Immunology Practice Questions

Q: To fully activate a naive CD4 T cell, what must the antigen-presenting cell express?

B7 and MHC class II molecules. ### Explanation To activate a naive CD4+ T cell, a **two-signal model** is required. This ensures that the immune system does not mount an accidental response against self-antigens. 1. **Signal 1 (Antigen Recognition):** The T-cell receptor (TCR) on the CD4 cell recognizes the specific peptide fragment presented by the **MHC Class II** molecule on the surface of a professional Antigen-Presenting Cell (APC) like a dendritic cell, macrophage, or B cell. 2. **Signal 2 (Co-stimulation):** This is the "confirmation" signal. The **B7 protein** (CD80/86) on the APC binds to the **CD28** receptor on the T cell. Without this interaction, the T cell becomes "anergic" (non-responsive). **Analysis of Options:** * **Option A:** MHC Class I is present on all nucleated cells and presents to CD8+ T cells, not CD4+ cells. * **Option B:** Interleukin-2 (IL-2) is a cytokine produced *by* the T cell after activation to promote clonal expansion; it is not expressed by the APC to initiate activation. * **Option D:** CD28 is located on the **T cell**, not the APC. The question asks what the **APC** must express. **High-Yield Clinical Pearls for NEET-PG:** * **Signal 1:** TCR + MHC II (CD4) or MHC I (CD8). * **Signal 2:** CD28 (T cell) + B7 (APC). * **Anergy:** If Signal 1 occurs without Signal 2, the T cell enters a state of prolonged inactivation. * **CTLA-4:** A molecule on T cells that binds B7 with higher affinity than CD28 but sends an *inhibitory* signal, acting as a "brake" on the immune response (target of checkpoint inhibitors in cancer).

Q: HLA typing is useful in:

Cases of parental dispute. **Explanation:** **HLA (Human Leukocyte Antigen)** typing, also known as tissue typing, identifies the specific MHC (Major Histocompatibility Complex) proteins on the surface of cells. These antigens are highly polymorphic and are inherited in a Mendelian codominant fashion (one haplotype from each parent). **Why Option D is Correct:** Because of the extreme diversity (polymorphism) of HLA alleles, the probability of two unrelated individuals having the same HLA profile is exceptionally low. Since a child must inherit one HLA haplotype from each biological parent, HLA typing serves as a powerful tool in **paternity testing and resolving parental disputes**. If a child possesses an HLA antigen not present in either the mother or the alleged father, that man is excluded as the biological father. **Why Other Options are Incorrect:** * **A. Blood Grouping:** This is determined by ABO and Rh antigens on RBCs, not HLA (which are primarily on nucleated cells). * **B. Assessing Prognosis:** While certain HLA types are associated with disease *susceptibility* (e.g., HLA-B27 and Ankylosing Spondylitis), they are generally used for diagnosis or risk assessment rather than predicting the clinical prognosis of an established disease. * **C. Cancer Therapy:** While HLA matching is vital for Bone Marrow Transplants (to prevent GVHD), it is not a standard "therapy" for cancer itself. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Location:** Encoded on the short arm of **Chromosome 6**. * **Organ Transplantation:** HLA-DR matching is the most important for successful renal transplant, followed by HLA-B and HLA-A. * **Key HLA-Disease Associations:** * **HLA-B27:** Ankylosing Spondylitis, Reiter’s syndrome. * **HLA-DR3/DR4:** Type 1 Diabetes Mellitus. * **HLA-DQ2/DQ8:** Celiac Disease. * **HLA-B51:** Behcet’s Disease.

Q: Which Toll-like receptor (TLR) is present on flagella of bacteria?

TLR-5. **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)**. **Why TLR-5 is correct:** TLR-5 is specifically designed to recognize **Flagellin**, the principal protein component of bacterial flagella. This receptor is primarily expressed on the surface of epithelial cells, monocytes, and dendritic cells. When flagellin binds to TLR-5, it triggers a signaling cascade (via the MyD88 pathway) that leads to the activation of NF-κB, resulting in the production of pro-inflammatory cytokines. **Analysis of Incorrect Options:** * **TLR-1:** Typically forms a heterodimer with TLR-2 to recognize **triacyl lipopeptides** found in bacteria and mycobacteria. * **TLR-3:** Located on endosomal membranes; it specifically recognizes **double-stranded RNA (dsRNA)**, which is a hallmark of viral replication. * **TLR-7:** Also located in endosomes; it recognizes **single-stranded RNA (ssRNA)** from viruses (similar to TLR-8). **High-Yield Clinical Pearls for NEET-PG:** * **TLR-4:** Recognizes **Lipopolysaccharide (LPS)** of Gram-negative bacteria (requires MD2 and CD14 co-receptors). This is a very frequent exam topic. * **TLR-2:** Recognizes **Peptidoglycan** and Lipoteichoic acid (Gram-positive bacteria). * **TLR-9:** Recognizes unmethylated **CpG DNA** motifs common in bacteria and viruses. * **Location Tip:** TLRs 1, 2, 4, 5, and 6 are found on the **cell surface** (detecting extracellular pathogens), while TLRs 3, 7, 8, and 9 are found in **endosomes** (detecting intracellular/nucleic acid PAMPs).

Q: Which of the following is NOT a function of complements?

Toxin neutralization. The complement system is a biochemical cascade of the innate immune system that helps clear pathogens. However, it lacks the structural ability to neutralize toxins. ### **Why Toxin Neutralization is the Correct Answer** **Toxin neutralization** is primarily a function of **antibodies** (specifically IgG and IgA). Antibodies bind to the active sites of toxins or block their entry into host cells. The complement system consists of plasma proteins that act on cell surfaces or viral envelopes but cannot chemically modify or "neutralize" small soluble protein toxins. ### **Explanation of Other Options** * **Cell Lysis (Option A):** This is a primary function mediated by the **Membrane Attack Complex (MAC)**, consisting of C5b-C9. It creates pores in the lipid bilayer of Gram-negative bacteria and infected cells, leading to osmotic lysis. * **Antiviral Action (Option B):** Complements contribute to antiviral immunity by opsonizing viral particles (C3b), promoting their phagocytosis, and directly lysing enveloped viruses via the MAC. * **Promotes Phagocytosis (Option C):** This occurs through **Opsonization**. **C3b** (and C4b) acts as a major opsonin, coating the pathogen surface. Phagocytes (neutrophils/macrophages) have CR1 receptors that bind to C3b, significantly enhancing the engulfment of the pathogen. ### **High-Yield Clinical Pearls for NEET-PG** * **C3b:** The most potent **Opsonin**. * **C5a:** The most potent **Chemotactic agent** and Anaphylatoxin. * **C5b-9:** The **Membrane Attack Complex (MAC)**; deficiency leads to recurrent *Neisseria* infections. * **C1 Esterase Inhibitor Deficiency:** Leads to **Hereditary Angioedema** (due to overproduction of bradykinin). * **CH50 Assay:** Used to screen for deficiencies in the Classical Pathway.

Q: Class I histocompatibility antigens are expressed on all of the following cell types except?

Lymphocyte. **Explanation:** The expression of Major Histocompatibility Complex (MHC) molecules is a fundamental concept in immunology. **MHC Class I molecules** (HLA-A, B, and C) are found on the surface of **all nucleated cells** in the body, as well as on **platelets**. Their primary role is to present endogenous antigens to CD8+ T-cytotoxic cells. **Why Option D (Red Blood Cells) is the correct answer:** Mature Red Blood Cells (RBCs) are **non-nucleated**. Since they lack a nucleus and the necessary protein synthesis machinery (ribosomes/endoplasmic reticulum) to process and display these surface glycoproteins, they do not express MHC Class I antigens. **Analysis of Incorrect Options:** * **A. Macrophages:** These are nucleated cells and professional Antigen Presenting Cells (APCs). They express **both** MHC Class I and MHC Class II. * **B. Lymphocytes:** Both B and T lymphocytes are nucleated and express MHC Class I. (Note: B-cells also express MHC Class II). * **C. Platelets:** Although platelets are anuclear fragments of megakaryocytes, they are a notable **exception** to the "nucleated cell" rule. They do express MHC Class I antigens on their surface, which is clinically significant in platelet transfusion refractoriness. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Class I:** Found on all nucleated cells + Platelets. (Presents to CD8+ T cells). * **MHC Class II:** Found only on Professional APCs (Macrophages, B-cells, Dendritic cells) and thymic epithelial cells. (Presents to CD4+ T cells). * **MHC Class III:** Includes components of the complement system (C2, C4) and TNF. * **Human exception:** The only nucleated cell that lacks MHC Class I is the **villous trophoblast**, which helps prevent maternal immune rejection of the fetus.

Q: Which antibody isotype is primarily associated with the mucosal immune system?

IgA. **Explanation:** **Correct Option: A (IgA)** Immunoglobulin A (IgA) is the hallmark antibody of the mucosal immune system. Specifically, **Secretory IgA (sIgA)** is the most abundant antibody at mucosal surfaces (GIT, respiratory tract, and genitourinary tract). It exists as a **dimer** held together by a **J-chain** and a **secretory component**, which protects the molecule from degradation by proteolytic enzymes in harsh mucosal environments. Its primary function is **immune exclusion**, where it prevents the attachment of bacteria and viruses to epithelial cells. **Incorrect Options:** * **B (IgD):** Found in trace amounts in serum; it primarily acts as a B-cell antigen receptor on the surface of mature, naive B-cells. It has no established role in mucosal defense. * **C (IgE):** Primarily involved in **Type I hypersensitivity** reactions and defense against **helminthic parasitic infections**. It binds to mast cells and basophils via high-affinity Fc receptors. * **D (IgM):** The first antibody produced in a primary immune response. While it can be secreted across mucosa (as a pentamer with a J-chain) in IgA-deficient individuals, it is not the primary mucosal isotype. **NEET-PG High-Yield Pearls:** * **Most abundant Ig in the body:** IgA (due to the vast surface area of the gut). * **Most abundant Ig in serum:** IgG. * **Selective IgA Deficiency:** The most common primary immunodeficiency; patients are often asymptomatic but may present with recurrent sinopulmonary infections or Giardiasis. * **Breast Milk:** Rich in secretory IgA, providing passive mucosal immunity to the neonate.

Q: A pregnant female is infected with Rubella. Which of the following immunoglobulins is produced by in-utero infection?

IgM. **Explanation:** The correct answer is **IgM**. **Why IgM is correct:** The human fetus begins producing its own immunoglobulins around the 20th week of gestation. However, the placenta is selective; only maternal **IgG** can cross the placental barrier to provide passive immunity. **IgM** is a pentameric molecule with a high molecular weight, making it too large to cross the placenta. Therefore, if IgM antibodies against Rubella are detected in a newborn or a fetus, it serves as definitive evidence of a **primary intrauterine infection**, as these antibodies could only have been synthesized by the fetal immune system in response to the virus. **Why other options are incorrect:** * **IgG:** While IgG is found in the fetus, it is predominantly of maternal origin (passive transfer). It does not signify an active fetal infection unless titers remain persistently high or rise after the disappearance of maternal antibodies (usually after 6–12 months). * **IgA:** IgA is primarily secreted in colostrum and breast milk. While the fetus can produce trace amounts, it is not the diagnostic marker for acute in-utero infection. * **IgD:** This immunoglobulin acts mainly as an antigen receptor on B cells and has no diagnostic significance in congenital infections. **High-Yield Clinical Pearls for NEET-PG:** * **Gregg’s Triad (Congenital Rubella Syndrome):** Cataracts, Sensorineural hearing loss (most common), and Congenital Heart Disease (PDA is most common; Peripheral Pulmonary Artery Stenosis is most specific). * **Blueberry Muffin Rash:** Characteristic finding in CRS due to extramedullary hematopoiesis. * **Risk Period:** The risk of malformation is highest if the infection occurs in the **first trimester** (up to 80% risk in the first 12 weeks). * **Diagnosis:** Detection of Rubella-specific IgM in the cord blood or neonatal serum is the gold standard for diagnosing CRS at birth.

Q: What is the most abundant complement protein in the body?

C3. **Explanation:** **C3** is the most abundant complement protein in human serum, with a normal concentration of approximately **1.2 mg/mL**. It serves as the central hub of the complement system because all three activation pathways (Classical, Alternative, and Lectin) converge at the step of C3 cleavage. Its high concentration is physiologically necessary because C3b (its cleavage product) acts as a major opsonin and is required to form the C5 convertase, which initiates the Membrane Attack Complex (MAC). **Analysis of Incorrect Options:** * **C1:** This is the first component of the classical pathway. While large in molecular size (a complex of C1q, C1r, and C1s), its serum concentration is significantly lower than C3. * **C2:** This is the least abundant complement component in the serum. It is often the rate-limiting factor in the classical pathway activation. * **C4:** Although C4 is present in higher concentrations than C2, it ranks below C3. It is primarily involved in the classical and lectin pathways. **Clinical Pearls for NEET-PG:** * **Central Molecule:** C3 is the most important component; its deficiency leads to severe, recurrent pyogenic infections (e.g., *S. pneumoniae*, *H. influenzae*). * **C3b Function:** "C3**b** **B**inds" to bacteria (Opsonization). * **C3a/C5a Function:** These are **Anaphylatoxins** (trigger mast cell degranulation). C5a is also a potent chemoattractant for neutrophils. * **Diagnostic Marker:** Low levels of C3 and C4 are used clinically to monitor disease activity in Systemic Lupus Erythematosus (SLE) and Post-Streptococcal Glomerulonephritis (PSGN).

Question 1

Tonsils are absent in which of the following conditions?

Accepted Answer

X linked agammaglobulinemia

Answer

Wiskott-Aldrich syndrome

Answer

DiGeorge syndrome

Answer

Chediak Higashi syndrome

Question 2

To fully activate a naive CD4 T cell, what must the antigen-presenting cell express?

Accepted Answer

B7 and MHC class II molecules

Answer

MHC class I and class II molecules

Answer

Interleukin-2

Answer

CD28 and MHC class II molecules

Question 3

HLA typing is useful in:

Accepted Answer

Cases of parental dispute

Answer

Blood grouping

Answer

Assessing prognosis of disease

Answer

Cancer therapy

Question 4

Which Toll-like receptor (TLR) is present on flagella of bacteria?

Accepted Answer

TLR-5

Answer

TLR-1

Answer

TLR-3

Answer

TLR-7

Question 5

Which statement is false about haptens?

Accepted Answer

Haptens are low molecular weight molecules

Answer

Haptens lack immunogenicity

Answer

Haptens retain antigenicity

Answer

Complex haptens contain two or more epitopes

Question 6

Which of the following is NOT a function of complements?

Accepted Answer

Toxin neutralization

Answer

Cell lysis

Answer

Antiviral action

Answer

Promotes phagocytosis

Question 7

Class I histocompatibility antigens are expressed on all of the following cell types except?

Accepted Answer

Lymphocyte

Answer

Macrophage

Answer

Platelets

Answer

Red Blood Cells

Question 8

Which antibody isotype is primarily associated with the mucosal immune system?

Accepted Answer

IgA

Answer

IgD

Answer

IgE

Answer

IgM

Question 9

A pregnant female is infected with Rubella. Which of the following immunoglobulins is produced by in-utero infection?

Accepted Answer

IgM

Answer

IgG

Answer

IgA

Answer

IgD

Question 10

What is the most abundant complement protein in the body?

Accepted Answer

C3

Answer

C1

Answer

C2

Answer

C4

Immunology — MCQs

Immunology — MCQs

On this page

Practice by Chapter

Want unlimited practice?