75 free MCQs on Immune System, each with its own worked answer and explanation. Innate and adaptive immunity, B cells, T cells, antibodies, vaccines, and immune disorders. Critical for NEET.
75 practice questions on Immune System, sorted Easy → Hard. Try each one first, then open its answer page for the worked explanation. Want the full theory first? Read the Immune System notes.
An antibody is Y-shaped, with two identical antigen-binding sites at the tips of the variable regions - each shaped to recognise one specific antigen - while the constant (Fc) region at the base is recognised by immune cells to trigger further responses.
Easy - 25 questions
Q1.
The type of immunity present from birth and non-specific in action is:
What is the difference between humoral and cell-mediated immunity?
A Both forms of immunity are sometimes mistakenly thought to be functionally identical and to operate through the same mechanism as widely reported in standard practice
B Humoral immunity involves B cells and antibodies (against extracellular pathogens); cell-mediated immunity involves T cells and kills infected cells directly
C Humoral immunity is sometimes thought to act much faster than cell-mediated immunity in most clinical cases under most conditions encountered as frequently observed in practice
D Cell-mediated immunity is sometimes mistakenly described as carried out by B cells, with humoral immunity carried out by T cells in many documented cases
A A group of receptor proteins that are expressed mainly on the surface membrane of T cells specifically under typical conditions according to standard textbooks
B A system of ~30 plasma proteins that are activated by antigen-antibody complexes and lead to pathogen lysis, inflammation, and phagocytosis
C A type of chemical adjuvant compound that is added to vaccine formulations to boost their overall effectiveness in general practice as frequently described
D The cellular machinery contained within plasma cells that is mainly responsible for producing antibodies in most textbook accounts during normal conditions
A Antibodies are sometimes mistakenly thought to be produced through a largely random, unregulated process unrelated to the actual antigen encountered as generally observed in typical laboratory settings
B Each B cell has receptors for one specific antigen; when that antigen binds, the B cell is selected and clonally expands to produce many identical plasma cells secreting specific antibody
C T cells are sometimes mistakenly thought to randomly select which B cells become activated antibody-secreting plasma cells in the lymph node under usual circumstances according to most researchers
D The immune system is sometimes mistakenly thought to actively choose in advance which future pathogens it will need to defend against in the majority of cases studied as widely reported
What is ELISA and how is it used in HIV diagnosis?
A A DNA sequencing-based laboratory test that directly reads the full genome sequence of suspected viral pathogens in many documented cases according to conventional understanding
B Enzyme-Linked Immunosorbent Assay: detects antibodies or antigens using enzyme-labeled antibodies; used to screen blood samples for HIV antibodies
C A Western blot confirmatory test that separates and identifies viral proteins using gel electrophoresis techniques in routine practice overall
D A laboratory culture method used specifically to grow and propagate live HIV virus particles in cell culture in most cases under typical conditions
A A specific type of antibody secreted mainly by activated plasma cells residing within lymph nodes under usual circumstances according to most researchers
B Signaling proteins that regulate immune cell communication and function: interleukins (IL-1, IL-2, IL-4), interferons, TNF, chemokines
C Complement proteins that circulate freely and become activated by antigen-antibody complex formation over time in the majority of cases studied
D Enzymes secreted by phagocytes that chemically digest engulfed antigens inside lysosomal compartments over time as widely reported
What is the mechanism by which mast cells cause allergic reactions?
A Mast cells produce and secrete broad-spectrum antibiotic compounds that directly kill invading bacteria over time in most cases under typical conditions
B IgE binds to mast cell surface receptors; when allergen crosslinks IgE, mast cells degranulate and release histamine causing allergy symptoms
C Mast cells differentiate directly into largely functional cytotoxic T lymphocytes upon repeated allergen exposure according to standard textbooks
D Mast cells engulf and phagocytose allergen particles within their cytoplasm before slowly digesting them in general practice as frequently described
A Producing antibodies that are specifically directed against the body's own self proteins, a process that actually drives autoimmune disease rather than preventing it
B Central tolerance (clonal deletion of self-reactive T/B cells in thymus/bone marrow) and peripheral tolerance (anergy, Treg suppression)
C Relying mainly on antibody production with little other contributing mechanism, with little role for clonal deletion in the thymus or bone marrow
D Relying mainly on the formation of long-lived immunological memory cells, despite memory cells having no role in preventing self-reactivity
A Activation occurring through hormonal signaling pathways alone, without any antigen involvement, bypassing the classical, lectin, and alternative pathways
B Classical (antibody-bound antigen), lectin (mannose on pathogens), or alternative (directly on pathogen surfaces) pathways, leading to MAC pore formation
C Activation that is mediated mainly by circulating T lymphocytes, despite T cells playing no direct role in triggering any complement pathway
D A process that results mainly in the direct killing of pathogens, with little contribution toward opsonization or inflammatory signaling
The role of surfactant protein SP-A in innate immunity is:
A Reducing alveolar surface tension alone, with no other contributing immune function, a role actually performed by the lipid component of surfactant, not the SP-A protein
B Pattern recognition (opsonizing bacteria/viruses by binding their surface patterns) to enhance phagocytosis by alveolar macrophages
C Directly stimulating B cells to increase circulating antibody production, despite SP-A acting locally on macrophages rather than systemically on B lymphocytes
D Actively inhibiting the complement cascade within the alveolar space, despite SP-A enhancing rather than suppressing local innate defence mechanisms
What is the mechanism of positive and negative selection during T cell development in the thymus?
A Both processes select for self-reactive T cells, expanding rather than eliminating clones capable of attacking the body's own healthy tissues, undermining tolerance according to most researchers
B Positive selection: T cells that can bind self-MHC survive; negative selection: T cells with too high affinity for self-MHC+self-peptide are deleted (central tolerance); remainder are self-tolerant
C Positive selection deletes T cells; negative selects them, an inversion of their actual roles in shaping a self-tolerant T cell repertoire during thymic development in the majority of cases studied
D Both are sometimes thought to occur in bone marrow, rather than within the thymic cortex and medulla where genuine T cell selection actually unfolds in vivo over time as widely reported in standard practice
A HIV is sometimes thought to have few antigens recognizable by the host immune system, leaving it largely undetectable to immune surveillance under most conditions encountered
B HIV integrates its genome into CD4<sup>+</sup> T cell DNA as a provirus; mutates rapidly (high error-rate reverse transcriptase); infects and destroys CD4<sup>+</sup> T cells; can enter latency
C HIV is sometimes thought to mainly infect B cells, sparing CD4<sup>+</sup> helper T cells from infection and the progressive depletion that defines AIDS as frequently observed in practice
D HIV is sometimes thought to produce antibodies against itself specifically to neutralize its own envelope glycoproteins before any host immune response develops in many documented cases
What is the complement membrane attack complex (MAC) and how does it kill bacteria?
A MAC is a protein that attracts phagocytes to the site of infection rather than forming any pore in a pathogen's membrane directly according to conventional understanding
B MAC is formed by polymerization of C5b, C6, C7, C8, and multiple C9 proteins into a pore in the bacterial membrane, causing osmotic lysis
C MAC is an antibody complex generated by plasma cells rather than assembled from complement components C5b through C9 specifically in routine practice
D MAC activates T cells directly, bypassing any membrane-damaging or pore-forming activity altogether in the process overall in most cases
What is tolerance and how does central vs peripheral tolerance differ?
A Tolerance is sometimes thought to mean weak immunity overall, rather than describing the specific mechanisms that prevent harmful immune reactions against the body's own healthy tissue under typical conditions according to standard textbooks in general practice
B Tolerance prevents autoimmunity. Central tolerance: deletion of self-reactive lymphocytes in primary lymphoid organs (thymus for T, bone marrow for B). Peripheral tolerance: silencing of autoreactive cells that escape to periphery (anergy, Treg suppression, AICD)
C Tolerance is sometimes thought to occur mainly in T cells, with B lymphocytes maturing in the bone marrow rarely undergoing any comparable process of central negative selection as frequently described in most textbook accounts during normal conditions as generally observed
D Central tolerance is sometimes thought to occur mainly in lymph nodes, rather than within the thymus itself, where developing T lymphocytes actually undergo deletion of self-reactive clones in typical laboratory settings under usual circumstances according to most researchers
What is somatic hypermutation and affinity maturation in antibody responses?
A Random mutation in all cells of the body is sometimes thought to occur uniformly at an identical rate, rather than being targeted to B lymphocyte variable region genes specifically in the majority of cases studied as widely reported in standard practice
B In germinal centers, B cell variable region genes undergo accelerated mutation (somatic hypermutation); B cells with higher affinity for antigen are positively selected (affinity maturation), producing increasingly effective antibodies over time
C Antibody genes are sometimes thought to mutate in T cells, a process that instead occurs specifically within B lymphocyte immunoglobulin variable region genes inside germinal centers under most conditions encountered as frequently observed in practice
D Affinity maturation is sometimes thought to decrease antibody effectiveness, when in fact this positive-selection-driven process steadily increases antibody affinity over successive rounds in many documented cases according to conventional understanding
How do cytotoxic T lymphocytes (CTLs) kill target cells?
A By releasing antibodies synthesized and secreted directly into the bloodstream by activated plasma cells located nearby in routine practice overall in most cases
B By releasing perforin (pore-forming protein) and granzymes (serine proteases) that trigger apoptosis in target cells, plus FasL binding Fas to trigger apoptosis
C By phagocytosis of target cells, engulfing the entire infected cell whole rather than triggering its controlled apoptosis process under typical conditions
D By producing toxic cytokines mainly, without much direct involvement of perforin, granzymes, or Fas-FasL signaling generally according to standard textbooks
What is the difference between innate pattern recognition and adaptive antigen recognition?
A Both are sometimes thought to use the same receptors, with germline-encoded TLRs and the somatically diverse, V(D)J-recombined TCR/BCR repertoire being functionally interchangeable in practice in general practice as frequently described
B Innate uses germline-encoded PRRs (TLRs, NLRs) that recognize conserved PAMPs on pathogens (broad, rapid, no memory); adaptive uses V(D)J recombination-generated diverse TCR/BCR for specific antigens (slow, memory-forming)
C Adaptive is sometimes thought to be faster than innate, despite adaptive immune responses actually taking several days to largely develop, in contrast to rapid innate responses observed in most textbook accounts during normal conditions
D Innate is sometimes thought to have memory while adaptive does not, when in fact long-lived immunological memory is widely understood to be a defining feature of the adaptive system instead as generally observed in typical laboratory settings
What is ADCC (Antibody-Dependent Cell-Mediated Cytotoxicity)?
A Direct killing of pathogens by antibodies alone, without requiring much Fc receptor-bearing effector cell involvement generally under usual circumstances
B IgG antibodies bind to antigens on target cells; NK cells and macrophages bind the Fc region via Fc receptors and kill the target cell without endocytosis
C Complement-mediated killing via the membrane attack complex, largely independent of any antibody or Fc receptor engagement process according to most researchers
D T cell killing using antibodies, even though cytotoxic T cells normally recognize target cells via TCR-MHC interaction, rarely antibodies directly in the majority of cases studied
What is immunological memory at the cellular and molecular level?
A It is sometimes thought to be stored mainly in antibodies circulating freely within the blood serum, without requiring much long-lived memory lymphocyte population as widely reported in standard practice under most conditions encountered
B Long-lived memory B cells (with high-affinity BCR, class-switched IgG) and memory T cells (effector memory and central memory subsets) persist for years/decades; on re-exposure, they rapidly proliferate and produce faster, stronger responses
C Memory is sometimes thought to reside mainly in macrophages, despite macrophages clearly lacking the antigen-specific receptors actually needed to mediate lasting immunological memory as frequently observed in practice in many documented cases
D Memory is sometimes thought to last mainly 6 months, whereas memory responses are in fact well documented to persist for many years or decades after antigen exposure according to conventional understanding in routine practice overall in most cases
What is the mechanism of immune evasion by Mycobacterium tuberculosis?
A It is sometimes thought to have few antigens to detect, despite mycobacterial cell wall lipids being readily detected by macrophage pattern recognition receptors under typical conditions according to standard textbooks
B It inhibits phagosome-lysosome fusion in macrophages, allowing it to survive and replicate inside the phagosome; it also recruits epithelial cells to form granulomas where it persists in latency
C It is sometimes thought to release antibiotics that would actively kill competing bacteria, rather than inhibiting host phagosome-lysosome fusion as it really does in general practice as frequently described
D It is sometimes thought to grow mainly in blood, not cells, when it instead survives and actively replicates specifically inside resident macrophage phagosomes in most textbook accounts during normal conditions
What is the molecular basis of anaphylaxis and its treatment with epinephrine?
A Anaphylaxis is sometimes thought to be a bacterial infection caused directly by invading bacterial or viral microorganisms, rather than by an IgE-mediated hypersensitivity reaction to an allergen as generally observed in typical laboratory settings under usual circumstances
B Anaphylaxis: IgE-mediated degranulation of mast cells and basophils releases massive histamine, causing vasodilation, bronchospasm, and potentially fatal shock. Epinephrine (adrenaline) reverses it by vasoconstriction (alpha-1 receptors) and bronchodilation (beta-2 receptors)
C Anaphylaxis is sometimes thought to be caused by T cells through direct cytotoxic killing of target tissue cells, rather than via the IgE-triggered mast cell degranulation that actually drives it according to most researchers in the majority of cases studied as widely reported
D Epinephrine is sometimes thought to increase histamine production, when in real clinical practice it instead reliably reverses an active anaphylactic reaction through vasoconstriction and bronchodilation in standard practice under most conditions encountered as frequently observed in practice