Question 1

Immunology: Which of the following statements about antigen epitopes (antigenic determinants) is incorrect?

Accepted Answer

Introduction: Epitopes are the specific structural features on antigens recognized by immune receptors. Understanding who recognizes what—B cells, antibodies, or T cells—is fundamental. This question asks you to identify the incorrect statement regarding epitope recognition patterns. Given Data / Assumptions: B-cell receptors (BCRs) and antibodies bind native, accessible structures (proteins, polysaccharides, lipids). T-cell receptors (TCRs) recognize peptides presented on MHC after antigen processing. Antigens often display many epitopes; cross-reactivity can occur when epitopes are shared. Concept / Approach: Antibody/BCR recognition favors native surface topologies (conformational or linear). T cells require processing into peptides and presentation by MHC. Therefore, the claim that B cells bind only processed epitopes is incorrect because it reverses the roles of B cells and T cells. Step-by-Step Solution: Review BCR/antibody binding: native macromolecular epitopes on intact antigens.Review TCR binding: peptide–MHC complexes arising from intracellular processing.Identify the inconsistency: saying B cells bind only processed epitopes contradicts immunologic principles.Select the incorrect statement accordingly. Verification / Alternative check: Experimental approaches (e.g., ELISA with native antigens) demonstrate antibody binding without antigen processing, while T-cell assays require peptide–MHC presentation, validating the distinction. Why Other Options Are Wrong: Shared epitopes and multiple epitopes per antigen: well established. Linear vs conformational epitopes: standard classification. T-cell recognition of peptide–MHC: core tenet of adaptive immunity. Common Pitfalls: Confusing epitope types seen by B cells vs T cells or assuming all recognition requires processing. Final Answer: B cells bind only processed (peptide-presented) epitopes and never native structures.

Question 2

In immunological dose–response, exposure to very low doses of antigen is most likely to induce which phenomenon?

Accepted Answer

Introduction: Immune responsiveness depends on antigen dose, timing, and context. At extremes of dosage, the immune system can become unresponsive rather than activated. This question targets the concept of low-zone tolerance—unresponsiveness induced by very small amounts of antigen, contrasted with high-zone tolerance at very high doses. Given Data / Assumptions: Very low antigen doses may fail to provide adequate costimulation or T-cell help. Tolerance can be peripheral (e.g., anergy) or central; here we focus on dose-dependent peripheral effects. Outcome measures include clonal deletion, anergy, or regulatory cell engagement. Concept / Approach: When antigen levels are too low, lymphocytes may receive insufficient signals (signal 1 without adequate signal 2), driving anergy rather than productive activation. This phenomenon is termed low-zone tolerance and is antigen-specific. It is distinct from immunological ignorance (lack of encounter) and from hypersensitivity (pathologic over-reaction). Step-by-Step Solution: Consider signal requirements: antigen recognition alone is not enough.At very low dose, APC activation and costimulatory molecules may be inadequate.Outcome: anergy or tolerance pathways dominate over effector differentiation.Memory formation is weak or absent under tolerogenic low-dose conditions. Verification / Alternative check: Experimental systems show bell-shaped dose–response curves: strong immunity at intermediate doses, tolerance at very low or very high doses (low-zone and high-zone tolerance, respectively). Why Other Options Are Wrong: Hypersensitivity: requires prior sensitization and is not dictated purely by tiny doses. Immunological ignorance: implies lack of encounter, not low-dose signaling. Low-zone immunity: contradicts tolerogenic outcome. Polyclonal activation: typically driven by mitogens or superantigens, not trace antigen doses. Common Pitfalls: Confusing low-zone tolerance with lack of exposure, or assuming any dose is stimulatory if repeated often (context and costimulation matter). Final Answer: Low-zone tolerance (antigen-specific unresponsiveness)

Question 3

CD (cluster of differentiation) antigens: which statement best describes their primary immunological use and meaning?

Accepted Answer

Introduction: CD (cluster of differentiation) designations provide a universal nomenclature for leukocyte surface molecules. They are essential for identifying, sorting, and studying immune cells. This question asks for the best description of their role in immunology and research practice. Given Data / Assumptions: CD molecules are surface proteins defined by specific monoclonal antibody reactivity. They can serve as receptors, coreceptors, adhesion molecules, or signaling components. Phenotyping often relies on panels of CD markers (e.g., CD3, CD4, CD8, CD19, CD56). Concept / Approach: The key utility of CD antigens is as standardized markers to classify leukocyte subsets and enable their physical separation (e.g., magnetic beads, flow cytometry). While certain CDs have receptor functions, the unifying concept is their use as reproducible surface identifiers rather than direct antigen-recognition receptors like TCR/BCR. Step-by-Step Solution: Define CD: consensus-based labels for specific surface molecules.Link to practice: used in gating strategies and magnetic sorting.Clarify function: some CDs are receptors, adhesion molecules, or coreceptors, but classification utility is primary.Select the statement emphasizing standardized phenotyping and separation. Verification / Alternative check: Clinical immunophenotyping (e.g., HIV monitoring with CD4 counts) and hematologic diagnostics rely on CD markers to define cell populations, illustrating their practical role. Why Other Options Are Wrong: Direct antigen recognition: performed by TCR/BCR, not generic CD markers. One cell type only: many CDs are shared across subsets or change with activation. Soluble antibodies: CDs are cell-surface molecules; antibodies detect them. Exclusively intracellular: contradicts their role as surface markers. Common Pitfalls: Assuming all CDs have the same function or that they uniquely define a single lineage without context (activation state and combinations matter). Final Answer: They are standardized surface markers used to classify and separate immune cell subsets (e.g., flow cytometry).

Question 4

Immunochemistry: A small non-immunogenic molecule can elicit an immune response after covalent conjugation to which type of macromolecule?

Accepted Answer

Introduction: Small molecules (haptens) are generally not immunogenic on their own. However, when covalently linked to a large, immunogenic macromolecule, they can induce specific antibody responses. This question asks you to identify the macromolecule that provides immunogenicity upon conjugation. Given Data / Assumptions: Haptens are small and non-immunogenic without a protein scaffold. Conjugation presents the hapten in a multivalent, T-cell-help-competent context. Protein carriers supply T-cell epitopes required for help-dependent antibody responses. Concept / Approach: The correct term for the macromolecule that confers immunogenicity is the carrier. The hapten is the small molecule; the adjuvant is a formulation component that enhances responses but is not the covalently linked scaffold; mitogens and superantigens activate many lymphocytes nonspecifically and are unrelated to hapten-carrier conjugation. Step-by-Step Solution: Define hapten: small, non-immunogenic antigenic determinant.Identify carrier: immunogenic protein that provides T-cell epitopes.Mechanism: conjugation enables processing/presentation → T-cell help → anti-hapten antibodies.Conclusion: the macromolecule is the carrier. Verification / Alternative check: Classical experiments (e.g., dinitrophenyl conjugated to keyhole limpet hemocyanin) demonstrate robust anti-hapten responses only when a protein carrier is present. Why Other Options Are Wrong: Adjuvant: boosts immunity but is not the covalent scaffold. Hapten: the small molecule itself, not the macromolecular partner. Mitogen/superantigen: cause polyclonal activation, not specific hapten responses. Common Pitfalls: Confusing the terms hapten and carrier or assuming adjuvants must be covalently attached. Final Answer: Carrier

Question 5

Which of the following factors does NOT influence the ability of an antigen to be immunogenic (to induce an immune response)?

Accepted Answer

Introduction: Immunogenicity depends on properties of the antigen and the context of exposure. This question asks you to identify a factor that is irrelevant to general immunogenic potential in typical experimental or clinical settings. Given Data / Assumptions: Larger, complex, and aggregated antigens are usually more immunogenic. Dose and route influence whether tolerance or immunity develops. Adjuvants enhance antigen presentation and costimulation. Concept / Approach: Tissue-specific entry into an organ like the thyroid is not a general determinant of whether an antigen is immunogenic. By contrast, size, dose, aggregation, adjuvants, and route are classical determinants that modulate immune activation versus tolerance. Step-by-Step Solution: List canonical determinants: size, complexity, dose, route, adjuvant, foreignness.Recognize aggregation increases APC uptake and immunogenicity.Note that organ tropism to the thyroid is not a standard factor in immunogenicity.Select the non-determinant accordingly. Verification / Alternative check: Textbook frameworks of immunogenicity emphasize molecular and exposure parameters rather than specific organ entry, except in specialized autoimmune contexts not implied here. Why Other Options Are Wrong: Aggregation: promotes uptake and danger signaling. Dose: too low or too high can induce tolerance; intermediate favors immunity. Size/complexity: larger, complex molecules elicit stronger responses. Adjuvant/route: shape innate cues and lymph node targeting. Common Pitfalls: Overinterpreting tissue tropism as a driver of immunogenicity outside autoimmunity models. Final Answer: Ability of the antigen to enter the thyroid specifically

Question 6

During the lag phase after first antigen exposure and before adaptive immune responses are detectable, which process best explains what is happening?

Accepted Answer

Introduction: The primary immune response shows a lag before specific antibodies or T-cell effectors become detectable. This question examines the immunological events that occur during this window and clarifies the respective roles of innate and adaptive immunity. Given Data / Assumptions: Innate immunity responds within minutes to hours (e.g., complement, phagocytes, interferons). Adaptive responses require antigen processing/presentation, clonal selection, proliferation, and differentiation. Naive lymphocytes with diverse specificities already exist prior to exposure. Concept / Approach: During the lag phase, innate defenses contain the threat while antigen-specific lymphocytes engage in activation and clonal expansion in lymphoid organs. Adaptive effectors are not yet abundant, which explains why specific serum antibodies or cytotoxic activity are initially undetectable. Step-by-Step Solution: Antigen is captured by dendritic cells and processed.Antigen-bearing APCs migrate to lymph nodes and present peptide–MHC to naive T cells.Clonal selection and proliferation occur; B cells receive T-cell help and begin class switching and affinity maturation.Innate mechanisms (complement, phagocytes, inflammation) are active immediately to limit spread. Verification / Alternative check: Time courses show detectable IgM appears after days, with IgG and effector T-cells later. Early cytokines and innate markers rise prior to adaptive readouts, confirming the sequence. Why Other Options Are Wrong: Antigen hiding in macrophages: macrophages process and present antigen; they do not sequester it to evade detection. Innate blocking adaptive: innate signals are generally required to activate adaptive immunity. De novo generation of specificity in bone marrow: specificity arises from pre-existing naive clones; bone marrow production is ongoing but not the immediate source of response. Peak adaptive effectors present but undetectable antibodies: contradicts observed kinetics. Common Pitfalls: Assuming detection failure means no activity is occurring; in reality, priming and expansion take time before effectors are measurable. Final Answer: Innate immune effectors act immediately while antigen-specific clones are expanding

Question 7

T cell antigen recognition in adaptive immunity  Which statement best describes the requirements and properties of antigen recognition by T lymphocytes in vertebrates?

Accepted Answer

Introduction: T lymphocytes recognize short peptide fragments derived from proteins, a process central to cell-mediated immunity. Unlike B cells, which bind native antigens via surface immunoglobulin, T cells engage peptide–MHC complexes using the T cell receptor (TCR). Understanding this distinction clarifies why protein denaturation usually does not impair T cell epitope recognition. Given Data / Assumptions: T cells recognize peptides presented by MHC molecules on antigen-presenting cells. Peptides are generated after antigen processing (proteolysis). Denaturation disrupts conformational epitopes but not the primary amino acid sequence. TCR is not an antibody; it is a distinct receptor with MHC restriction. Concept / Approach: Because T cells recognize linear peptides bound to MHC, the native 3D conformation of a protein is not required. Denaturation may even facilitate processing. In contrast, B cell epitopes are often conformational and can be lost upon denaturation. Step-by-Step Solution: 1) Antigen enters an antigen-presenting cell and is degraded into peptides.2) Peptides load onto MHC class I or class II molecules.3) The TCR interacts with the peptide–MHC complex; recognition depends on peptide sequence and MHC, not native folding.4) Therefore, denaturation typically does not reduce (and can enhance) T cell epitope generation. Verification / Alternative check: Experimental systems show T cells responding to chemically denatured proteins after processing, whereas many B cell antibodies fail to bind denatured antigens because conformational epitopes collapse. Why Other Options Are Wrong: Option A: T cells use TCRs, not membrane antibodies (those are on B cells). Option C: MHC is essential (MHC restriction); removing MHC abrogates TCR recognition. Option D: Antigen exposure during thymic maturation leads to tolerance, not a requirement for later recognition. Option E: Some lipids and polysaccharides can be presented via specialized pathways, but direct recognition without presentation is not the general rule for conventional αβ T cells. Common Pitfalls: Confusing B cell conformational epitopes with T cell linear peptide epitopes; assuming all antigen recognition mechanisms are identical across lymphocyte subsets. Final Answer: Denaturation of the antigen generally does not reduce T cell epitope recognition

Question 8

Definition of a pathogen and examples  In the context of infectious disease, what can be considered a pathogen?

Accepted Answer

Introduction: A pathogen is any biological agent capable of causing disease in a host. This question assesses basic infectious disease terminology and recognition of common pathogen types. Given Data / Assumptions: Pathogens include diverse classes: viruses, bacteria, fungi, protozoa, helminths, and prions. “Agent that causes disease” is a generic definition. Visibility under a light microscope is not a criterion; many viruses are submicroscopic. Concept / Approach: Since both viruses and bacteria are well-established causes of disease, and a pathogen is by definition any disease-causing agent, a comprehensive option that encompasses all is correct. Step-by-Step Solution: 1) Define pathogen as “disease-causing agent.”2) Recognize that viruses and bacteria are subtypes of pathogens.3) Therefore, the inclusive choice that lists all correct subtypes and definitions is the best answer. Verification / Alternative check: Textbook definitions of pathogenesis consistently categorize viruses and bacteria among primary pathogen types, alongside other microorganisms. Why Other Options Are Wrong: Option A, B, C: Each is partially correct but incomplete compared to the inclusive correct choice. Option E: Size or light-microscopy visibility does not determine pathogenicity; viruses are not visible by standard light microscopy but are pathogens. Common Pitfalls: Assuming “pathogen” refers only to living cells; viruses and prions challenge that assumption. Final Answer: All of these

Question 9

Penicillin allergy and immunochemistry  Penicillin alone does not induce antibodies but, after covalently binding to serum proteins, the complex elicits an antibody response in some people. Penicillin is therefore best classified as what?

Accepted Answer

Introduction: Small molecules that fail to induce an immune response on their own but can become antigenic when attached to larger carriers are called haptens. Classic drug allergies, including penicillin hypersensitivity, illustrate this principle in clinical immunology. Given Data / Assumptions: Free penicillin is too small/simple to be immunogenic by itself. Penicillin can form covalent adducts with host proteins (e.g., penicilloyl–protein). The penicillin–protein conjugate can be processed and presented, eliciting antibodies. Concept / Approach: By definition, a hapten is non-immunogenic alone but becomes antigenic when linked to a carrier, enabling T cell help and B cell activation. The scenario described matches this definition precisely. Step-by-Step Solution: 1) Identify the failure of the free molecule to induce antibodies (non-immunogenic alone).2) Recognize covalent binding to serum proteins creates a new antigenic determinant.3) Conclude the small molecule behaves as a hapten requiring a carrier for immunogenicity. Verification / Alternative check: Drug hypersensitivity literature frequently refers to penicillin as a hapten that modifies self-proteins, enabling T-dependent antibody production, clinically manifesting as allergy. Why Other Options Are Wrong: Option A/C: These imply intrinsic immunogenicity, which contradicts the premise. Option D: While the conjugate is antigenic, the classification of the small molecule itself is “hapten,” not “both.” Option E: Penicillin clearly can elicit responses once conjugated; it is not purely tolerogenic. Common Pitfalls: Confusing antigenicity (binding by antibodies) with immunogenicity (ability to induce an immune response). A hapten is antigenic only when coupled to a carrier. Final Answer: A hapten

Question 10

Where are specific lymphocytes activated after an antigen is injected into peripheral tissue?  Select the most appropriate anatomical site for primary activation.

Accepted Answer

Introduction: Antigen location determines where adaptive immune responses initiate. After antigens enter peripheral tissues via injection or injury, antigen-presenting cells transport processed antigen to regional lymph nodes where naive lymphocytes are primed. Given Data / Assumptions: Antigen is introduced into peripheral tissue (not directly into blood or mucosa). Dendritic cells migrate via afferent lymphatics to nearby nodes. Naive T and B cells recirculate through secondary lymphoid organs. Concept / Approach: The immune system compartmentalizes surveillance. Tissue antigens drain to regional lymph nodes; blood-borne antigens are filtered by the spleen; mucosal antigens are sampled by MALT. Matching the route of entry to the corresponding organ identifies the activation site. Step-by-Step Solution: 1) Identify antigen entry: peripheral tissue injection.2) Dendritic cells capture/process antigen and migrate to the nearest node.3) In the draining lymph node, antigen-bearing APCs present peptides to naive T cells; B cells encounter antigen and receive T cell help.4) Activated lymphocytes proliferate and differentiate, then exit via efferent lymphatics to circulation. Verification / Alternative check: Clinical observation: ipsilateral lymphadenopathy near injection sites reflects activation and clonal expansion in local nodes. Why Other Options Are Wrong: Option A: Blood is a conduit, not the primary activation site. Option C: MALT specializes in mucosal antigen (e.g., gut, respiratory tract), not typical intradermal/subcutaneous injections. Option D: The spleen focuses on antigens in the bloodstream. Option E: The thymus is for T cell development, not antigen-driven activation. Common Pitfalls: Assuming all antigens activate in the spleen; forgetting route-specific immune organ specialization. Final Answer: Draining lymph nodes

Question 11

Primary sites of lymphocyte activation by antigen  Where are naive lymphocytes typically activated after encountering antigen from peripheral tissues?

Accepted Answer

Introduction: Adaptive immune responses are initiated in specialized secondary lymphoid tissues. Recognizing the correct anatomical site helps interpret clinical signs such as regional lymph node enlargement during infections or after vaccination. Given Data / Assumptions: Antigen originates from peripheral tissues (e.g., skin, muscle). Dendritic cells transport processed antigen via lymphatics. Naive T and B cells continuously traffic through lymph nodes. Concept / Approach: Lymph nodes are designed for antigen presentation: afferent lymph brings antigen/APCs; distinct microanatomical zones (T cell area, B cell follicles) facilitate activation and help. Step-by-Step Solution: 1) Tissue antigen is captured by antigen-presenting cells.2) APCs migrate to the nearest lymph node.3) T cells recognize peptide–MHC on APCs; B cells recognize native antigen and receive T help.4) Clonal expansion occurs, generating effector and memory cells. Verification / Alternative check: Vaccine responses correlate with activation in regional lymph nodes, evidenced by germinal center formation and node swelling. Why Other Options Are Wrong: Option A: Blood transports cells and antigen but is not the main activation site. Option B: Bone marrow is a primary organ for hematopoiesis and some B cell development, not peripheral activation. Option C: Liver filters blood and performs metabolic functions; not a canonical activation center. Option E: Skin contains innate sentinels, but naive lymphocyte activation requires lymphoid organs. Common Pitfalls: Confusing lymphoid development sites (bone marrow, thymus) with activation sites (lymph nodes, spleen, MALT). Final Answer: Lymph nodes

Question 12

Designing antiviral vaccines for cytotoxic T cell (CD8+) activation  Which vaccine formulation is most likely to elicit strong cytotoxic T lymphocyte responses?

Accepted Answer

Introduction: Cytotoxic T lymphocytes (CTLs, CD8+) recognize peptides presented on MHC class I, typically derived from endogenous proteins synthesized inside infected cells. Vaccine designs that place antigen in the cytosol efficiently prime CTLs. Given Data / Assumptions: MHC I presentation favors intracellularly produced antigens. Live attenuated viruses replicate to limited degrees and generate endogenous antigen. Inactivated or purely extracellular antigens mainly drive MHC II helper responses unless cross-presentation occurs. Concept / Approach: Live attenuated vaccines mimic natural infection, ensuring robust MHC I presentation and strong CTL memory. While cross-presentation can occur with certain adjuvants or delivery systems, it is less reliable than true intracellular synthesis. Step-by-Step Solution: 1) Identify pathway: CTLs require peptide–MHC I derived from intracellular antigen.2) Select vaccine type that delivers antigen to the cytosol: live attenuated virus.3) Predict strong CD8+ priming with additional CD4+ help for optimal memory.4) Conclude live attenuated formulation is most consistent for robust CTL activation. Verification / Alternative check: Historically, live attenuated viral vaccines (where safe) generate durable cellular and humoral immunity, including CTL responses. Why Other Options Are Wrong: Option A: High dose inactivated virus favors antibody responses; CTL priming is limited without cross-presentation. Option B: Adjuvants enhance innate signals but cannot substitute for antigen and proper presentation pathway. Option D/E: Exogenous peptides/subunits may not reach MHC I efficiently unless specialized delivery or cross-presentation is ensured. Common Pitfalls: Assuming dose or adjuvant alone determines CTL responses; the intracellular location of antigen synthesis is the key determinant. Final Answer: Live virus (attenuated) capable of intracellular replication

Antigen Questions