Immunology Practice Questions

Q: Which leukotriene functions as an adhesion factor for neutrophils on the cell surface to attach to the endothelium?

Leukotriene B4. ### Explanation **Correct Option: A. Leukotriene B4 (LTB4)** Leukotriene B4 is a potent inflammatory mediator derived from arachidonic acid via the **5-lipoxygenase pathway**. Its primary role in the inflammatory response is the **recruitment and activation of neutrophils**. Specifically, LTB4 functions as a powerful **chemotactic agent** and an **adhesion factor**. It induces the expression of adhesion molecules (integrins) on the surface of neutrophils, facilitating their firm attachment to the vascular endothelium before they undergo diapedesis (transmigration) into the tissues. **Why the other options are incorrect:** * **Leukotriene C4, D4, and E4 (Option B, C, D):** These are collectively known as **cysteinyl leukotrienes** (or the Slow-Reacting Substance of Anaphylaxis - SRS-A). Their primary physiological effects include intense bronchoconstriction, increased vascular permeability (edema), and mucus secretion. They are central to the pathogenesis of bronchial asthma but do not play a significant role in neutrophil adhesion or chemotaxis. --- ### High-Yield Clinical Pearls for NEET-PG: * **Chemotactic "Big Four":** Remember the four most important substances that attract neutrophils: **LTB4**, **IL-8**, **C5a**, and **Bacterial products** (N-formyl methionine). * **Pharmacology Link:** **Zileuton** inhibits 5-lipoxygenase (preventing all LT synthesis), while **Montelukast/Zafirlukast** are receptor antagonists specifically for the cysteinyl leukotrienes (LTC4, LTD4, LTE4). * **LTB4 vs. LTC4/D4/E4:** Think of **LTB4** as "Neutrophil **B**olting" (adhesion/chemotaxis) and **LTC4/D4/E4** as "**C**onstriction" (bronchospasm).

Q: Which immunoglobulin is least important in human beings?

IgD. **Explanation:** The correct answer is **IgD**. In human physiology, IgD is considered the least important immunoglobulin because it has no known primary effector function in the systemic circulation. It is present in extremely low concentrations in the serum (<1% of total serum globulins) and has a very short half-life of about 2–3 days. While it serves as a surface receptor on B-lymphocytes (alongside IgM) to signal B-cell activation, its absence does not lead to significant clinical deficiency or disease. **Why other options are incorrect:** * **IgG:** The most abundant immunoglobulin (75-80%). It is crucial for secondary immune responses, opsonization, and is the only antibody that crosses the placenta to provide passive immunity to the fetus. * **IgA:** The primary secretory antibody. It provides essential mucosal immunity in the gut, respiratory tract, and urogenital tract, and is found in breast milk (colostrum). * **IgE:** Although present in trace amounts, it is vital for mediating Type I hypersensitivity (allergic) reactions and provides defense against helminthic (parasitic) infections. **High-Yield Facts for NEET-PG:** * **IgD & IgM:** These are the only two immunoglobulins co-expressed on the surface of **naive B-cells**. * **Heat Labile:** IgD and IgE are the most heat-labile antibodies. * **Molecular Weight:** IgM is the largest (Pentamer), but IgD has a relatively high molecular weight due to its long hinge region, making it susceptible to proteolysis. * **Serum Concentration Order:** IgG > IgA > IgM > IgD > IgE (Mnemonic: **GAMDE**).

Q: What is true about IgM?

Primary response. **Explanation:** **IgM (Immunoglobulin M)** is the first antibody produced by the immune system in response to an initial exposure to an antigen. This makes it the hallmark of the **Primary Immune Response**. It is a large pentameric molecule (the largest immunoglobulin) held together by a J-chain, which provides it with high avidity to neutralize pathogens effectively before the more specific IgG is produced. **Analysis of Options:** * **Option B (Correct):** IgM is the first isotype to appear after antigen exposure. In clinical diagnostics, the presence of IgM indicates an **acute or recent infection**. * **Option A (Incorrect):** The **Prausnitz-Küstner (PK) reaction** is mediated by **IgE**. This reaction was historically used to demonstrate immediate hypersensitivity (Type I) by transferring serum from an allergic individual to a non-allergic one. * **Option C (Incorrect):** Only **IgG** can be transported across the placenta. IgM is too large (pentameric structure) to cross the placental barrier. Therefore, the detection of IgM in a newborn’s blood indicates a **congenital infection** (e.g., TORCH), as it cannot be maternal in origin. * **Option D (Incorrect):** The **Secondary (anamnestic) response** is primarily mediated by **IgG**, which appears faster, reaches higher titers, and persists longer due to memory B-cell activation. **High-Yield Clinical Pearls for NEET-PG:** * **Structure:** Pentamer (in serum), Monomer (on B-cell surface as a receptor). * **Complement Activation:** IgM is the **most efficient** activator of the classical complement pathway. * **Evolutionary Fact:** It is the oldest immunoglobulin class phylogenetically. * **Valency:** It has a theoretical valency of 10, but an effective valency of 5 due to steric hindrance.

Q: Which cells are primarily associated with humoral immunity?

B cells. **Explanation:** **Humoral immunity** (antibody-mediated immunity) is the aspect of the adaptive immune system mediated by macromolecules found in extracellular fluids. The primary mediators of this response are **B cells (B lymphocytes)**. 1. **Why B cells are correct:** Upon encountering a specific antigen, B cells differentiate into **plasma cells**, which secrete antibodies (Immunoglobulins). These antibodies neutralize pathogens, activate the complement system, and promote opsonization. This process occurs in the "humors" (body fluids), hence the name. 2. **Why other options are incorrect:** * **T cells:** These are the primary mediators of **Cell-Mediated Immunity (CMI)**. They do not produce antibodies but instead act directly against intracellular pathogens (CD8+ Cytotoxic T cells) or coordinate the immune response (CD4+ Helper T cells). * **NK (Natural Killer) cells:** These are part of the **innate immune system**. They provide a rapid response to virally infected cells and tumor cells without prior sensitization. * **Null cells:** These are lymphocytes that lack the characteristic surface markers of either B or T cells (primarily consisting of NK cells). **High-Yield Clinical Pearls for NEET-PG:** * **Origin:** Both B and T cells originate in the bone marrow, but B cells mature in the **bone marrow**, while T cells mature in the **thymus**. * **Markers:** B cells are identified by surface markers **CD19, CD20, and CD21**. * **Memory:** Humoral immunity is characterized by "memory"; subsequent exposure to the same antigen leads to a faster and more robust IgG response (Secondary immune response). * **Deficiency:** Bruton’s Agammaglobulinemia is a classic clinical example of a pure B-cell (humoral) immunodeficiency.

Q: A 15-year-old boy presents 1 week after being bitten by an Ixodes tick with fatigue, fever, headache, and a reddish rash over his trunk and extremities. A positive IgM antibody titer (1:200) to Borrelia burgdorferi is associated with which of the following?

Acute Lyme disease. **Explanation:** The clinical presentation of a tick bite followed by fever, headache, and a characteristic rash (Erythema migrans) is classic for **Lyme disease**, caused by the spirochete *Borrelia burgdorferi*. In immunology, **IgM** is the first antibody isotype produced during a primary immune response. A high IgM titer (1:200) within one week of symptom onset confirms an **acute infection**. **Why the other options are incorrect:** * **Fifth Disease (Erythema Infectiosum):** Caused by Parvovirus B19, it typically presents with a "slapped-cheek" rash in children and is not transmitted by ticks. * **Hepatitis B Infection:** Diagnosis relies on HBsAg and anti-HBc IgM markers. While IgM is present in acute HBV, the clinical history of a tick bite and skin rash is inconsistent with hepatitis. * **Subacute Sclerosing Panencephalitis (SSPE):** This is a late, progressive neurological complication of a Measles virus infection. It is characterized by extremely high titers of **IgG** (not IgM) in both serum and CSF, occurring years after the initial infection. **High-Yield Clinical Pearls for NEET-PG:** * **Vector:** *Ixodes* tick (also transmits Babesia and Anaplasma). * **Early Localized Stage:** Erythema migrans (target-like/bull’s eye rash). * **Serology:** Two-tier testing is recommended (ELISA followed by Western Blot). IgM appears in 1–2 weeks; IgG appears in 4–6 weeks. * **Treatment:** Doxycycline is the drug of choice (Amoxicillin in children <8 years or pregnant women).

Q: What is the important step played by Interleukin in the activation of naive CD4+ T cells and initiation of cell-mediated immune response?

Interleukin-2. **Explanation:** The activation of naive CD4+ T cells is a two-signal process. Signal 1 involves the TCR-MHC II interaction, and Signal 2 involves costimulation (B7-CD28). Once these signals are received, the T cell undergoes **clonal expansion and differentiation**, a process driven primarily by **Interleukin-2 (IL-2)**. **Why Interleukin-2 is the correct answer:** IL-2 is known as the **T-cell growth factor**. Upon activation, the naive T cell begins to secrete IL-2 and simultaneously expresses the high-affinity IL-2 receptor (CD25). This creates an **autocrine loop** where IL-2 binds back to the same cell, triggering rapid cell division (proliferation) and survival. This step is essential for the initiation of a robust cell-mediated immune response. **Analysis of Incorrect Options:** * **Interleukin-1 (IL-1):** Produced by macrophages; it acts as a pyrogen and a pro-inflammatory mediator but is not the primary driver of T-cell clonal expansion. * **Interleukin-3 (IL-3):** Acts as a colony-stimulating factor (CSF) that supports the growth and differentiation of hematopoietic stem cells in the bone marrow. * **Interleukin-4 (IL-4):** Primarily involved in the differentiation of naive T cells into **Th2 cells** and promotes B-cell class switching to IgE; it is not the universal "activation" interleukin for all CD4+ T cells. **High-Yield NEET-PG Pearls:** * **CD25** is the alpha chain of the IL-2 receptor; it is a marker for activated T cells and Regulatory T cells (Tregs). * **Cyclosporine and Tacrolimus** (immunosuppressants) work by inhibiting calcineurin, which prevents the transcription of IL-2, thereby halting T-cell activation. * **Sirolimus (Rapamycin)** acts later by inhibiting the mTOR pathway, blocking the T-cell response *to* IL-2.

Q: Which of the following is responsible for phagocytosis?

C3b. ### Explanation The correct answer is **C3b**. **1. Why C3b is correct:** C3b is the primary **opsonin** of the complement system. Opsonization is the process by which specific molecules (opsonins) coat a pathogen, making it "tasty" and easily recognizable to phagocytes (neutrophils and macrophages). Phagocytes possess specific **CR1 receptors** that bind to C3b attached to the microbial surface, significantly enhancing the efficiency of phagocytosis. **2. Why other options are incorrect:** * **C5a & C3a:** These are known as **Anaphylatoxins**. They trigger mast cell degranulation, leading to histamine release and increased vascular permeability. Specifically, **C5a** is also a potent **chemoattractant** that recruits neutrophils to the site of inflammation, but it does not directly mediate the attachment phase of phagocytosis. * **TNF-α:** This is a pro-inflammatory cytokine produced mainly by macrophages. While it activates endothelial cells and induces fever, it does not act as an opsonin. **3. Clinical Pearls for NEET-PG:** * **Major Opsonins:** The two most important opsonins in the body are **C3b** (complement) and **IgG** (specifically the Fc portion). * **C3b Function:** Apart from opsonization, C3b also helps in the clearance of immune complexes and contributes to the formation of C5 convertase. * **Deficiency:** Patients with C3 deficiency suffer from recurrent pyogenic infections (e.g., *S. pneumoniae*, *H. influenzae*) because they cannot effectively opsonize encapsulated bacteria. * **Mnemonic:** **C3b** **B**inds **B**acteria (Opsonization); **C3a/C5a** mediate **A**cute **A**llergic-like reactions (Anaphylaxis).

Q: Which of the following is a T-cell marker?

CD8. **Explanation:** The identification of lymphocytes is based on **Cluster of Differentiation (CD)** markers, which are surface molecules used to categorize white blood cells. **Why CD8 is the correct answer:** CD8 is a transmembrane glycoprotein that serves as a co-receptor for the **T-cell receptor (TCR)**. It is specifically expressed on **Cytotoxic T-cells**. These cells recognize antigens presented by **MHC Class I** molecules. Along with CD4 (found on Helper T-cells), CD8 is a definitive marker for mature T-cell subsets. **Analysis of Incorrect Options:** * **CD45 (Option A):** Known as the **Leukocyte Common Antigen (LCA)**. It is expressed on *all* hematologic cells (except mature erythrocytes and platelets), not just T-cells. It is used in pathology to differentiate lymphomas from carcinomas. * **IL-3 (Option B):** This is a **cytokine** (interleukin) secreted by activated T-cells to stimulate the bone marrow stem cells; it is not a surface marker. * **CD19 (Option D):** This is a classic **B-cell marker**. It is expressed from the earliest stages of B-cell development until just before differentiation into plasma cells. **High-Yield Clinical Pearls for NEET-PG:** * **Pan-T-cell markers:** CD2, **CD3** (most specific), CD5, and CD7. * **Pan-B-cell markers:** CD19, CD20, and CD21 (also the receptor for Epstein-Barr Virus). * **NK cell markers:** CD16 (FcγRIII) and CD56. * **Rule of 8:** T-cells follow a simple multiplication rule: CD4 × MHC II = 8 and **CD8 × MHC I = 8**.

Q: Contact dermatitis is a type of:

Type-IV hypersensitivity. **Explanation:** **Correct Answer: D. Type-IV hypersensitivity** Contact dermatitis is a classic example of **Type-IV (Delayed-type) hypersensitivity**. Unlike other types, this is **cell-mediated** rather than antibody-mediated. When a hapten (e.g., nickel, poison ivy, or chemicals in cosmetics) penetrates the skin, it binds to skin proteins to become antigenic. These are processed by Langerhans cells and presented to **T-helper 1 (Th1) cells**. Upon re-exposure, sensitized T-cells release cytokines (IFN-γ, IL-2), recruiting macrophages that cause epidermal damage and vesicle formation. The reaction typically peaks **48–72 hours** after exposure. **Why other options are incorrect:** * **Type-I (Immediate):** Mediated by **IgE** and mast cell degranulation (e.g., Anaphylaxis, Urticaria). It occurs within minutes. * **Type-II (Cytotoxic):** Mediated by **IgG or IgM** against antigens on cell surfaces (e.g., Rh incompatibility, Myasthenia Gravis). * **Type-III (Immune-complex):** Caused by deposition of **antigen-antibody complexes** in tissues (e.g., SLE, Serum sickness, Arthus reaction). **NEET-PG High-Yield Pearls:** * **Patch Test:** The gold standard diagnostic tool for identifying the allergen in contact dermatitis (read at 48 and 72 hours). * **Key Mediators:** CD4+ T-cells (Th1) and Macrophages. * **Other Type-IV Examples:** Mantoux test (Tuberculin reaction), Lepromin test, Graft rejection (acute/chronic), and Granuloma formation (e.g., Sarcoidosis). * **Mnemonic:** **ACID** (Type **A**naphlyactic, **C**ytotoxic, **I**mmune-complex, **D**elayed).

Question 1

Which leukotriene functions as an adhesion factor for neutrophils on the cell surface to attach to the endothelium?

Accepted Answer

Leukotriene B4

Answer

Leukotriene C4

Answer

Leukotriene D4

Answer

Leukotriene E4

Question 2

Which immunoglobulin is least important in human beings?

Accepted Answer

IgD

Answer

IgE

Answer

IgG

Answer

IgA

Question 3

MHC restriction is a part of all except?

Accepted Answer

Autoimmune disorder

Answer

Antiviral cytotoxic T cell

Answer

Antibacterial helper T cell/cytotoxic cells

Answer

Allograft rejection

Question 4

What is true about IgM?

Accepted Answer

Primary response

Answer

Mediates Prausnitz-kustner reaction

Answer

Transported across placenta

Answer

Secondary response

Question 5

Which cells are primarily associated with humoral immunity?

Accepted Answer

B cells

Answer

NK cells

Answer

T cells

Answer

Null cells

Question 6

A 15-year-old boy presents 1 week after being bitten by an Ixodes tick with fatigue, fever, headache, and a reddish rash over his trunk and extremities. A positive IgM antibody titer (1:200) to Borrelia burgdorferi is associated with which of the following?

Accepted Answer

Acute Lyme disease

Answer

Fifth disease

Answer

Possible hepatitis B infection

Answer

Possible subacute sclerosing panencephalitis (SSPE)

Question 7

What is the important step played by Interleukin in the activation of naive CD4+ T cells and initiation of cell-mediated immune response?

Accepted Answer

Interleukin-2

Answer

Interleukin-1

Answer

Interleukin-3

Answer

Interleukin-4

Question 8

Which of the following is responsible for phagocytosis?

Accepted Answer

C3b

Answer

C5a

Answer

C3a

Answer

TNF-a

Question 9

Which of the following is a T-cell marker?

Accepted Answer

CD8

Answer

CD45

Answer

IL3

Answer

CD19

Question 10

Contact dermatitis is a type of:

Accepted Answer

Type-IV hypersensitivity

Answer

Type-I hypersensitivity

Answer

Type-II hypersensitivity

Answer

Type-III hypersensitivity

Immunology — MCQs

Immunology — MCQs

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