Immunology Practice Questions

Q: A young patient presents with severe recurrent pyogenic bacterial infections, yet has normal T-cell and B-cell numbers. Testing reveals a defect in the CD40 ligand of the patient's CD4 T-helper cells. Which immunoglobulin, characterized by its presence as a monomer on B-cell surfaces, a pentamer in serum, and its initial appearance in the primary immune response, is significantly elevated in this patient?

IgM. **Explanation:** The clinical presentation describes **Hyper-IgM Syndrome (Type 1)**, an X-linked immunodeficiency. The core defect lies in the **CD40 ligand (CD154)** on T-cells, which fails to interact with the **CD40 receptor** on B-cells. This interaction is mandatory for **Isotype Class Switching** and **Somatic Hypermutation**. 1. **Why IgM is correct:** Because B-cells cannot receive the "signal" to switch from producing IgM to other classes (IgG, IgA, or IgE), they continue to produce only IgM. Consequently, serum levels of IgM are normal to significantly elevated, while other isotopes are severely deficient. IgM is the first antibody produced in a primary response, exists as a **monomer** on B-cell surfaces (BCR), and forms a **pentamer** (with a J-chain) in serum. 2. **Why other options are incorrect:** * **IgG:** Levels are low because class switching from IgM to IgG is blocked. IgG is the most abundant serum Ig and crosses the placenta. * **IgA:** Levels are low due to the class-switch defect. IgA is primarily found in secretions (dimer) and protects mucosal surfaces. * **IgD:** While present on B-cell surfaces alongside IgM, it is not the primary antibody elevated in this syndrome and does not exist as a pentamer in serum. **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Most common form is X-linked (CD40L deficiency). * **Clinical Clue:** Recurrent pyogenic infections (due to low IgG) + *Pneumocystis jirovecii* pneumonia (due to T-cell signaling defect). * **Diagnosis:** Flow cytometry showing absent CD154 on activated T-cells. * **Treatment:** IVIG replacement and Hematopoietic Stem Cell Transplant (HSCT).

Q: Which of the following statements regarding IgE antibodies is NOT true?

It can cross the placenta and fix complement.. ### Explanation The correct answer is **D**, as IgE does **not** cross the placenta nor does it fix complement via the classical pathway. #### Why Option D is the Correct Answer (The False Statement) * **Placental Transfer:** Only **IgG** is capable of crossing the placenta to provide passive immunity to the fetus, due to the presence of specific Fc receptors (FcRn) on placental cells. * **Complement Fixation:** The classical complement pathway is activated by **IgM** (most potent) and **IgG** (subclasses 1, 2, and 3). IgE lacks the binding site for C1q and therefore cannot fix complement. #### Why the Other Options are Incorrect (True Statements) * **Option A & B:** IgE is the primary mediator of **Type I Hypersensitivity** (allergic) reactions. It binds to high-affinity receptors (FcεRI) on **mast cells and basophils**. Upon re-exposure to an allergen, cross-linking of IgE triggers degranulation, releasing histamine, leukotrienes, and prostaglandins. * **Option C:** IgE plays a crucial role in **helminthic (parasitic) infections**. It facilitates Antibody-Dependent Cellular Cytotoxicity (ADCC) by recruiting **eosinophils**, which release major basic protein to destroy the parasite. #### NEET-PG High-Yield Pearls * **Heat Lability:** IgE is the most heat-labile immunoglobulin (inactivated at 56°C for 30 minutes). * **Prausnitz-Küstner (PK) Reaction:** Historically used to detect IgE (reaginic antibody) by passive cutaneous anaphylaxis. * **Serum Levels:** IgE has the lowest serum concentration and the shortest half-life (~2 days) among all immunoglobulins. * **Structure:** It is a monomer with an extra constant domain (**CH4**) on its heavy chain.

Q: Which of the following statements is FALSE regarding acquired immunity?

Immunological memory responses are absent. ### Explanation The correct answer is **D. Immunological memory responses are absent.** This statement is false because **immunological memory** is a hallmark characteristic of acquired (adaptive) immunity, distinguishing it from innate immunity. #### Why Option D is the Correct Answer (The False Statement) Acquired immunity is characterized by the ability to "remember" a specific pathogen. Upon initial exposure (primary response), the body produces **memory B and T cells**. On subsequent exposure to the same antigen (secondary response), these memory cells ensure a faster, more vigorous, and more effective immune attack. In contrast, innate immunity lacks this memory and responds identically to every exposure. #### Why the Other Options are Incorrect (True Statements) * **Option A:** Acquired immunity is not present at birth; it **develops only after exposure** to a foreign antigen (via infection or vaccination). * **Option B:** The receptors on B cells (BCRs) and T cells (TCRs) are **highly specific**. Unlike the broad Pattern Recognition Receptors (PRRs) of innate immunity, these receptors are generated through genetic rearrangement to recognize unique epitopes. * **Option C:** Acquired immunity is **antigen-specific**. It can distinguish between even minor molecular differences in different microbial strains. #### High-Yield Clinical Pearls for NEET-PG * **Components:** Acquired immunity is divided into **Humoral** (B-cells/Antibodies) and **Cell-Mediated** (T-cells). * **Active vs. Passive:** Active immunity (long-lasting, has memory) involves the host's own immune system; Passive immunity (short-acting, no memory) involves the transfer of pre-formed antibodies (e.g., IgA in breast milk, Tetanus antitoxin). * **Lag Period:** Acquired immunity has a distinct lag period during the first exposure, whereas innate immunity is immediate.

Q: Mast cells synthesize and/or secrete which of the following substances?

Histamine. **Explanation:** Mast cells are key effector cells of the innate immune system, primarily known for their role in Type I (Immediate) Hypersensitivity reactions. **Why Histamine is the Correct Answer:** Mast cells contain numerous basophilic granules packed with pre-formed inflammatory mediators. Upon activation (cross-linking of IgE receptors), these cells undergo degranulation. **Histamine** is the most significant pre-formed mediator released. It acts on H1 receptors to cause vasodilation, increased vascular permeability (leading to edema), and smooth muscle contraction (bronchospasm). **Analysis of Incorrect Options:** * **Adrenaline (Option A):** This is a hormone and neurotransmitter synthesized by the adrenal medulla and sympathetic nervous system. It is actually the drug of choice to *counteract* mast cell degranulation during anaphylaxis. * **Acetylcholine (Option B):** This is the primary neurotransmitter of the parasympathetic nervous system and neuromuscular junctions, not a secretory product of mast cells. * **Heparin (Option D):** While mast cells *do* contain heparin (an anticoagulant), it serves primarily as a structural matrix for storing histamine within the granules. In the context of standard medical examinations, **Histamine** is the primary functional mediator associated with mast cell clinical manifestations. **High-Yield Clinical Pearls for NEET-PG:** * **Markers:** Tryptase is the most specific marker for mast cell activation (used to diagnose anaphylaxis). * **Receptors:** Mast cells express high-affinity receptors for the Fc portion of IgE (**FcεRI**). * **Location:** They are abundant in tissues exposed to the external environment (skin, GI tract, respiratory tract). * **C-kit (CD117):** This is a crucial surface marker for identifying mast cells in pathology.

Q: The technique of immunoblotting used to analyze RNA is named as?

Northern blot. **Explanation:** The correct answer is **Northern blot**. In molecular biology, blotting refers to the transfer of biological macromolecules (DNA, RNA, or proteins) from a gel to a carrier membrane for identification. 1. **Why Northern Blot is correct:** This technique is specifically designed to detect and analyze **RNA** sequences. It involves separating RNA samples by size using gel electrophoresis, transferring them to a membrane (like nitrocellulose), and then using a labeled complementary nucleic acid probe to identify specific RNA strands. It is widely used to study gene expression. 2. **Why other options are incorrect:** * **Southern blot:** Named after Edwin Southern, this technique is used for the detection of specific **DNA** sequences. * **Western blot:** This technique is used to identify specific **proteins** using labeled antibodies. It is clinically significant as a confirmatory test for HIV (detecting antibodies against gp120, gp41, and p24). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic (SNOW DROP):** * **S**outhern = **D**NA * **N**orthern = **R**NA * **O** = **O** (No match) * **W**estern = **P**rotein * **Southwestern Blot:** A hybrid technique used to identify **DNA-binding proteins** (e.g., transcription factors like c-Jun and c-Fos). * **Eastern Blot:** Used to analyze post-translational modifications of proteins (e.g., carbohydrates or lipids). * **ELISA vs. Western Blot:** In HIV screening, ELISA is the highly sensitive initial test, while Western Blot is the highly specific confirmatory test.

Q: A 21-year-old woman has a history since childhood of recurrent episodes of swelling of the submucosal and subcutaneous tissue of the gastrointestinal and respiratory tracts. Her C1 inhibitor level is less than 5% of the reference value. These findings support a diagnosis of:

Hereditary angioedema. **Explanation:** The clinical presentation of recurrent, non-pitting edema of the subcutaneous and submucosal tissues (especially the GI tract and airway) without urticaria, combined with a deficiency in **C1 esterase inhibitor (C1-INH)**, is pathognomonic for **Hereditary Angioedema (HAE)**. **Why the correct answer is right:** C1-INH is a serine protease inhibitor that regulates the classical complement pathway and the kinin-generating system. A deficiency leads to the unregulated activation of the kallikrein-kinin cascade, resulting in excessive production of **bradykinin**. Bradykinin increases vascular permeability, leading to the characteristic episodes of swelling. It is inherited in an autosomal dominant fashion. **Why incorrect options are wrong:** * **DiGeorge Syndrome:** A T-cell deficiency caused by 22q11.2 deletion, characterized by thymic hypoplasia, hypocalcemia, and cardiac defects. It does not involve C1-INH. * **Nutritional based immune deficiency:** Usually presents with generalized lymphopenia or specific vitamin/mineral deficiencies (e.g., Zinc) leading to opportunistic infections, not localized angioedema. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** Caused by a deficiency of GPI-anchored proteins (CD55/CD59) on RBCs, leading to complement-mediated hemolysis and thrombosis, not C1-INH deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Screen with **C4 levels** (consistently low during and between attacks). Confirm with C1-INH levels/function. * **Management:** Acute attacks are treated with **C1-INH concentrate** or **Icatibant** (bradykinin B2 receptor antagonist). * **Contraindication:** ACE inhibitors are contraindicated as they prevent bradykinin breakdown, worsening the edema. * **Key Distinction:** Unlike allergic angioedema, HAE does **not** present with itching or hives (urticaria).

Q: What is the most important cytokine for type II lepra reaction?

TNF alpha. **Explanation:** **Type II Lepra Reaction (Erythema Nodosum Leprosum - ENL)** is a classic example of a **Type III Hypersensitivity reaction** (Immune-complex mediated). It typically occurs in patients with multibacillary leprosy (lepromatous or borderline lepromatous) where there is a high bacterial load. **Why TNF-alpha is the correct answer:** TNF-alpha (Tumor Necrosis Factor-alpha) is the central mediator in the pathogenesis of ENL. During the reaction, there is a massive systemic release of TNF-alpha from activated macrophages and monocytes. This cytokine is responsible for the systemic symptoms (fever, malaise) and the acute inflammatory skin lesions. The clinical effectiveness of **Thalidomide** in treating Type II reactions is specifically due to its potent ability to inhibit TNF-alpha synthesis. **Analysis of Incorrect Options:** * **IL-1 and IL-6:** While these are pro-inflammatory cytokines that may be elevated during systemic inflammation, they are secondary mediators and not the primary drivers or therapeutic targets specific to ENL. * **IFN-gamma:** This is the hallmark cytokine of **Type 1 Lepra Reaction** (Reversal Reaction), which involves a Type IV Delayed Hypersensitivity response and a shift toward a Th1 immune profile. **High-Yield Clinical Pearls for NEET-PG:** * **Type I Reaction:** Type IV Hypersensitivity; involves IFN-gamma and IL-2; treated with Steroids. * **Type II Reaction (ENL):** Type III Hypersensitivity; involves TNF-alpha; treated with **Thalidomide** (drug of choice) or Clofazimine. * **Clinical Presentation of ENL:** Tender evanescent subcutaneous nodules, fever, arthralgia, and iridocyclitis. * **Trigger:** Often precipitated by the initiation of Multidrug Therapy (MDT).

Q: Which of the following is coded by the HLA III gene?

Complement. The Human Leukocyte Antigen (HLA) complex, located on the short arm of **Chromosome 6**, is divided into three classes. Understanding the distinct functions of these classes is high-yield for NEET-PG. ### **Explanation of the Correct Answer** **Option B (Complement)** is correct because the **HLA Class III** region codes for several secreted proteins involved in the immune response that are *not* cell-surface markers. Specifically, it codes for: * **Complement components:** C2, C4 (C4A and C4B), and Factor B. * **Cytokines:** Tumor Necrosis Factor (TNF-α and TNF-β). * **Heat Shock Proteins (HSP).** Unlike Class I and II, Class III molecules do not participate in antigen presentation but play a vital role in the inflammatory cascade. ### **Analysis of Incorrect Options** * **Options A & C (Graft Rejection / GVHD):** These reactions are primarily mediated by **HLA Class I** (A, B, C) and **HLA Class II** (DR, DQ, DP) molecules. Class I molecules are found on all nucleated cells and are the main targets in acute cellular rejection, while Class II molecules are restricted to antigen-presenting cells and are crucial for T-helper cell activation. * **Option D (Immunoglobulins):** These are produced by B-lymphocytes and are coded by genes located on **Chromosomes 14** (Heavy chains), **2** (Kappa light chains), and **22** (Lambda light chains), not the HLA complex on Chromosome 6. ### **High-Yield Clinical Pearls for NEET-PG** * **Class I HLA:** Coded by A, B, and C loci; presents endogenous antigens to **CD8+ T-cells**. * **Class II HLA:** Coded by DP, DQ, and DR loci; presents exogenous antigens to **CD4+ T-cells**. * **Ankylosing Spondylitis:** Strongly associated with **HLA-B27** (Class I). * **Narcolepsy:** Strongly associated with **HLA-DR2/DQB1*06:02** (Class II). * **Structure:** Class I has one heavy chain and one **β2-microglobulin** (coded on Chromosome 15); Class II has two heavy chains (α and β).

Question 1

A young patient presents with severe recurrent pyogenic bacterial infections, yet has normal T-cell and B-cell numbers. Testing reveals a defect in the CD40 ligand of the patient's CD4 T-helper cells. Which immunoglobulin, characterized by its presence as a monomer on B-cell surfaces, a pentamer in serum, and its initial appearance in the primary immune response, is significantly elevated in this patient?

Accepted Answer

IgM

Answer

IgG

Answer

IgA

Answer

IgD

Question 2

Which of the following statements regarding IgE antibodies is NOT true?

Accepted Answer

It can cross the placenta and fix complement.

Answer

It mediates the release of histamine and other chemical mediators.

Answer

It is the primary antibody involved in allergic reactions.

Answer

It is involved in anti-parasitic immune responses.

Question 3

Which of the following statements is FALSE regarding acquired immunity?

Accepted Answer

Immunological memory responses are absent

Answer

Develops following antigenic exposure

Answer

Host cell receptors are specific

Answer

Responds to specific microbial antigens

Question 4

Mast cells synthesize and/or secrete which of the following substances?

Accepted Answer

Histamine

Answer

Adrenaline

Answer

Acetylcholine

Answer

Heparin

Question 5

The technique of immunoblotting used to analyze RNA is named as?

Accepted Answer

Northern blot

Answer

Southern blot

Answer

Western blot

Answer

None of the above

Question 6

A 21-year-old woman has a history since childhood of recurrent episodes of swelling of the submucosal and subcutaneous tissue of the gastrointestinal and respiratory tracts. Her C1 inhibitor level is less than 5% of the reference value. These findings support a diagnosis of:

Accepted Answer

Hereditary angioedema

Answer

DiGeorge syndrome

Answer

Nutritional based immune deficiency

Answer

Paroxysmal nocturnal hemoglobinuria

Question 7

What is the most important cytokine for type II lepra reaction?

Accepted Answer

TNF alpha

Answer

IL 1

Answer

IL 6

Answer

INF gamma

Question 8

What region of the immunoglobulin molecule contains the antigen binding site?

Accepted Answer

Hypervariable region

Answer

Variable region

Answer

Constant region

Answer

Idiotype

Question 9

What is the heterophile agglutination test?

Accepted Answer

A heterophile antibody that reacts with a microorganism or cells of unrelated species due to common antigen sharing.

Answer

The test is performed in hypertonic saline (5% saline) or albumin saline.

Answer

Coomb, Mourant, and Race devised a reagent: Rabbit anti-human gamma globulin.

Answer

Helps to detect the blood group and for cross-matching.

Question 10

Which of the following is coded by the HLA III gene?

Accepted Answer

Complement

Answer

Immunological reaction in graft rejection

Answer

Graft versus host reaction

Answer

Immunoglobulins

Immunology — MCQs

Immunology — MCQs

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