced in a primary immune response and exists mainly as a large pentamer, which is cleared more rapidly from the circulation. * **IgE:** Has the shortest half-life, approximately **2–3 days** in the serum, as it binds rapidly and with high affinity to mast cells and basophils. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Serum Concentration:** **GAMDE** (IgG > IgA > IgM > IgD > IgE). * **Placental Transfer:** IgG is the **only** immunoglobulin that crosses the placenta (IgG1, G3, and G4 specifically). * **Complement Activation:** IgM is the most efficient activator of the classical complement pathway, followed by IgG. * **Heat Lability:** IgE is unique for being heat-labile (inactivated at 56°C for 30 minutes).

Q: What is the most common primary immunodeficiency?

Isolated IgA immunodeficiency. **Explanation:** **Isolated (Selective) IgA Deficiency** is the most common primary immunodeficiency disorder worldwide, with an estimated prevalence of approximately 1 in 600 individuals in Western populations. It is characterized by serum IgA levels less than 7 mg/dL with normal levels of IgG and IgM. The underlying pathology involves a failure of B-cells to differentiate into IgA-secreting plasma cells. **Analysis of Options:** * **Option A: Common Variable Immunodeficiency (CVID):** While it is the most common *clinically significant* (symptomatic) antibody deficiency, its overall prevalence is much lower than IgA deficiency. * **Option C: Wiskott-Aldrich Syndrome:** This is a rare X-linked recessive disorder characterized by the triad of eczema, thrombocytopenia, and recurrent infections. * **Option D: AIDS:** This is a **secondary** (acquired) immunodeficiency caused by HIV. The question specifically asks for a **primary** (genetic/congenital) immunodeficiency. **High-Yield Clinical Pearls for NEET-PG:** 1. **Asymptomatic Nature:** Most patients are asymptomatic, but those who are symptomatic present with recurrent sinopulmonary infections and diarrhea (Giardiasis). 2. **Blood Transfusion Risk:** A critical complication is **Anaphylaxis during blood transfusion**. This occurs because patients develop anti-IgA antibodies; therefore, they must receive washed RBCs or IgA-deficient blood products. 3. **Associations:** Strongly associated with autoimmune diseases (SLE, Rheumatoid Arthritis) and Celiac disease (false-negative IgA anti-transglutaminase tests are common). 4. **False Positive:** Can cause a false positive pregnancy test in some assays due to heterophile antibodies.

Q: Major histocompatibility complex class 1 is expressed on which of the following cell types?

Macrophages only. **Explanation:** The expression of **Major Histocompatibility Complex (MHC) Class I** molecules is a fundamental concept in immunology and neuroanatomy. Under normal physiological conditions, MHC Class I is expressed on **all nucleated cells** [1] in the body to present endogenous antigens to CD8+ T-cells [3]. However, the **Central Nervous System (CNS)** is an "immunologically privileged" site. In the healthy brain, MHC Class I expression is remarkably low or absent on neurons and glial cells to prevent autoimmune-mediated damage. Among the options provided, **Macrophages** (and their CNS counterparts, **Microglia** [2]) are the primary cells that constitutively express MHC Class I (and Class II) as they function as professional antigen-presenting cells (APCs) [4]. **Analysis of Options:** * **A. Macrophages only (Correct):** In the context of this specific question's constraints, macrophages/microglia [2] are the dominant cells in the neural environment expressing these markers for immune surveillance [4]. * **B. All nucleated cells:** While true for the general body [1], this is often restricted in the CNS to avoid neuroinflammation. * **C. B cells only:** B cells express MHC I, but they are not the *only* cells to do so. * **D. All blood cells except erythrocytes:** This is incorrect because platelets (which are non-nucleated) also express MHC Class I. **High-Yield NEET-PG Pearls:** * **MHC Class I:** Presents to **CD8+** T-cells (Rule of 8: 1 x 8 = 8) [1]. * **MHC Class II:** Expressed only on **Professional APCs** (Macrophages, B-cells, Dendritic cells) and presents to **CD4+** T-cells (Rule of 8: 2 x 4 = 8) [4]. * **RBCs:** Lack MHC Class I because they are non-nucleated; this is why they cannot be infected by viruses that require MHC I for presentation. * **Microglia:** The "macrophages of the brain," derived from the yolk sac (mesoderm), unlike other glial cells which are ectodermal [2].

Q: All of the following statements regarding hypersensitivity reactions are true, except:

The Schick test is an example of delayed hypersensitivity.. ### Explanation The correct answer is **C**. The **Schick test** is not an example of delayed hypersensitivity; rather, it is a **neutralization test** used to determine susceptibility to *Corynebacterium diphtheriae*. In this test, diphtheria toxin is injected intradermally. If the person lacks antibodies (non-immune), the toxin causes local inflammation (positive result). If antibodies are present, they neutralize the toxin, and no reaction occurs. **Analysis of other options:** * **Option A (Erythema Nodosum Leprosum):** This is a classic example of **Type III hypersensitivity** (Arthus-type). It occurs due to the deposition of immune complexes (antigen-antibody) in tissues, typically during the treatment of lepromatous leprosy. * **Option B (Post-streptococcal Glomerulonephritis):** This is a **Type III hypersensitivity** reaction where circulating immune complexes (formed against Group A Streptococcus) deposit in the glomerular basement membrane, leading to inflammation. * **Option D (Mismatched Blood Transfusion):** This is a **Type II hypersensitivity** (Cytotoxic) reaction. Pre-formed antibodies (IgM/IgG) bind to antigens on the transfused RBCs, leading to complement activation and cell lysis. **High-Yield Clinical Pearls for NEET-PG:** * **Type IV (Delayed) Hypersensitivity Examples:** Mantoux test (Tuberculin), Lepromin test, Mitsuda reaction, Contact dermatitis, and Graft rejection. * **Type III Examples:** SLE, Rheumatoid Arthritis, Serum Sickness, and Farmer’s Lung. * **Type II Examples:** Myasthenia gravis, Graves' disease, Goodpasture syndrome, and Rheumatic fever. * **Mnemonic for Hypersensitivity (Gell & Coombs):** **ACID** (**A**naphylactic - I, **C**ytotoxic - II, **I**mmune Complex - III, **D**elayed - IV).

Q: Which type of cell secretes Interferon-alpha (IFN-α)?

Leukocytes. **Explanation:** Interferons (IFNs) are a group of signaling proteins (cytokines) released by host cells in response to viral infections. They are classified into three types based on their receptor specificity and cellular origin. **1. Why Leukocytes is correct:** **Interferon-alpha (IFN-α)**, also known as **Leukocyte Interferon**, is primarily produced by mononuclear phagocytes (monocytes, macrophages) and B-lymphocytes. These cells secrete IFN-α in response to viral stimulation or exposure to double-stranded RNA. Its primary function is to induce an antiviral state in neighboring cells by inhibiting viral protein synthesis. **2. Why the other options are incorrect:** * **Fibroblasts (Option B):** These cells primarily produce **Interferon-beta (IFN-β)**. Together, IFN-α and IFN-β are classified as **Type I Interferons**. * **T helper cells and Cytotoxic T cells (Options C & D):** These are the primary sources of **Interferon-gamma (IFN-γ)**, also known as **Immune Interferon** or **Type II Interferon**. IFN-γ is secreted by activated T-cells and Natural Killer (NK) cells to enhance the microbicidal activity of macrophages and promote Th1 differentiation. **High-Yield Clinical Pearls for NEET-PG:** * **Type I IFNs (α, β):** Acid-stable; primary role is **antiviral** defense. * **Type II IFN (γ):** Acid-labile; primary role is **immunomodulation** (activates macrophages and increases MHC expression). * **Clinical Use:** Recombinant IFN-α is used therapeutically in Chronic Hepatitis B, Hepatitis C, Hairy Cell Leukemia, and Kaposi Sarcoma. * **Mechanism:** IFNs do not kill viruses directly; they induce the production of **ribonuclease L** (degrades viral mRNA) and **protein kinase R** (inhibits protein synthesis).

Q: The Tuberculin test is an example of which type of immune reaction?

Cell mediated. The Tuberculin (Mantoux) test is a classic example of a **Type IV Hypersensitivity reaction**, also known as **Delayed-Type Hypersensitivity (DTH)**. ### Why "Cell mediated" is correct: Unlike other hypersensitivity types, Type IV reactions do not involve antibodies. Instead, they are mediated by **T-lymphocytes** (specifically Th1 cells). When Purified Protein Derivative (PPD) is injected intradermally, sensitized T-cells recognize the antigen, release cytokines (like IFN-γ), and recruit macrophages. This process takes **48–72 hours** to manifest as induration, hence the term "delayed." ### Why other options are incorrect: * **Option A (Anaphylaxis mediated):** This refers to **Type I Hypersensitivity**, which is IgE-mediated and occurs within minutes (e.g., asthma, urticaria). * **Option C (Antibody mediated):** This refers to **Type II Hypersensitivity**, where IgG or IgM antibodies bind to antigens on cell surfaces, leading to complement activation or ADCC (e.g., Rh incompatibility). * **Option D (Immune complex mediated):** This refers to **Type III Hypersensitivity**, involving the deposition of antigen-antibody complexes in tissues (e.g., SLE, Arthus reaction). ### High-Yield Clinical Pearls for NEET-PG: * **Reading the test:** Measure the **induration** (palpable hardness), not the erythema (redness), at 48–72 hours. * **False Negative:** Can occur in miliary TB, malnutrition, sarcoidosis, or immunosuppression (e.g., HIV/AIDS) due to **anergy**. * **False Positive:** Often seen in individuals previously vaccinated with **BCG** or infected with atypical mycobacteria. * **Other Type IV examples:** Lepromin test, Contact dermatitis (nickel/poison ivy), and Graft rejection.

Question 1

ABO antibodies are primarily which immunoglobulin class?

Accepted Answer

IgM

Answer

IgG

Answer

IgA

Answer

IgD

Question 2

Which immunoglobulin is predominantly found in Peyer's patches?

Accepted Answer

IgA

Answer

IgM

Answer

IgG

Answer

IgD

Question 3

All of the following statements are true regarding Bare lymphocyte syndrome, except?

Accepted Answer

MHC overexpression

Answer

Autosomal recessive inheritance

Answer

Defect in b2-Microglobulin

Answer

MHC non-expression

Question 4

Which immunoglobulin has the longest half-life?

Accepted Answer

IgG

Answer

IgA

Answer

IgM

Answer

IgE

Question 5

What is the most common primary immunodeficiency?

Accepted Answer

Isolated IgA immunodeficiency

Answer

Common variable immunodeficiency

Answer

Wiskott-Aldrich syndrome

Answer

AIDS

Question 6

Major histocompatibility complex class 1 is expressed on which of the following cell types?

Accepted Answer

Macrophages only

Answer

All nucleated cells

Answer

B cells only

Answer

All blood cells except erythrocytes

Question 7

Diagnosis of X-linked agammaglobulinemia should be suspected if which of the following is present?

Accepted Answer

Absent tonsils and no palpable lymph nodes on physical examination

Answer

Female sex

Answer

High isohemagglutinin titers

Answer

Low CD3 count

Question 8

All of the following statements regarding hypersensitivity reactions are true, except:

Accepted Answer

The Schick test is an example of delayed hypersensitivity.

Answer

Erythema nodosum leprosum is a Type III hypersensitivity reaction.

Answer

Post-streptococcal glomerulonephritis is a Type III hypersensitivity reaction.

Answer

Mismatched blood transfusion is a Type II hypersensitivity reaction.

Question 9

Which type of cell secretes Interferon-alpha (IFN-α)?

Accepted Answer

Leukocytes

Answer

Fibroblasts

Answer

T helper cells

Answer

Cytotoxic T cells

Question 10

The Tuberculin test is an example of which type of immune reaction?

Accepted Answer

Cell mediated

Answer

Anaphylaxis mediated

Answer

Antibody mediated

Answer

Immune complex mediated

Immunology — MCQs

Immunology — MCQs

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