Immunology Practice Questions

Q: The Fernandez reaction in the lepromin test is a type of?

Type 4 Hypersensitive reaction. ### Explanation The **Lepromin test** is a skin test used to determine the cell-mediated immunity (CMI) of a patient against *Mycobacterium leprae*. It involves two distinct clinical readings: the **Fernandez reaction** and the **Mitsuda reaction**. **Why Option D is Correct:** The Fernandez reaction is an early response read at **48–72 hours**. It is a classic example of a **Type 4 (Delayed-type) Hypersensitivity reaction**. It occurs due to the infiltration of sensitized T-lymphocytes and macrophages at the site of lepromin injection, indicating prior exposure to the leprosy bacillus. (Note: The Mitsuda reaction, read at 3–4 weeks, is also a Type 4 reaction but signifies a granulomatous response). **Why Other Options are Incorrect:** * **Option A (Type 1):** These are immediate reactions mediated by **IgE antibodies** and mast cell degranulation (e.g., Anaphylaxis, Asthma). The Fernandez reaction takes days, not minutes, to develop. * **Option B (Type 2):** These are **cytotoxic reactions** where antibodies (IgG/IgM) react with antigens on cell surfaces (e.g., ABO incompatibility). * **Option C (Type 3):** These are **immune-complex mediated** reactions (e.g., Arthus reaction, Serum sickness). While Type 3 reactions can occur in leprosy (specifically **Erythema Nodosum Leprosum** or Type 2 Lepra reaction), they do not define the Fernandez reaction. **High-Yield Clinical Pearls for NEET-PG:** * **Fernandez Reaction:** Read at 48–72 hours (Early). * **Mitsuda Reaction:** Read at 21 days/3 weeks (Late). It is more clinically significant as it correlates with the patient's prognosis and helps classify the type of leprosy. * **Prognostic Value:** The Lepromin test is **positive** in Tuberculoid Leprosy (strong CMI) and **negative** in Lepromatous Leprosy (weak CMI). * **Diagnostic Value:** It is **NOT** used to diagnose leprosy; it is used for classification and prognosis.

Q: Which of the following statements is true regarding Toll-like receptors?

Part of innate immunity. ### Explanation **Toll-like Receptors (TLRs)** are a class of **Pattern Recognition Receptors (PRRs)** that play a pivotal role in the body's first line of defense. **Why Option D is correct:** TLRs are fundamental components of **Innate Immunity**. They are evolutionarily conserved receptors expressed on sentinel cells like macrophages and dendritic cells. They recognize highly conserved microbial structures known as **Pathogen-Associated Molecular Patterns (PAMPs)**—such as LPS, flagellin, or viral RNA—allowing the immune system to detect the presence of "non-self" immediately upon entry, without prior exposure. **Why other options are incorrect:** * **Option A & C:** TLRs are **not antigen-specific** and are not part of adaptive immunity. Unlike B-cell or T-cell receptors, which undergo genetic rearrangement to recognize specific unique epitopes, TLRs have broad specificity for entire classes of microbes. * **Option B:** While TLR activation *leads* to the production of cytokines (via the NF-κB pathway), the receptors themselves do not "act by cytokine release." They act by **ligand binding and signal transduction**. Cytokine release is the *result* of TLR activation, not the mechanism of the receptor itself. --- ### High-Yield Facts for NEET-PG * **Location:** TLRs can be **extracellular** (TLR 1, 2, 4, 5, 6—detecting bacteria/fungi) or **endosomal** (TLR 3, 7, 8, 9—detecting nucleic acids/viruses). * **Key TLRs to Remember:** * **TLR-4:** Recognizes **Lipopolysaccharide (LPS)** of Gram-negative bacteria (associated with septic shock). * **TLR-2:** Recognizes Peptidoglycan/Teichoic acid (Gram-positive bacteria). * **TLR-3:** Recognizes dsRNA. * **TLR-5:** Recognizes Flagellin. * **TLR-9:** Recognizes unmethylated CpG DNA. * **Adapter Protein:** Most TLRs (except TLR-3) utilize the **MyD88** signaling pathway to activate NF-κB.

Q: In ataxia-telangiectasia, which immunoglobulin is absent?

IgA. **Explanation:** **Ataxia-Telangiectasia (AT)** is an autosomal recessive multisystem disorder caused by a mutation in the **ATM (Ataxia-Telangiectasia Mutated) gene** on chromosome 11. This gene is responsible for repairing double-stranded DNA breaks. **Why IgA is the correct answer:** The defect in DNA repair leads to impaired **class-switch recombination**, which is essential for producing different immunoglobulin isotypes. In AT, the most common and characteristic immunologic finding is a **selective deficiency of IgA** (seen in about 70% of patients). While IgG subclasses (IgG2/IgG4) and IgE may also be low, the complete absence or profound deficiency of IgA is the classic diagnostic hallmark mentioned in high-yield medical literature. **Analysis of Incorrect Options:** * **IgG:** While IgG levels can be low (hypogammaglobulinemia) in some patients, it is rarely completely absent. * **IgM:** IgM levels are typically **normal or even elevated** in AT because the defect lies in switching *away* from IgM to other classes. * **Abnormal structure of IgA:** The pathology in AT is a quantitative failure of production (deficiency), not a qualitative defect in the molecular structure of the immunoglobulin itself. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Cerebellar ataxia (early childhood), Oculocutaneous telangiectasia (spider veins in eyes/skin), and recurrent sinopulmonary infections. * **Laboratory Marker:** Characteristically **elevated Alpha-Fetoprotein (AFP)** levels in children >1 year old. * **Complications:** High risk of malignancies (Lymphomas and Leukemias) and extreme sensitivity to ionizing radiation (X-rays/CT scans).

Q: Which one of the following statements regarding hypersensitivity reactions is FALSE?

Serum sickness is a Type II hypersensitivity reaction.. **Explanation:** The correct answer is **B** because **Serum sickness is a Type III hypersensitivity reaction**, not Type II. **Understanding the Concept:** Hypersensitivity reactions are classified by the Gell and Coombs system. **Type III (Immune Complex-mediated)** reactions occur when soluble antigen-antibody complexes deposit in tissues (like blood vessels or joints), activating the complement system and causing systemic inflammation. Serum sickness typically occurs after the administration of foreign proteins (e.g., anti-thymocyte globulin or snake antivenom), leading to fever, rash, and arthralgia. **Analysis of Other Options:** * **Option A (True):** The **Theobald-Smith phenomenon** refers to experimental systemic anaphylaxis in guinea pigs, which is a classic example of a **Type I (IgE-mediated)** reaction. * **Option C (True):** **Allograft rejection** (specifically acute and chronic cellular rejection) is primarily mediated by T-cells, making it a **Type IV (Delayed-type)** hypersensitivity reaction. * **Option D (True):** **Transfusion reactions** (ABO incompatibility) involve antibodies (IgM/IgG) binding to antigens on the surface of red blood cells, leading to complement-mediated lysis. This is a hallmark of **Type II (Cytotoxic)** hypersensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **Type II vs. Type III:** Remember, Type II involves antigens fixed **on cell surfaces** (e.g., Myasthenia Gravis, Goodpasture syndrome), while Type III involves **soluble** antigens forming circulating complexes (e.g., SLE, Post-streptococcal glomerulonephritis). * **Arthus Reaction:** This is the localized form of Type III hypersensitivity, whereas Serum Sickness is the systemic form. * **Mnemonic for Gell & Coombs:** **ACID** (Type I: **A**nanphylactic/Atopic; Type II: **C**ytotoxic; Type III: **I**mmune Complex; Type IV: **D**elayed).

Q: Interferon interferes with virus replication at which stage?

Protein synthesis. **Explanation:** Interferons (IFNs) are host-encoded glycoproteins produced in response to viral infections. They do not directly kill viruses but induce an **antiviral state** in neighboring uninfected cells. **Why Protein Synthesis is the Correct Answer:** Once IFN binds to the receptors of a healthy cell, it triggers the production of several antiviral proteins. The two most critical pathways target the translation machinery: 1. **Protein Kinase R (PKR):** This enzyme phosphorylates and inactivates the elongation factor **eIF-2**, effectively halting the initiation of protein synthesis. 2. **2',5'-Oligoadenylate Synthetase:** This activates **RNase L**, which degrades viral (and cellular) mRNA. By destroying mRNA and disabling the translation initiation complex, interferons specifically block the **synthesis of viral proteins**. **Analysis of Incorrect Options:** * **B. DNA/RNA Replication:** While some secondary mechanisms exist, the primary and most characteristic action of IFN is the inhibition of translation, not the direct inhibition of the polymerase enzymes responsible for genome replication. * **C & D. Entry and Uncoating:** These are early stages of the viral life cycle. Interferons do not prevent the virus from attaching to, entering, or uncoating within the host cell; the virus enters the cell normally, but its genetic message cannot be translated into functional proteins. **High-Yield Clinical Pearls for NEET-PG:** * **Type I IFNs (IFN-α, IFN-β):** Produced by most nucleated cells; primarily antiviral. * **Type II IFN (IFN-γ):** Produced by T-cells and NK cells; primarily immunomodulatory (activates macrophages). * **Clinical Use:** IFN-α is used in the treatment of Chronic Hepatitis B, Hepatitis C, and Kaposi Sarcoma. * **Side Effect:** "Flu-like symptoms" (fever, myalgia) are the most common side effects of IFN therapy.

Q: Which IgG subclass exhibits the greatest individual variation?

IgG1. **Explanation:** The correct answer is **IgG1**. In human serum, IgG is the most abundant immunoglobulin class, further divided into four subclasses based on structural differences in their heavy chain constant regions. **Why IgG1 is correct:** IgG1 is the most predominant subclass, accounting for approximately **60-70%** of total serum IgG. Because it is the most abundant, it exhibits the **greatest individual variation** in absolute serum concentration among different people. While all IgG subclasses have genetic variants (allotypes), the sheer volume and primary role of IgG1 in the immune response to protein antigens make its quantitative fluctuations most prominent in clinical profiles. **Analysis of Incorrect Options:** * **IgG2:** This is the second most common subclass (approx. 20%). It is primarily involved in the immune response against polysaccharide antigens (e.g., *S. pneumoniae*). Deficiencies in IgG2 are common in children with recurrent sinopulmonary infections. * **IgG3:** Known for having the longest hinge region and being the most effective complement activator. However, it has a much shorter half-life (7 days) compared to the others (23 days) and lower serum concentration. * **IgG4:** The least abundant subclass ( IgG2 > IgG3 > IgG4. * **Placental Transfer:** IgG1 is transferred most efficiently across the placenta (IgG2 is the least efficient). * **Complement Activation:** IgG3 is the most potent activator, followed by IgG1 and IgG2 (IgG4 does not activate complement). * **Half-life:** All IgG subclasses have a half-life of ~23 days, **except IgG3**, which lasts only ~7 days.

Q: Which of the following class-specific antigenic determinants of an immunoglobulin is associated with the H-chain?

H-chain. ### Explanation The classification of immunoglobulins into five distinct classes (IgG, IgA, IgM, IgD, and IgE) is determined by the **Isotypic determinants**. These determinants are based on the constant region of the **Heavy (H) chain**. **Why the H-chain is correct:** Immunoglobulins are defined by their heavy chain type: $\gamma$ (gamma) for IgG, $\alpha$ (alpha) for IgA, $\mu$ (mu) for IgM, $\delta$ (delta) for IgD, and $\epsilon$ (epsilon) for IgE. Because these antigenic differences are located in the constant region of the heavy chain, the H-chain is the structural component that dictates the class-specific identity and biological effector functions (like complement fixation or placental transfer). **Analysis of Incorrect Options:** * **L-chain (Light chain):** There are only two types of light chains ($\kappa$ and $\lambda$). Both types can be found in any class of immunoglobulin; therefore, they do not determine the specific class. * **J-chain (Joining chain):** This is a polypeptide found only in polymeric forms of antibodies (secretory IgA and pentameric IgM). It facilitates polymerization but does not define the immunoglobulin class itself. * **Variable region:** This region (found on both H and L chains) is responsible for antigen-binding specificity (idiotypes), not for determining the class (isotype) of the antibody. **High-Yield NEET-PG Pearls:** * **Isotypes:** Determined by Heavy chain constant regions (defines Class). * **Allotypes:** Determined by allelic differences at specific loci (individual variations within a species). * **Idiotypes:** Determined by the hypervariable regions in the Fab portion (unique to a specific antigen-binding site). * **Memory Trick:** **H**eavy chain = **H**ierarchy (Class/Isotype).

Q: Which portion of the MHC class I complex forms the antigen-presenting part?

Distal part of the alpha chain. **Explanation:** The **MHC Class I molecule** is a heterodimer consisting of a heavy **$\alpha$ (alpha) chain** (with three domains: $\alpha$1, $\alpha$2, and $\alpha$3) and a light chain called **$\beta$2-microglobulin**. The **antigen-binding cleft** (the site where endogenous peptides are presented to CD8+ T-cells) is formed by the folding of the **$\alpha$1 and $\alpha$2 domains**. These two domains are located at the **distal (outermost) end** of the molecule, furthest from the cell membrane. Therefore, the distal part of the alpha chain forms the antigen-presenting part. **Analysis of Options:** * **Option A & D:** $\beta$2-microglobulin does not participate in forming the peptide-binding groove. Its primary role is to provide structural support and stabilize the MHC-I complex on the cell surface. * **Option C:** The proximal part of the alpha chain refers to the **$\alpha$3 domain**, which is located closest to the cell membrane. This domain is highly conserved and serves as the binding site for the **CD8 co-receptor** of T-cells, rather than the antigen itself. **High-Yield Facts for NEET-PG:** * **MHC Class I:** Presents **endogenous antigens** (e.g., viral or tumor proteins) to **CD8+ Cytotoxic T-cells**. Found on all nucleated cells. * **MHC Class II:** Antigen-binding cleft is formed by **$\alpha$1 and $\beta$1 domains**. It presents **exogenous antigens** to **CD4+ Helper T-cells**. Found only on Professional Antigen Presenting Cells (APCs). * **Rule of 8:** MHC I × CD8 = 8; MHC II × CD4 = 8. * **Human Leukocyte Antigens (HLA):** MHC Class I corresponds to HLA-A, B, and C.

Question 1

The Fernandez reaction in the lepromin test is a type of?

Accepted Answer

Type 4 Hypersensitive reaction

Answer

Type 1 Hypersensitive reaction

Answer

Type 2 Hypersensitive reaction

Answer

Type 3 Hypersensitive reaction

Question 2

Which of the following statements is true about a hapten?

Accepted Answer

It needs a carrier to induce an immune response.

Answer

It induces a brisk immune response.

Answer

It is a T-independent antigen.

Answer

It has no association with MHC.

Question 3

Which of the following statements is true regarding Toll-like receptors?

Accepted Answer

Part of innate immunity

Answer

Antigen specific

Answer

Acts by cytokine release

Answer

Part of adaptive immunity

Question 4

In ataxia-telangiectasia, which immunoglobulin is absent?

Accepted Answer

IgA

Answer

IgG

Answer

IgM

Answer

Abnormal structure of IgA

Question 5

Which one of the following statements regarding hypersensitivity reactions is FALSE?

Accepted Answer

Serum sickness is a Type II hypersensitivity reaction.

Answer

Theobald-Smith phenomenon is a Type I hypersensitivity reaction.

Answer

Allograft rejection is a Type IV hypersensitivity reaction.

Answer

Transfusion reaction is a Type II hypersensitivity reaction.

Question 6

Interferon interferes with virus replication at which stage?

Accepted Answer

Protein synthesis

Answer

DNA/RNA replication

Answer

When the virus enters the cell

Answer

Uncoating of the virus protein capsule

Question 7

Which IgG subclass exhibits the greatest individual variation?

Accepted Answer

IgG1

Answer

IgG2

Answer

IgG3

Answer

IgG4

Question 8

Which of the following class-specific antigenic determinants of an immunoglobulin is associated with the H-chain?

Accepted Answer

H-chain

Answer

L-chain

Answer

J-chain

Answer

Variable region

Question 9

Which portion of the MHC class I complex forms the antigen-presenting part?

Accepted Answer

Distal part of the alpha chain

Answer

Between alpha 1 and beta 2 microglobulin

Answer

Proximal part of the alpha chain

Answer

Between alpha subunit and beta 2 microglobulin

Question 10

One of the most remarkable aspects of the human immune system is its diversity, that is, the ability to recognize a wide range of antigens and to mount a specific antibody response. This is called clonal selection. At the cellular level, which of the following are primarily responsible for such specificity?

Accepted Answer

Hypervariable regions in domains of B cells

Answer

Cytotoxic T cells

Answer

The major histocompatibility complex

Answer

Specific T cell receptors

Immunology — MCQs

Immunology — MCQs

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