Anaphylaxis refers to which of the following?
What is the definition of an allograft?
Which precipitate forms at 50-60 o C but disappears on heating?
Administration of the DPT vaccine (diphtheria toxoid, pertussis vaccine, and tetanus toxoid) would stimulate which of the following types of immunity?
Which cells express immunoglobulins as surface antigens?
During the physical examination of a 22-year-old man, a purified protein derivative isolated from Mycobacterium tuberculosis is injected into the skin. Three days later, the injection site appears raised and indurated. Which of the following glycoproteins was directly involved in antigen presentation during the initiation phase of delayed hypersensitivity in this patient?
Which type of hypersensitivity reaction is mediated by immune complexes?
What is the molecular mass of IgG in kDa?
What is the term for the specific part of an antigen molecule that is recognized by an antibody?
A 21-year-old Rh-negative pregnant female is about to deliver. The baby's father is Rh-positive. What procedure should be ordered to reduce the chance of hemolytic disease of the newborn?
Explanation: ### Explanation **1. Why Option A is Correct:** Anaphylaxis is a **Type I Hypersensitivity reaction** (IgE-mediated). The fundamental requirement for any hypersensitivity reaction is **prior sensitization**. When a "sensitized" individual (one who has already produced specific IgE antibodies against a protein/antigen) is re-exposed to that same antigen, it leads to the cross-linking of IgE on the surface of mast cells and basophils. This triggers immediate degranulation and the release of potent mediators like **histamine**, leukotrienes, and prostaglandins, resulting in a systemic, life-threatening reaction. **2. Why Other Options are Incorrect:** * **Option B:** A primary (first) injection cannot cause anaphylaxis because the body has not yet produced the specific IgE antibodies required for the reaction. * **Option C:** This describes **Active Immunity** or desensitization protocols, not anaphylaxis. Repeated injections usually lead to the production of IgG (blocking antibodies) rather than the explosive IgE response seen in anaphylaxis. * **Option D:** This describes **Atopy**. While atopy involves sensitivity to common environmental allergens (like pollen or dust), it typically manifests as localized conditions (allergic rhinitis, asthma) rather than the systemic, acute clinical syndrome defined as anaphylaxis. **3. NEET-PG High-Yield Pearls:** * **Mediators:** Histamine is the primary mediator; however, **Tryptase** levels are measured clinically to confirm a diagnosis of anaphylaxis post-event. * **Drug of Choice:** **Adrenaline (Epinephrine)** 1:1000 concentration, administered **Intramuscularly (IM)** in the anterolateral thigh. * **Mechanism:** It is an "Immediate" hypersensitivity occurring within minutes. * **Prausnitz-Küstner (PK) Reaction:** A historical test used to demonstrate Type I hypersensitivity by passive transfer of serum.
Explanation: ### Explanation The classification of grafts is based on the genetic relationship between the donor and the recipient. This is a fundamental concept in transplant immunology, as the degree of genetic disparity determines the intensity of the immune response (rejection). **Correct Answer: C. A graft from a member of the same species** An **Allograft** (or homograft) is a transplant between two genetically different individuals of the same species (e.g., human to human). Because the donor’s Human Leukocyte Antigens (HLA) are different from the recipient’s, allografts trigger an immune response, necessitating the use of immunosuppressive therapy to prevent rejection. **Analysis of Incorrect Options:** * **A. A graft from oneself:** This is an **Autograft**. Since the donor and recipient are the same person, there is no genetic disparity, and no immune rejection occurs (e.g., skin grafting in burns). * **B. A graft from an identical twin:** This is an **Isograft** (or syngeneic graft). Because monozygotic twins are genetically identical, the recipient’s immune system recognizes the graft as "self," and rejection does not occur. * **D. A graft from a different species:** This is a **Xenograft** (or heterograft). Examples include using porcine (pig) heart valves in humans. These carry the highest risk of hyperacute rejection. **High-Yield NEET-PG Pearls:** 1. **Order of Immunogenicity:** Xenograft > Allograft > Isograft = Autograft. 2. **MHC/HLA:** The primary targets of allograft rejection are the **MHC Class I and II** molecules. 3. **Hyperacute Rejection:** Occurs within minutes due to pre-formed antibodies; most commonly seen in ABO-incompatible or xenografts. 4. **Most Common:** Allografts are the most common type of transplant performed in clinical practice.
Explanation: This question refers to the unique biochemical properties of **Bence-Jones proteins**, which are free monoclonal **light chains** (either kappa or lambda) found in the urine of patients with plasma cell dyscrasias. ### Explanation of the Correct Answer **Bence-Jones proteins (Light chains)** exhibit a characteristic thermal behavior known as **thermosolubility**. When urine containing these light chains is heated: 1. They begin to precipitate at **40–60°C**, forming a visible cloudy white precipitate. 2. Upon further heating to **100°C (boiling)**, the precipitate **redissolves** and the urine becomes clear again. 3. On cooling, the precipitate reappears at 60°C and disappears once more below 40°C. This occurs because the light chains undergo reversible denaturation and aggregation at specific temperatures, unlike standard proteins (like albumin) which coagulate permanently when boiled. ### Why Incorrect Options are Wrong * **Heavy chains (Option A):** Heavy chains are larger molecules and do not exhibit this specific reversible thermosolubility. In "Heavy Chain Disease," these proteins are excreted but do not show the Bence-Jones phenomenon. * **Both heavy and light chains (Option C):** Only the free light chains possess the specific structural properties required for this unique precipitation-redissolution cycle. Intact immunoglobulins (heavy + light) do not behave this way. ### High-Yield Clinical Pearls for NEET-PG * **Clinical Association:** Bence-Jones proteinuria is a hallmark of **Multiple Myeloma** (found in ~50-80% of cases) and Waldenström macroglobulinemia. * **Diagnostic Note:** Standard urine dipsticks often fail to detect Bence-Jones proteins because they primarily react with albumin. **Sulphosalicylic acid (SSA) test** or **Urine Protein Electrophoresis (UPEP)** is required for detection. * **Renal Impact:** These light chains are nephrotoxic and can lead to "Myeloma Kidney" (cast nephropathy).
Explanation: ### Explanation The correct answer is **Artificial active immunity**. **1. Why "Artificial Active" is correct:** Immunity is classified based on how it is acquired (Natural vs. Artificial) and how the body responds (Active vs. Passive). * **Active:** The individual’s own immune system is stimulated to produce antibodies and memory cells. In the DPT vaccine, the antigens (toxoids and killed bacteria) trigger an endogenous immune response. * **Artificial:** The exposure to the antigen is intentional and medical, rather than through a clinical or subclinical infection. Therefore, any **vaccination** (like DPT) falls under artificial active immunity. **2. Why the other options are incorrect:** * **Adoptive (A):** This involves the transfer of immune cells (usually lymphocytes) from a donor to a recipient (e.g., bone marrow transplant or certain cancer immunotherapies). * **Artificial Passive (C):** This involves the administration of pre-formed antibodies (immunoglobulins) to provide immediate protection. Examples include Tetanus Immunoglobulin (TIG) or Anti-rabies serum (ARS). * **Natural Active (D):** This occurs when a person is exposed to a live pathogen in the environment and develops the disease (e.g., recovering from a natural Measles or Chickenpox infection). **3. High-Yield Clinical Pearls for NEET-PG:** * **Active Immunity:** Slow onset but long-lasting (due to memory cells). * **Passive Immunity:** Immediate onset but short-acting (no memory cells). * **DPT Components:** Diphtheria and Tetanus are **toxoids** (exotoxins modified to lose toxicity but retain antigenicity), while the Pertussis component in the standard DPT is **killed (whole-cell)** bacteria. * **Combined Immunity:** In cases of a "dirty" wound in an unimmunized person, both Tetanus Toxoid (Active) and TIG (Passive) are given at different sites; this is known as **simultaneous immunization**.
Explanation: ### Explanation **Correct Answer: D. B cells** **Mechanism:** B cells are the primary mediators of humoral immunity. The hallmark of a mature B cell is the expression of **Surface Immunoglobulins (sIg)**, which function as the **B-cell Receptor (BCR)**. These surface antibodies (primarily **IgM and IgD**) allow the B cell to specifically recognize and bind to exogenous antigens. Once an antigen binds to these surface immunoglobulins, the B cell undergoes activation, proliferation, and differentiation into plasma cells, which then secrete soluble antibodies. **Why other options are incorrect:** * **Neutrophils (A) and Monocytes (B):** These are phagocytic cells of the innate immune system. They do not produce or express intrinsic immunoglobulins. Instead, they possess **Fc receptors** (e.g., CD16, CD32, CD64) that allow them to bind to the tail portion of antibodies already attached to pathogens (opsonization). * **NK Cells (C):** These are large granular lymphocytes that lack antigen-specific receptors like BCRs or TCRs. While they express **CD16** (an Fc receptor) to mediate Antibody-Dependent Cellular Cytotoxicity (ADCC), they do not express immunoglobulins as their own surface antigens. **High-Yield Clinical Pearls for NEET-PG:** * **B-cell Markers:** Apart from sIg, other characteristic markers include **CD19, CD20, CD21** (receptor for EBV), and **MHC Class II**. * **Pre-B cells:** These express cytoplasmic $\mu$ heavy chains but do **not** yet have surface immunoglobulins. * **Mature B cells:** Characterized by the co-expression of **surface IgM and IgD**. * **Plasma Cells:** These are the end-stage cells that secrete antibodies but, notably, **lose** most of their surface immunoglobulin expression.
Explanation: ### Explanation **1. Why Class II HLA molecules is correct:** The scenario describes a **Tuberculin (Mantoux) test**, which is a classic example of **Type IV (Delayed-type) Hypersensitivity**. * **Initiation Phase:** When the purified protein derivative (PPD) is injected, it acts as an exogenous antigen. It is taken up by local **Antigen-Presenting Cells (APCs)**, such as Dendritic cells or Macrophages. * **Mechanism:** Exogenous antigens are processed via the endocytic pathway and presented on **Class II HLA molecules** (HLA-DP, DQ, DR). These molecules present the antigen to **CD4+ T-helper (Th1) cells**. * **Effector Phase:** Upon re-exposure, these sensitized Th1 cells release cytokines (IFN-γ, TNF-α), leading to macrophage activation and the characteristic induration seen 48–72 hours later. **2. Why the other options are incorrect:** * **Class I HLA molecules:** These present **endogenous** antigens (like viral proteins or tumor antigens) to **CD8+ Cytotoxic T cells**. While CD8+ cells play a minor role in some Type IV reactions, the primary initiation of the PPD response is CD4+ mediated via Class II. * **Class III HLA molecules:** These genes encode components of the **complement system** (C2, C4) and certain cytokines (TNF). They are not involved in the structural process of antigen presentation. * **Non-HLA dependent antigen presentation:** While some lipids are presented via CD1 molecules, protein derivatives like PPD strictly require HLA molecules for T-cell recognition. **3. Clinical Pearls for NEET-PG:** * **Type IV Hypersensitivity** is the only hypersensitivity reaction that is **cell-mediated** (no antibodies involved). * **Key Cells:** Macrophages (APCs) and Th1 cells. * **Key Cytokine:** **IFN-γ** (Interferon-gamma) is the most important cytokine for activating macrophages in this reaction. * **Histology:** Look for "perivascular cuffing" by lymphocytes and macrophages. * **Other Examples:** Contact dermatitis (nickel, poison ivy), Sarcoidosis, and Granuloma formation.
Explanation: **Explanation:** Hypersensitivity reactions are exaggerated immune responses that cause tissue damage. The correct answer is **Type III**, as it is specifically defined by the formation and deposition of **antigen-antibody (immune) complexes**. **1. Why Type III is Correct:** Type III hypersensitivity involves soluble antigens binding to antibodies (usually IgG or IgM) to form complexes. When these complexes are not cleared, they deposit in tissues (like blood vessel walls, joints, or kidneys), activating the **complement system**. This leads to the recruitment of neutrophils, release of lysosomal enzymes, and subsequent tissue inflammation (vasculitis). **2. Why Other Options are Incorrect:** * **Type I (Immediate):** Mediated by **IgE** antibodies binding to mast cells and basophils, leading to histamine release (e.g., Anaphylaxis, Asthma). * **Type II (Cytotoxic):** Mediated by **IgG or IgM** binding directly to antigens on **cell surfaces** or extracellular matrix, leading to cell lysis (e.g., Rheumatic fever, Goodpasture syndrome). * **Type IV (Delayed):** The only **cell-mediated** type. It involves T-lymphocytes (CD4+ or CD8+) rather than antibodies (e.g., Mantoux test, Contact dermatitis). **3. NEET-PG High-Yield Clinical Pearls:** * **Mnemonic (ACID):** **A**naphlyactic (I), **C**ytotoxic (II), **I**mmune-Complex (III), **D**elayed (IV). * **Classic Type III Examples:** Systemic Lupus Erythematosus (SLE), Post-streptococcal glomerulonephritis (PSGN), Serum Sickness (systemic), and Arthus Reaction (local). * **Key Feature:** Type III reactions typically involve a **low serum complement level** (C3, C4) because the complement is "consumed" during the inflammatory process.
Explanation: **Explanation:** The correct answer is **150 kDa**. Immunoglobulin G (IgG) is the most abundant antibody in human serum. Structurally, it is a monomer consisting of four polypeptide chains: two identical **Heavy (H) chains** (~50 kDa each) and two identical **Light (L) chains** (~25 kDa each). These are linked by disulfide bonds. * **Calculation:** (2 × 50) + (2 × 25) = **150 kDa**. **Analysis of Incorrect Options:** * **B (400 kDa):** This is approximately the molecular weight of **Secretory IgA (sIgA)**. While serum IgA is a monomer (160 kDa), secretory IgA exists as a dimer with a J-chain and a secretory component, totaling about 385–400 kDa. * **C (1000 kDa / 1 million Da):** This corresponds to **IgM**. Because IgM exists as a pentamer (five units of 180 kDa each plus a J-chain), it is the largest immunoglobulin, often referred to as the "millionaire molecule." * **D (1500 kDa):** This value does not correspond to any standard human immunoglobulin. **High-Yield Clinical Pearls for NEET-PG:** * **Abundance:** IgG is the most abundant (75-80%) and has the longest half-life (~23 days). * **Placental Transfer:** IgG is the **only** antibody that crosses the placenta, providing passive immunity to the fetus (specifically IgG1, IgG3, and IgG4). * **Functions:** It is the primary antibody in the secondary (anamnestic) immune response and is responsible for opsonization, complement activation (classical pathway), and neutralizing toxins. * **Subclasses:** There are four subclasses (IgG1 > IgG2 > IgG3 > IgG4). IgG3 is the most effective complement activator.
Explanation: ### Explanation **Correct Answer: B. Epitope** **Concept:** An **epitope**, also known as an **antigenic determinant**, is the specific chemical group or structural configuration on the surface of an antigen that is recognized by and binds to the **paratope** (the antigen-binding site) of an antibody or a T-cell receptor. A single antigen can possess multiple different epitopes, each capable of stimulating a distinct immune response. **Analysis of Incorrect Options:** * **A. Hapten:** These are small, non-immunogenic molecules (e.g., penicillin) that cannot induce an immune response on their own. They only become immunogenic when conjugated to a larger **carrier protein**. * **C. Complement:** This refers to a system of plasma proteins (C1-C9) that enhance (complement) the ability of antibodies and phagocytic cells to clear pathogens. They are part of the innate immune system, not a structural part of an antigen. * **D. Variable region:** This is a structural component of the **antibody** (specifically the N-terminal ends of the light and heavy chains), not the antigen. It contains the paratope which determines the antibody's specificity. **High-Yield NEET-PG Pearls:** * **Paratope vs. Epitope:** Remember the mnemonic: **P**aratope is on the **P**rotein (Antibody); **E**pitope is on the **E**nemy (Antigen). * **Valency:** The number of epitopes on an antigen surface is called its valency. * **Types of Epitopes:** * **Linear (Sequential):** Recognized based on amino acid sequence; remains intact even if the protein is denatured. * **Conformational (Discontinuous):** Formed by the 3D folding of the protein; lost if the protein is denatured. * **Adjuvant:** A substance injected with an antigen to enhance the immune response (e.g., Alum). Unlike haptens, adjuvants do not bond covalently to the antigen.
Explanation: ### Explanation **Correct Answer: B. Administration of anti-Rh antibodies to the mother after delivery** **Underlying Medical Concept:** Hemolytic Disease of the Newborn (HDN) or Erythroblastosis Fetalis occurs when an Rh-negative mother is sensitized to Rh-positive fetal RBCs. During delivery, fetal cells enter maternal circulation, triggering a primary immune response (IgM). In subsequent pregnancies, memory cells produce IgG antibodies that cross the placenta and attack fetal RBCs. Administering **anti-Rh antibodies (RhoGAM/Anti-D)** to the mother within 72 hours of delivery acts as **passive immunization**. These exogenous antibodies bind to and mask the Rh antigens on any fetal RBCs in the mother’s blood, leading to their clearance before her immune system can recognize them and initiate an active immune response (sensitization). **Why Incorrect Options are Wrong:** * **Option A:** Administering antibodies to the fetus is ineffective; the goal is to prevent the *mother's* immune system from forming its own long-term memory cells. * **Option C:** Transfusing the father has no clinical relevance to the mother’s immune sensitization process. * **Option D:** Transfusing an Rh-negative mother with Rh-positive blood would cause a massive transfusion reaction and accelerate sensitization, worsening the risk for future pregnancies. **High-Yield NEET-PG Pearls:** * **Type of Hypersensitivity:** HDN is a classic example of **Type II Hypersensitivity**. * **Timing of RhoGAM:** Standard protocol involves administration at **28 weeks of gestation** and again within **72 hours of delivery**. * **Diagnostic Tests:** * **Indirect Coombs Test (ICT):** Done on maternal serum to detect anti-Rh antibodies. * **Direct Coombs Test (DCT):** Done on fetal/neonatal cord blood to detect antibodies coated on fetal RBCs. * **Kleihauer-Betke Test:** Used to quantify the amount of fetal-maternal hemorrhage to determine the required dose of Anti-D.
Cells and Organs of Immune System
Practice Questions
Innate Immunity
Practice Questions
Adaptive Immunity
Practice Questions
Antigens and Antibodies
Practice Questions
Major Histocompatibility Complex
Practice Questions
Complement System
Practice Questions
Cytokines and Chemokines
Practice Questions
Hypersensitivity Reactions
Practice Questions
Autoimmunity and Autoimmune Diseases
Practice Questions
Immunodeficiency Disorders
Practice Questions
Transplantation Immunology
Practice Questions
Tumor Immunology
Practice Questions
Get full access to all questions, explanations, and performance tracking.
Start For Free