Immunology Practice Questions

Q: Which Toll-like receptor is associated with viruses?

TLR3. **Explanation:** Toll-like receptors (TLRs) are a class of Pattern Recognition Receptors (PRRs) that play a crucial role in the innate immune system by detecting Pathogen-Associated Molecular Patterns (PAMPs). **1. Why TLR3 is Correct:** TLR3 is specifically localized in the **endosomal membranes** (intracellularly) rather than the cell surface. Its primary ligand is **double-stranded RNA (dsRNA)**, which is a hallmark of viral replication. When TLR3 detects dsRNA, it triggers the production of Type I Interferons (IFN-α and IFN-β), which are essential for the antiviral response. **2. Analysis of Incorrect Options:** * **TLR1:** This receptor forms a heterodimer with TLR2 to recognize **triacyl lipopeptides** found primarily in bacteria and mycobacteria. * **TLR2:** Located on the cell surface, it recognizes **peptidoglycan**, lipoteichoic acid, and lipoproteins. It is the primary receptor for **Gram-positive bacteria**. * **TLR4:** This is the classic receptor for **Lipopolysaccharide (LPS)** found in the outer membrane of **Gram-negative bacteria**. It is also associated with the MD2 and CD14 complex. **3. NEET-PG High-Yield Pearls:** * **Viral TLRs:** Remember the "Viral Trio": **TLR3** (dsRNA), **TLR7/8** (ssRNA), and **TLR9** (unmethylated CpG DNA). * **Location:** TLRs 1, 2, 4, 5, and 6 are on the **plasma membrane** (detecting extracellular pathogens). TLRs 3, 7, 8, and 9 are **endosomal** (detecting intracellular/nucleic acid PAMPs). * **TLR5:** Specifically recognizes **Flagellin** (bacterial flagella). * **Clinical Correlation:** Deficiency of TLR3 is associated with an increased susceptibility to **Herpes Simplex Encephalitis (HSE)**.

Q: In which of the following conditions is the prozone phenomenon most evident?

Secondary syphilis. **Explanation:** The **Prozone Phenomenon** is a false-negative result in agglutination or precipitation tests due to an **excess of antibodies** (antibody excess zone). When antibody concentration is extremely high, each antigen is coated by antibodies without forming the necessary cross-linkages (lattices) required for visible clumps. **Why Secondary Syphilis is the Correct Answer:** In **Secondary Syphilis**, the bacterial load of *Treponema pallidum* is at its peak, triggering a massive humoral immune response. This results in very high titers of non-specific antibodies (reagins). When performing screening tests like **VDRL or RPR**, these excessive antibodies prevent lattice formation, leading to a false-negative result. The phenomenon is resolved by **diluting the patient’s serum**, which reduces the antibody concentration to the "zone of equivalence," allowing agglutination to occur. **Analysis of Incorrect Options:** * **A, B, and C (Tularaemia, Legionnaires, Plague):** While these are significant bacterial infections, they do not typically present with the extreme antibody titers required to frequently trigger the prozone phenomenon in standard diagnostic assays. Diagnosis for these often relies on culture, PCR, or specific titer rises rather than high-volume reaginic screening. **High-Yield Clinical Pearls for NEET-PG:** * **Post-zone Phenomenon:** Occurs due to **antigen excess** (rare in clinical practice). * **Zone of Equivalence:** The ideal ratio of antigen to antibody where maximum precipitation occurs. * **Syphilis Testing:** VDRL is used for screening and monitoring treatment (titer falls after treatment), while TPHA/FTA-ABS are specific treponemal tests used for confirmation. * **Other conditions for Prozone:** Occasionally seen in **Brucellosis** (due to blocking antibodies) and **HIV** (due to polyclonal B-cell activation).

Q: At what age does the capacity for producing IgG develop?

6 months. **Explanation:** The development of the humoral immune system in a neonate follows a specific chronological pattern. At birth, the infant has high levels of **maternal IgG**, which is actively transported across the placenta during the third trimester. This passive immunity provides protection for the first few months of life. **Why 6 months is correct:** Endogenous production of IgG (the infant's own antibodies) begins shortly after birth, but it remains at low levels while maternal IgG is still dominant. Maternal IgG levels begin to decline significantly around 3–4 months. By **6 months of age**, the infant’s own lymphoid system matures sufficiently to take over, and the capacity for significant endogenous IgG production is firmly established. This transition period (3–6 months) is known as the period of **"Physiological Hypogammaglobulinemia."** **Why other options are incorrect:** * **1 year:** By this age, the infant’s IgG levels are already approximately 60% of adult levels. The *capacity* to produce it starts much earlier. * **2 and 3 years:** These ages represent milestones for other isotopes. For example, adult levels of IgG are reached by 5–8 years, while IgA (the slowest to develop) takes until puberty to reach adult levels. **High-Yield Clinical Pearls for NEET-PG:** * **IgM:** The first immunoglobulin produced by the fetus (starts at 20 weeks gestation). Elevated IgM at birth indicates **intrauterine infection** (TORCH), as IgM does not cross the placenta. * **IgA:** Present in colostrum/breast milk, providing local mucosal immunity, but endogenous production is the slowest to reach adult levels. * **Placental Transfer:** Only **IgG** crosses the placenta (specifically via neonatal Fc receptors, FcRn). * **Transient Hypogammaglobulinemia of Infancy:** A condition where the infant’s endogenous IgG production is delayed beyond the normal 6-month mark, leading to recurrent infections.

Q: A patient presents with recurrent swelling of the lips. He has no itching and a positive family history. Which of the following is deficient in this patient?

C1 inhibitor. The clinical presentation of recurrent, non-pruritic swelling (angioedema) without urticaria (itching), coupled with a positive family history, is the classic triad for **Hereditary Angioedema (HAE)**. ### **Explanation of the Correct Answer** **Hereditary Angioedema** is caused by a deficiency or dysfunction of the **C1 esterase inhibitor (C1-INH)**. * **Mechanism:** C1-INH normally inhibits the classical complement pathway and the kinin system. Its deficiency leads to the uncontrolled activation of the kallikrein-kinin cascade, resulting in excessive production of **bradykinin**. * **Clinical Effect:** Bradykinin increases vascular permeability, leading to the characteristic episodic swelling of the face, lips, airway (life-threatening), and gastrointestinal tract. ### **Analysis of Incorrect Options** * **A. C1, C2, C4:** Deficiencies in early classical pathway components are strongly associated with **Systemic Lupus Erythematosus (SLE)** and other immune-complex diseases, as they are required for clearing apoptotic debris. * **C. C3b inactivator (Factor I):** Deficiency leads to the continuous consumption of C3. This results in low C3 levels and presents clinically as recurrent infections with **pyogenic bacteria** (e.g., *S. pneumoniae*). * **D. C5-C8:** Deficiencies in the Membrane Attack Complex (MAC) components (C5–C9) specifically predispose individuals to recurrent **Neisserial infections** (Meningitis and Gonorrhea). ### **NEET-PG High-Yield Pearls** * **Biochemical Marker:** The best screening test for HAE is a **low C4 level**, even between attacks. * **Treatment:** Acute attacks are treated with C1-INH concentrate or **Icatibant** (bradykinin B2 receptor antagonist). * **Contraindication:** Patients with HAE should avoid **ACE inhibitors**, as they prevent bradykinin breakdown and can trigger severe attacks.

Q: Which of the following statements best applies to the given diagram?

Found on T and B lymphocytes and all nucleated cells. ***Found on T and B lymphocytes and all nucleated cells*** - **MHC Class I molecules** are present on all nucleated cells in the body, including **T lymphocytes** and **B lymphocytes**, to present intracellular peptides to **CD8+ T cells**. - This universal distribution allows the immune system to monitor all cells for **intracellular pathogens** or **abnormal proteins** like those from viruses or tumors. *Depicts the cell-membrane MHC product associated with narcolepsy* - **Narcolepsy** is associated with **HLA-DQB1*06:02**, which is an **MHC Class II molecule**, not the MHC Class I molecule shown in the diagram. - **MHC Class II molecules** are found on **antigen-presenting cells** like dendromes, macrophages, and B cells, not on all nucleated cells. *Essential for the transplacental passage of antibody* - **Transplacental antibody passage** is mediated by the **neonatal Fc receptor (FcRn)**, which binds **IgG antibodies**, not MHC molecules. - **FcRn** allows maternal **IgG antibodies** to cross the placenta and provide passive immunity to the fetus. *Present on macrophages but not neutrophils* - This describes the distribution of **MHC Class II molecules**, which are found on **antigen-presenting cells** like macrophages but not on neutrophils. - **MHC Class I molecules** (shown in the diagram) are present on **both macrophages and neutrophils** since both are nucleated cells.

Q: Antigens processed by the exogenous antigen presentation pathway are presented in association with which of the following?

MHC class II molecules. ### Explanation **Correct Answer: D. MHC class II molecules** The immune system utilizes two distinct pathways for antigen presentation based on the source of the antigen: 1. **Exogenous Pathway (MHC II):** Extracellular pathogens (bacteria, toxins) are internalized by **Antigen-Presenting Cells (APCs)** like macrophages, B cells, and dendritic cells via phagocytosis or endocytosis. These antigens are degraded in endolysosomes and then loaded onto **MHC Class II** molecules. These complexes are presented to **CD4+ T-helper cells**. 2. **Endogenous Pathway (MHC I):** Intracellular antigens (viruses, tumor proteins) are processed by proteasomes in the cytosol and loaded onto **MHC Class I** molecules in the endoplasmic reticulum. These are presented to **CD8+ Cytotoxic T cells**. #### Why Incorrect Options are Wrong: * **A. Fc receptors:** These are found on the surface of various immune cells (like NK cells and mast cells) and bind to the Fc portion of antibodies; they do not present antigens to T cells. * **B. IgG heavy chains:** These are structural components of the immunoglobulin molecule, responsible for determining the antibody class, not for antigen presentation. * **C. MHC class I molecules:** These present **endogenous** antigens (derived from within the cell) to CD8+ T cells. #### High-Yield Clinical Pearls for NEET-PG: * **Rule of 8:** MHC **II** × CD**4** = 8; MHC **I** × CD**8** = 8. * **Invariant Chain (Ii):** In the exogenous pathway, the invariant chain prevents premature binding of self-peptides to MHC II in the ER. * **Cross-presentation:** A unique process where dendritic cells can present exogenous antigens via MHC I to activate CD8+ T cells (essential for anti-tumor immunity). * **MHC II Distribution:** Unlike MHC I (found on all nucleated cells), MHC II is restricted to professional APCs.

Q: What is the earliest immunoglobulin synthesized by the fetus?

IgM. **Explanation:** The correct answer is **IgM**. **Why IgM is correct:** Immunoglobulin M (IgM) is the first antibody class to be synthesized by the fetus, beginning around the **20th week of intrauterine life**. Because IgM is a large pentameric molecule, it cannot cross the placental barrier. Therefore, the presence of specific IgM antibodies in a neonate’s serum is a definitive diagnostic marker for **congenital infections** (e.g., TORCH infections), as it indicates an active fetal immune response rather than maternal transfer. **Why the other options are incorrect:** * **IgG:** While IgG is the most abundant immunoglobulin in the fetus, it is **not synthesized** by the fetus in significant amounts initially. Instead, it is actively transported across the placenta from the mother (starting at 12 weeks) to provide passive immunity. * **IgA:** This is primarily a secretory antibody. Fetal synthesis of IgA begins much later (around 30 weeks) and levels remain very low at birth. It is primarily acquired postnatally through colostrum and breast milk. * **IgE:** This is involved in type I hypersensitivity and parasitic infections. It is produced in negligible amounts by the fetus and does not cross the placenta. **High-Yield Clinical Pearls for NEET-PG:** * **Order of synthesis:** IgM is the first to be synthesized, followed by IgG and then IgA. * **Placental Transfer:** **IgG** is the *only* immunoglobulin that crosses the placenta (via neonatal Fc receptors). * **Adult levels:** IgG reaches adult levels by 5–8 years, while IgM reaches adult levels by 1 year of age. * **Colostrum:** Rich in **Secretory IgA**, providing local mucosal immunity to the neonate’s gut.

Question 1

Which Toll-like receptor is associated with viruses?

Accepted Answer

TLR3

Answer

TLR1

Answer

TLR2

Answer

TLR4

Question 2

In which of the following conditions is the prozone phenomenon most evident?

Accepted Answer

Secondary syphilis

Answer

Tularaemia

Answer

Legionnaires disease

Answer

Plague

Question 3

Which of the following conditions represents a disorder of T-cell function?

Accepted Answer

Purine nucleoside phosphorylase (PNP) deficiency

Answer

Bruton disease

Answer

Chediak-Higashi Syndrome

Answer

Job's Syndrome

Question 4

At what age does the capacity for producing IgG develop?

Accepted Answer

6 months

Answer

1 year

Answer

2 years

Answer

3 years

Question 5

Which of the following statements regarding agglutination reaction is NOT true?

Accepted Answer

It is less sensitive than precipitation reaction for detecting antibodies.

Answer

It works on the same principle as that of precipitation reaction.

Answer

It is the method used for cross-matching and blood grouping.

Answer

Agglutination occurs optimally when antigens and antibody react in equivalent proportions.

Question 6

A patient presents with recurrent swelling of the lips. He has no itching and a positive family history. Which of the following is deficient in this patient?

Accepted Answer

C1 inhibitor

Answer

C1, C2, C4

Answer

C3b inactivator

Answer

C5-C8

Question 7

Division and differentiation of B cells leading to production of plasma cells both require:

Accepted Answer

IL-4 and IL-6

Answer

CD4 and CD8

Answer

Interleukin (IL)-1 and IL-5

Answer

IL-5 only

Question 8

Which of the following statements best applies to the given diagram?

Accepted Answer

Found on T and B lymphocytes and all nucleated cells

Answer

Depicts the cell-membrane MHC product associated with narcolepsy

Answer

Essential for the transplacental passage of antibody

Answer

Present on macrophages but not neutrophils

Question 9

Antigens processed by the exogenous antigen presentation pathway are presented in association with which of the following?

Accepted Answer

MHC class II molecules

Answer

Fc receptors

Answer

IgG heavy chains

Answer

MHC class I molecules

Question 10

What is the earliest immunoglobulin synthesized by the fetus?

Accepted Answer

IgM

Answer

IgA

Answer

IgG

Answer

IgE

Immunology — MCQs

Immunology — MCQs

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