Immune System — Practice Questions with Answers

Q1.

The first line of defence against pathogens is

• A Antibodies circulating in the blood plasma
• B Skin and mucous membranes
• C T lymphocytes patrolling the lymphatic system
• D Fever raising the body's core temperature

Q2.

Where do B lymphocytes mature?

• A Thymus
• B Spleen
• C Bone marrow
• D Lymph nodes

Q3.

Where do T lymphocytes mature?

• A Bone marrow
• B Thymus
• C Spleen
• D Lymph nodes

Q4.

What do antibodies do?

• A Inject toxic enzymes directly into pathogen cells to rupture their membranes
• B Recognize and bind to specific antigens on pathogens, marking them for destruction
• C Trigger localized inflammation and swelling at the site of pathogen entry
• D Digest engulfed pathogens inside the phagocyte's lysosomal compartments

Q5.

What is an antigen?

• A A specialized type of circulating white blood cell frequently found within lymph nodes and spleen
• B Any foreign molecule (usually protein/polysaccharide) that triggers an immune response
• C An antibody protein produced specifically by activated plasma cells against one pathogen
• D A weakened or otherwise inactivated pathogen preparation frequently used in a vaccine dose

Q6.

Active immunity means

• A Receiving ready-made antibodies transferred from another source or organism
• B The body produces its own antibodies after exposure to antigen
• C Immunity that is already present in an individual from the moment of birth
• D Antibodies passed from mother to fetus across the placental barrier

Q7.

Passive immunity is obtained by

• A Becoming vaccinated with a weakened or killed pathogen preparation administered each season
• B Receiving pre-formed antibodies from another source (e.g., antiserum, breast milk)
• C Recovering naturally after successfully surviving a prior natural infection episode
• D Taking a long prescribed course of broad-spectrum antibiotic medication

Q8.

Which cells produce antibodies?

• A T cells, which instead directly attack infected cells
• B Macrophages, which primarily engulf and digest pathogens
• C Plasma cells (activated B cells)
• D Natural killer cells, which target virus-infected cells

Q9.

HIV destroys which type of cell?

• A B cells
• B CD8+ T cells
• C CD4+ T helper cells
• D Macrophages only

Q10.

What is the purpose of vaccination?

• A To directly kill any bacteria that are already circulating in the bloodstream using strong chemical agents
• B To stimulate immune memory without causing disease, so the body can respond faster to future infection
• C To directly supply the body with a temporary dose of ready-made antibodies against one disease
• D To permanently and substantially increase the total circulating white blood cell count in the body

Q11.

What is the main antibody class in blood serum?

• A IgA
• B IgM
• C IgE
• D IgG

Q12.

Lysozyme found in tears and saliva protects by

• A Producing antibodies against incoming airborne pathogens
• B Digesting the cell walls of bacteria
• C Activating cytotoxic T cells at mucosal surfaces
• D Triggering phagocytosis by resident neutrophils

Q13.

What causes the symptoms of inflammation (redness, swelling, heat, pain)?

• A Direct mechanical damage inflicted on tissue by the invading pathogen itself over time
• B Release of histamine and other chemicals that increase blood flow and vascular permeability
• C Activation of cytotoxic T cells that are circulating near the wound site
• D Formation of new antibodies by plasma cells residing within nearby lymph nodes

Q14.

What is the role of memory cells in immunity?

• A They attack and lyse pathogens directly on contact, without ever needing antigen recognition first
• B They remain in the body long-term and enable rapid, stronger response on re-exposure to the same antigen
• C They synthesize antibiotic-like compounds that directly and immediately kill invading bacteria
• D They respond in an identical, non-specific way to absolutely any antigen they ever encounter

Q15.

Which antibody class is found in secretions like saliva, breast milk, and tears?

• A IgG
• B IgM
• C IgA
• D IgE

Q16.

Natural killer (NK) cells are part of which immune response?

• A Adaptive (specific) immunity
• B Innate (non-specific) immunity
• C Both adaptive and innate
• D Passive immunity

Q17.

Which process do neutrophils use to destroy pathogens?

• A Secreting antibodies directly into the bloodstream
• B Phagocytosis (engulfing and digesting pathogens)
• C Releasing antiviral interferon signaling proteins
• D Raising local tissue temperature to kill germs

Q18.

What type of vaccine is MMR?

• A Killed (inactivated) vaccine preparation
• B Subunit vaccine using isolated antigen
• C Live attenuated (weakened) vaccine
• D Toxoid vaccine made from a toxin

Q19.

What is allergy?

• A A normal, appropriately calibrated immune response that the body mounts against a genuine invading pathogen
• B Hypersensitivity reaction where the immune system responds excessively to a harmless antigen (allergen)
• C A congenital deficiency of circulating T lymphocytes that has been present in the bloodstream since birth
• D A type of autoimmune disease in which antibodies mistakenly target and damage the body's own healthy cells

Q20.

BCG vaccine protects against which disease?

• A Malaria
• B Typhoid
• C Tuberculosis
• D Cholera

Q21.

Lymph nodes filter lymph and contain:

• A Red blood cells filtered from circulating lymph fluid
• B B and T lymphocytes (immune cells)
• C Platelets that have leaked into the lymphatic system
• D Mainly plasma proteins filtered from circulating lymph

Q22.

Immunoglobulins (antibodies) are produced by:

• A T cells, which instead attack infected cells directly
• B Macrophages, which engulf and digest pathogens
• C B cells (plasma cells)
• D Neutrophils, which respond first to acute infection

Q23.

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

Q24.

What is MHC (Major Histocompatibility Complex) and why is it important?

• A A specific type of antibody molecule that is secreted into general circulation by activated plasma cells according to conventional understanding
• B Cell surface proteins that present antigen fragments to T cells; essential for T cell activation and self/non-self recognition
• C A type of complement protein that is sometimes thought to activate specifically during the alternative pathway in routine practice
• D The receptor protein found on B cell surfaces that circulating antibodies are generally designed to bind overall in most cases

Q25.

The structure of an antibody molecule consists of

• A Two identical heavy polypeptide chains alone, joined together without any light chains present
• B Four polypeptide chains: 2 heavy chains + 2 light chains, held by disulfide bonds, forming a Y shape
• C Six separate polypeptide chains arranged together in a closed hexagonal ring-like structure
• D A single continuous polypeptide chain folded back to form two separate antigen-binding regions

Q26.

What is complement system?

• 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

Q27.

What is clonal selection theory?

• 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

Q28.

What are interferons and what is their role in antiviral defence?

• A A class of antibiotic compounds that are sometimes thought to act specifically against established viral infections
• B Proteins secreted by virus-infected cells that signal neighboring cells to produce antiviral proteins, limiting viral spread
• C Proteins released by infected cells that are sometimes thought to directly bind to and inactivate free virus particles
• D Complement proteins that are sometimes thought to become activated specifically in response to viral surface antigens

Q29.

What is opsonization?

• A The direct killing of bacteria carried out exclusively by circulating natural killer (NK) cells
• B Coating of pathogens with antibodies or complement, enhancing their recognition and phagocytosis
• C Formation of the complement membrane attack complex (MAC) pore within a cell membrane
• D Activation of a resting B lymphocyte immediately upon its first contact with a matching antigen

Q30.

What distinguishes a primary immune response from a secondary immune response?

• A The primary response is generally faster and produces a noticeably greater quantity of antibodies overall in standard practice
• B Secondary is faster and produces more antibodies due to memory cells; IgG predominates in secondary; IgM predominates in primary
• C Both the primary and secondary immune responses are largely similar to one another in most measurable respects under most conditions encountered
• D The primary response involves mainly B lymphocytes, while the secondary response involves mainly T lymphocytes as frequently observed in practice

Q31.

What are autoimmune diseases? Give two examples.

• A Diseases caused entirely by invading external bacterial or viral pathogens from outside the body
• B Diseases where the immune system attacks the body's own tissues
• C Genetic diseases that are inherited directly from one or both biological parents
• D Diseases resulting from a congenital deficiency in the total number of immune cells

Q32.

What is the role of CD4+ T helper cells in immune response?

• A They are sometimes thought to directly recognize and kill virus-infected target cells without further assistance
• B They coordinate both humoral and cell-mediated immunity by secreting cytokines that activate B cells and cytotoxic T cells
• C They are sometimes mistaken for the primary cell type directly responsible for synthesizing and secreting antibodies
• D They are sometimes thought to function mainly within the thymus gland, rarely circulating beyond that organ

Q33.

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

Q34.

What is the difference between IgM and IgG in immune response timing?

• A IgG is sometimes produced as one of the first antibody classes in many immune responses according to standard textbooks in general practice
• B IgM is produced first (pentameric, good agglutinator); IgG follows (indicates mature response and provides long-term immunity)
• C IgM is sometimes thought to be largely absent throughout the entirety of a secondary immune response as frequently described
• D Both IgM and IgG antibody classes are sometimes thought to be produced simultaneously at the same early timepoint in most textbook accounts

Q35.

What is herd immunity?

• A A specific form of collective immunity that develops mainly within domesticated farm animal populations during normal conditions
• B When enough people in a population are immune that the pathogen cannot spread efficiently, protecting even unvaccinated individuals
• C A form of immunity that is sometimes thought to be acquired specifically through eating particular nutrient-rich foods as generally observed
• D A specialized type of passive immunity that some believe is transferred directly between family members in typical laboratory settings

Q36.

What are cytokines and give examples?

• 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

Q37.

What is the thymus and what happens to it with age?

• A Thymus is mainly a lymph node located in the neck region of the body in standard practice under most conditions encountered
• B Thymus is a gland in the chest where T cells mature; it is large in childhood and involutes (shrinks) after puberty
• C Thymus remains fairly active and largely unchanged in overall size throughout most of a human lifetime as frequently observed in practice
• D Thymus is sometimes mistakenly described as the principal organ where B lymphocytes undergo maturation in many documented cases

Q38.

What are monoclonal antibodies and how are they made?

• A Antibodies derived collectively from many different activated B cell clones combined together over time according to conventional understanding
• B Identical antibodies from a single B cell clone; produced by fusing a B cell with a myeloma cell (hybridoma technology)
• C Antibodies that are sometimes thought to be synthesized largely artificially using no living cells in routine practice
• D A type of complement protein specifically involved in the classical complement activation pathway process overall

Q39.

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

Q40.

What are T regulatory cells (Tregs) and why are they important?

• A T cells whose primary biological role is to further activate and stimulate other nearby T cells over time in most textbook accounts
• B Specialized T cells (CD4+CD25+FoxP3+) that suppress immune responses, preventing autoimmunity and excessive inflammation
• C T cells that differentiate into antibody-secreting plasma cells under sustained cytokine stimulation during normal conditions
• D T cells that mostly migrate to and reside mainly within the bone marrow stroma over time as generally observed in typical laboratory settings

Q41.

Immune tolerance prevents autoimmunity through:

• 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

Q42.

The complement system is activated by:

• 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

Q43.

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

Q44.

Neutrophil killing of bacteria involves:

• A Mainly physical engulfment of the bacterium by the cell's plasma membrane folding largely around it under typical conditions
• B Oxidative burst (NADPH oxidase producing superoxide), MPO (hypochlorous acid from H2O2 + Cl-), defensins, and elastase
• C Mainly degranulation of preformed granules releasing their antimicrobial contents alone each time according to standard textbooks
• D Mainly T cell activation by helper cells, with little role for neutrophils themselves in the process in general practice

Q45.

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

Q46.

How does HIV evade the immune system?

• 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+ T cell DNA as a provirus; mutates rapidly (high error-rate reverse transcriptase); infects and destroys CD4+ T cells; can enter latency
• C HIV is sometimes thought to mainly infect B cells, sparing CD4+ 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

Q47.

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

Q48.

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

Q49.

What is the significance of the T cell costimulation requirement (two-signal model)?

• A T cells are sometimes thought to need only one signal to activate, with TCR engagement of MHC-peptide alone being sufficient for full activation
• B T cells require BOTH signal 1 (TCR binding MHC-peptide) AND signal 2 (CD28 binding B7/CD80/86 on APCs); signal 1 alone causes anergy, not activation
• C Two signals are sometimes thought to cause cell death of the T cell rather than driving its proliferation and full effector differentiation process
• D Costimulation is sometimes thought to be mainly for B cells, despite CD28 binding to B7 occurring specifically and mainly on T lymphocytes

Q50.

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

Q51.

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

Q52.

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

Q53.

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

Q54.

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

Q55.

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

Q56.

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