Term
| What is hypersenstiivity? |
|
Definition
| state of heightened reactivity to antigen |
|
|
Term
| What is a hypersensitivity reaction? |
|
Definition
| immune responses to innocuous antigens that lead to symptomatic reactions upon REEXPOSURE |
|
|
Term
| What is important about hypersenstivity/"allergic" reactions? |
|
Definition
| they are dependent upon REEXPOSURE |
|
|
Term
| What type of immune reactant is involved in Type I hypersensitivity reactions? |
|
Definition
|
|
Term
| What type of antigen is involved in Type I hypersensitivity? |
|
Definition
|
|
Term
| what is the effector mechanism of IgE type I hypersenstivity? |
|
Definition
|
|
Term
| What are some examples of hypersensitivity reactions? |
|
Definition
| allergic rhinitis, (allergic) asthma, systemic anaphylaxis |
|
|
Term
| What is hypersenstiviity disease? |
|
Definition
| damage to host tissues caused by hypersenstiviity reactions to typically innocuous antigens |
|
|
Term
| How did Coombs and Gel classify hypersenstiivty reactions? |
|
Definition
| Type I, II, II, IV based on types of antigens that are recognized and the types of immune responses that are involves |
|
|
Term
| What else might people call a Type I hypersenstivity reaction? |
|
Definition
|
|
Term
| What does Type II hypersenstiivty involve (which immune reactant)? |
|
Definition
|
|
Term
| What are the two types of antigens involved in Type II? |
|
Definition
| cell or matrix associated antigen/cell surface receptor |
|
|
Term
| What is the effector mechanism involved in Type II and with what antigens are they involved? |
|
Definition
| Complement, FcR+ cells (phagocytes, NK cells) with cell/matrix associated antigen; antibody alters signaling in cell-surface receptors |
|
|
Term
| What are examples of hypersensitivity reactions? |
|
Definition
| some drug allergies (eg penicillin- complement effector mechanism); chronic urticaria (hives)- antibody against FCepsilonRIalpha receptor |
|
|
Term
| What is a type III hypersenstivity? |
|
Definition
| involves production of antigen-antibody complexes |
|
|
Term
| Which immune reactant is associated with Type III and what type of antigen? |
|
Definition
|
|
Term
| What is effector mechanism of Type III? |
|
Definition
|
|
Term
| What are some examples of Type III? |
|
Definition
| serum sickness, arthrus reaction |
|
|
Term
| What is Type IV hypersensitivity? |
|
Definition
| T cell mediated hypersenstivity |
|
|
Term
| Which immune reactants are involved in Type IV? |
|
Definition
|
|
Term
| What type of antigens are associated with Type IV? |
|
Definition
| soluble antigens (Th1 and Th2); cell associated antigen (CTL) |
|
|
Term
| What are the effector mechanisms of Type IV? |
|
Definition
| Th1: macrophage activation; Th2: IgE production, eosinophil activation, mastocytosis; CTL: cytotoxicity |
|
|
Term
| What are examples of Type IV reactions? |
|
Definition
| Th1: contact dermatitis, tuberculin; Th2: chronic asthma, chronic allergic rhinitis; CTL: graft rejection |
|
|
Term
| What are antigens that selectively stimulate Th2 cells to drive an IgE response and why Th2? |
|
Definition
| those antigens are also known as allergens; they stimulate Th2 cells because those CD4s can induce class switching from IgM to IgE |
|
|
Term
| Describe some properties of allergens. |
|
Definition
| small proteins; highly soluble; carried on desiccated particles like pollen or mite feces; usually presented at very low doses |
|
|
Term
| What happens once allergens come into contact with the mucosa of the airways? |
|
Definition
| the soluble antigens elute from the delivery particles and iffuse into the mucosa |
|
|
Term
| What happens with antigens presented to Th0 cells at low doses? |
|
Definition
| elicit differentiation into Th2 CD$ cells |
|
|
Term
| What is the maximum exposure to the common pollen allergens of ragweed? |
|
Definition
| less than 1 microgram/year/person- even so, many people suffer irritating and even life threatening to TH2 driven IgE responses to these antigens |
|
|
Term
| Do all people exposed to a particular allergen have an allergic reaction? |
|
Definition
|
|
Term
| Do all allergens have enzymatic activity? |
|
Definition
| no, not all, but many common allergens have enzymatic activity |
|
|
Term
| Why might the enzymatic activity of allergens be important? |
|
Definition
| IgE is a very important isotype of antibody in the immune response to parasites and many parasites produce and secrete proteolytic enzymes that break down connective tissues to allow worms access to host tissues |
|
|
Term
| What is special about proteases? |
|
Definition
| believed to be particularly strong inducers of Th2 type responses |
|
|
Term
| How do Th2 cells stimulate class switching to IgE? |
|
Definition
| by delivering several molecular signals that favor class switching in B lymphocytes to IgE |
|
|
Term
| Describe the signaling process of Th2 stimulating class switching to IgE. |
|
Definition
| when the TCR of a Th2 cells becomes ligated, the Th2 cell produces and secretes IL-4, IL-5, and IL-13, upregulating surface expression of CD40L and CD23 |
|
|
Term
| What do CD40L and CD23 do? |
|
Definition
| costimulatory molecules bind counter receptors (CD40 and CD2) on presenting B cell to induce class switching to IgE |
|
|
Term
|
Definition
| low affinity receptor for IgE |
|
|
Term
| What are Type I reactions initiated by? |
|
Definition
| mast cells (eosinophils and basophils also involved |
|
|
Term
| What do mast cells, eosinophils, and basophils express that is important for Type I reactions? |
|
Definition
| they express the high affinity IgE receptor (FcEpsilonRI) |
|
|
Term
| What happens when IgE binds to mast cells/eosinophils/basophils? |
|
Definition
| crosslinked by specific antigen, degranulate, releasing a variety of inflammatory mediators that initiate inflammatory responses |
|
|
Term
| What are basophil mediators simmilar to? |
|
Definition
| the immunological mediators produced by eosinophils |
|
|
Term
| How are type I hypersenstivity reactions initated? |
|
Definition
| degranulation of mast cells; mediators initate inflammation and recruit eosinophils and basophils to the site of inflammation; eosinophils and basophils contribute to inflammatory response by releasing the contents of their granules |
|
|
Term
| Is there a genetic component to allergy? |
|
Definition
| yes, there is a genetic basis to allergic predisposition |
|
|
Term
| How do you describe the condition of being predisposed to allergies? |
|
Definition
|
|
Term
| Who is more likely to produce IgE responses to common environmental allergens? |
|
Definition
| 40% of Caucasian population of North America and Europe |
|
|
Term
| How do atopic individuals differ from non-atopic individuals? |
|
Definition
| higher levels of soluble IgE and more circulating eosinophils than non-atopic individuals |
|
|
Term
| Which chromosomes are involved in allergic predisposition? |
|
Definition
| chromosome 11 encodes a gene for beta subunit of high affinity IgE receptor; chromosome 5 encodes a cluster of genes encoding IL-3,4,5,9,13 and GM-CSF |
|
|
Term
| What are the proteins encodd by chromosome 5 involved in? |
|
Definition
| isotype switching, eosinophil survival and mast cell proliferation |
|
|
Term
| What is correlated with elevated IL-4 levels in atopic individuals? |
|
Definition
| inherited sequence in the promoter region of the IL-4 gene |
|
|
Term
| Wha else might affect IgE response to certain allergens (HLA)? |
|
Definition
| HLA class II polymorphism; response to seveeral pollen antigens of ragweed correlate with expression of HLA class II allotype DRB1*1501 |
|
|
Term
| What does HLA class II polymorphism involvement in IgE response to certain allergens suggest? |
|
Definition
| HLA class II:peptide combination predisposes to stimulation of Th2 response |
|
|
Term
| Can you test an individual's sensitivity to a particular allergen? |
|
Definition
| yes, it can be tested easily by observing a 2 step response |
|
|
Term
| What is the 1st step of the allergic response test? |
|
Definition
| injection of allergen into skin of a sensitive individual produces a chracteristic inflammatory reaction known as a wheal and flare at the injection site |
|
|
Term
|
Definition
| an immediate reaction (appearing within minutes) that is the result of mast cell-degranulation in the skin; released histamine and other mediators cause increased permeability of lcoal blood vessels (fluid enters tissue causing swelling or edema); swelling=wheal; increased blood flow causes redness=flare |
|
|
Term
| How long do immediate allergic reactions last? |
|
Definition
|
|
Term
| What is the 2nd step of the allergic response test? |
|
Definition
| 6-8 hours post injection; a "late phase reaction" that occurs at the site of injection with more widespread swelling, mediated by leukotrienes, chemokines, and cytokines produced by mast cells following IgE mediated activation |
|
|
Term
| When reexposed to an allergen, what does the resulting Type I reaction depend upon? |
|
Definition
| when reexposed to an allergen, the resulting reaction depends upon tissues that come in contact with the allergen and only the mast cells residing at the site of allergen contact will be induced to degranulate (by IgE crosslinking with allergen) |
|
|
Term
| What are the various ways allergens gain access? |
|
Definition
| airborne and irritate mucose of respiratory tract; food borned and irritate mucosa of GI tract; gain access to connective tissue and blood via insect bites; gain access to blood via absorption via gut and respiratory mucosa |
|
|
Term
| What promotes degranulation? |
|
Definition
| crosslinking of allergen specific IgE bound to high affinity IgE receptor on mast cells |
|
|
Term
| What does degranulation of mast cells induce? |
|
Definition
| strong inflammatory response |
|
|
Term
| What is believed about IgE response? |
|
Definition
| evolved as a mechanism of defense against invertebrate parasites (worms); violent expulsion of airways (coughing and sneezing) and contents of stomach (vomiting) and intestines (diarrhea) initated by mast cells may have develops as a means of expulsion of parasites from body |
|
|
Term
| What is systemic anaphylaxis caused by? |
|
Definition
|
|
Term
| What is systemic anaphylaxis? |
|
Definition
| wide spread activation of mast cell degranulation causing both an incrase in vascular permeability and a widespread constriction of smooth muscle |
|
|
Term
| What is anaphylactic shock? |
|
Definition
| fluid leaving blood during systemic anaphylaxis causes dramatic reduction of blood pressure |
|
|
Term
| What happens to connective tissues during systemic anaphylaxis? |
|
Definition
| swelling due to influx of fluid |
|
|
Term
| What happens to organ systems during systemic anapylaxis? |
|
Definition
| damage can be sustained, impairing function |
|
|
Term
| What happens to airways/epiglottis during systemic anaphylaxis? |
|
Definition
| constriction of airways and swelling of epiglottis leading to asphyxiation/death (could result) |
|
|
Term
| How many deaths in the US from anaphylaxis? |
|
Definition
|
|
Term
| How can potential allergens be intorduced directly into blood (systemic)? |
|
Definition
| insect sting; drug injections |
|
|
Term
| Can food or drugs taken orally incude anaphylaxis? |
|
Definition
| yes, if the allergen is absorbed rapidly from gut into blood; examples include peanuts and brazil nuts |
|
|
Term
| What is the most common cause of anaphylaxis? |
|
Definition
| IgE mediated allergy to penicillin or other drugs (ingestion or injection); 100 fatalities/year in US |
|
|
Term
| what are anaphalactoid reactions? |
|
Definition
| resemble anaphylactic reactions but do not involve interaction between allergen and IgE |
|
|
Term
| how do you treat anaphylactic and anaphalactoid reactions? |
|
Definition
|
|
Term
| How does epinephrine work to help anaphylaxis? |
|
Definition
| stimulates reformation of tight junctions between endothlial cells, reducing the permeability of blood vessels, diminishing ttissue swelling, raising blood pressure; relaxes bronchial constriction and stimulates heart |
|
|
Term
| What should patients with anaphylactic sensitivity carry? |
|
Definition
| "epi-pen" (syringe full of epinephrine) |
|
|
Term
| What is rhinitis and asthma caused by? |
|
Definition
|
|
Term
|
Definition
| allergic rhinitis- mile allergic response chracterized by violent bursts of sneezing and runny nose in response to inhaled allergens |
|
|
Term
| What is allergic rhinitis caused by? |
|
Definition
| allergens diffusing across mucous membranes of nasal passages and activating mucosal mast cells beneath the nasal epithelium |
|
|
Term
| What characterizes allergic rhinitis? |
|
Definition
| local edema obstructing nasal airways + nasal dischrage of eosinophil-rich mucus; histamine release that causes general irritation of nasal passages |
|
|
Term
| What are secondary allergic rhinitis symptoms? |
|
Definition
| reaction can extend to ear/thraod leading to accumulation of fluid in sinuses and Eustachian tubes (conducive to bacterial infection) and conjunctiva of eye (allergic conjunctivitis) |
|
|
Term
|
Definition
| more serious condition than allergic rhinitis; when commonly inhaled allergens cause chronic breathing difficulties |
|
|
Term
| How is allergic asthma triggered? |
|
Definition
| when allergen/IgE interaction stimulates submucosal mast cells in lower respiratory tract |
|
|
Term
| What characterizes allergic asthma? |
|
Definition
| increase in fluid and mucus secretions into respiratory tract; bronchial constriction due to contraction of smooth muscle surrounding airways; chronic inflammation of airways involving persistent infiltration of leukocytes (Th2, eosinophils, neutrophils) |
|
|
Term
| What is the overall effect of allergic asthmatic attack? |
|
Definition
| trapping of air in the lungs making breathing more difficult (can be fatal) |
|
|
Term
| What is unique about allergic asthma? |
|
Definition
| initally driven by response to an allergen but chronic inflammation that develops can be perptuated in absence of further allergen |
|
|
Term
| What can almost totally occlude the airways in allergic asthma? |
|
Definition
|
|
Term
| What develops in the airways in allergic asthma? |
|
Definition
| generalized hypersenstivity; chemical irritants that are commonly present in air (cigarette smoke, sulfur dioxide) can trigger attacks |
|
|
Term
| What can exacerbate asthmatic disease? |
|
Definition
| immune responses to bacterial or viral infection of respiratory tract, especially infection that elicit Th2 responses |
|
|
Term
| What is chronic asthma considered? |
|
Definition
|
|
Term
|
Definition
| hives; itchy swellings caused by release of histamine by mast cells in the skin, following activation by allergen; reaction is essentially a wheal and flare |
|
|
Term
|
Definition
| inflammation caused by activation by activation of mast cells in deep subcutaneous tissue; swelling is more diffusie than observed for utricaria |
|
|
Term
| What causes both urticaria and angioedema? |
|
Definition
| food or drug allergens carried to the skin via bloodstream; can occur during anaphylactic reaction |
|
|
Term
| What can food allergies cause? |
|
Definition
| systemic effects and gut reactions |
|
|
Term
| What is interesting about humans and their foodstuffs? |
|
Definition
| humans eat a wider variety of "foodstuffs" than other living things; food is composed of a number of different proteins (many potentailly immunogenic) but only a few proteins ilicit IgE Ab responses |
|
|
Term
| What foods cause food allergens (typically)? |
|
Definition
| grains, nuts, fruits, elgumes, fish, shellfish, eggs, milk |
|
|
Term
| What happens once a person is sensitized to a food allergen? |
|
Definition
| subsequent intake of that allergen leads to an immediate reaction in the GI tract |
|
|
Term
| What do food allergens do in the gut? |
|
Definition
| pass through wall of gut, bind to IgE on mast cells of GI tract, triggering degranulation |
|
|
Term
| What does histamine in food allergen/mast cell reaction do? |
|
Definition
| causes increase in permeability of blood vessels, leading to accumulation of fluid in gut lumen |
|
|
Term
| What do smooth muscles of stomach walls do in food allergen sensitivity? The itestine? |
|
Definition
| contract, producing cramps and vomiting; same reaction in intestine, causing diarrhea |
|
|
Term
| How can you treat/prevent allergic reactions? |
|
Definition
| modification of behavior; pharmacological; immunological |
|
|
Term
| Describe modificaiton of behavior to preventing allergies? |
|
Definition
| modify patient's behavior and/or environment to eliminate contact with allergen |
|
|
Term
| Describe the pharmacological approach to treating/preventing allergies? |
|
Definition
| use drugs that reduce impact of allergen contact; drugs that block effector pathways of allergic response and limit inflammation |
|
|
Term
| What are some examples of anti-allergy drugs? |
|
Definition
| antihistamines; corticosteroirds; cromolyn sulfate; epinephrine |
|
|
Term
| What do antihistamines do? |
|
Definition
| reduce rhinitis and urticaria by preventing histamine from binding to H1 histamine receptors on vascular endothelium |
|
|
Term
| What do corticosteroids do in anti-allergy treatment? |
|
Definition
| suppresses leukocyte function; treat chronic inflammation of asthma, rhinitis, eczema |
|
|
Term
| What does cromolyn sulfate do in anti-allergy treamtnt? |
|
Definition
| prophylactic inhalant; prevents degranulation of activated mast cells and granulocytes |
|
|
Term
| What does epinephrine do in anti-allergy treatment? |
|
Definition
|
|
Term
| What does immunological treatment of allergies do? |
|
Definition
| prevents production of allergen specific IgE; modules immune resonse so that it shift from an IgE response to an IgG response |
|
|
Term
| Describe some of the immunological strategies for anti-allergy treatment. |
|
Definition
| 1) desensitization: series of injections of increasing doses of the allergen; gradulaly changes a Th2 (IgE) response to a Th1 respone in which no IgE is produced; can reuslt in anaphylaxis so be careful; 2) vaccinte patients with allergen derived peptides known to be presented by HLA class II molecules to Th2 CD4 cells in an attempt to induce anergy |
|
|
Term
| What is unique about people who experience parasite infections? |
|
Definition
| rare develop allergic disease |
|
|
Term
| Why might people infected with parasites rarely develop allergic disease? |
|
Definition
| parasites induce very potent imune responses that are typically Th2 driven and produce large quantities of IgE |
|
|
Term
| How much IgE is parasite-specific? |
|
Definition
|
|
Term
| What is true of the remainder of the IgE (that which is not parasite specific)? |
|
Definition
| highly heterogenous and represents product of non-specific polyclonal B and T cell activation by parasite |
|
|
Term
| What does nonspecific IgE dO? |
|
Definition
| outcompetes the parasite specific IgE for binding to high affinity IgE receptor on mast cells, basophils, and eosinophils (strtegy prevents parsite from triggering IgE mediated effector mechanisms, allowing parasite to evade immune response) |
|
|
Term
| What is a byproduct of the parasitic strategy to evade immune response? |
|
Definition
| people living in regions with high incidence of parasitic infections (and high concentrations of IgE experience reduced incidence of allergic disease compared to people that live in areas with low incidence of parasitic infections) |
|
|
Term
| What is type II hypersenstiivy? |
|
Definition
| reactions caused by antibodies specific for altered components of human cells |
|
|
Term
| What are some common examples of type II hypersensitivity reactions? |
|
Definition
| hemolytic anemia and thrombocytopenia (caused by destruction of red blood cells or platelets, respecitvely), following the administration of a drugs |
|
|
Term
| What can type II hypersenstiivty reactions be associated with? |
|
Definition
| Adminstration of drugs penicillin, quinidine (treats cardiac arrhythmia) and methyldopa (treats high blood prssure) |
|
|
Term
| What do the drugs do in Type II hypersensitivity reactions? |
|
Definition
| chemically active drugs bind to surface of red blood cells or platelets and create new epitopes to which immune system is not tolerant |
|
|
Term
| What happens in penicillin induced type II hypersensitivity? |
|
Definition
| new epitopes generated by penicillin stimulate production of IgM and IgG antibody specific for new epitopes; penicillin-modified RBCs must be coated with complement which facilitates phagocytosis by macrophages via complement receptors |
|
|
Term
| What is a side effect of complement activation by infection being treated with penicillin? |
|
Definition
| penicillin=modified RBCs must be coated with complement |
|
|
Term
| What do macrophages do in pencillin induced type II? |
|
Definition
| present newly formed epitopes to naïve CD4 T cells to produced armed effector Th2 cells |
|
|
Term
| What do effector Th2 cells do in penicillin induced type II? |
|
Definition
| those that are specific for new epitopes supply help to antigen-specific B cells, IgG specific for new epitopes is produced |
|
|
Term
| What do the IgG antibodies do in penicillin induced type II? |
|
Definition
| bind to altered RBCs and stimulate either complement activation or phagcytosis by macrophages |
|
|
Term
| What is the end result of penicillin induced type II? |
|
Definition
| altered RBCs are destroyed (lysed, phagocytosed) |
|
|
Term
| What causes type III hypersenstivity reactions? |
|
Definition
| immune complexes formed from IgG and soluble antigens |
|
|
Term
| When are antigen:antibody complexes generated? |
|
Definition
| in almost all immune responses (in most cases, they are cleared without causing tissue damage) |
|
|
Term
| What is the size of immune complexes? |
|
Definition
| very small (single complex of 1 antigen molecule and 1 Ab molecule) or very large (containing milions of each) |
|
|
Term
| What is true of large immune complexes? |
|
Definition
| they fix complement efficiently and are readily taken up by macrophages and removed without incident |
|
|
Term
| What is true of smaller immune complexes ? |
|
Definition
| less efficient at complement fixing; tend to remain in circulation and become deposited in blood vessel walls |
|
|
Term
| When does tissue damage (type III) occur? |
|
Definition
| whne sufficient immune complexes accumulate |
|
|
Term
| What happens once immune complexes accumulate? |
|
Definition
| circulating leukocytes recognize the immune complexes through their Fc and complement receptors, activating their inflammatory activities |
|
|
Term
| What is the Arthus reaction? |
|
Definition
| inflammtory response caused by antigen-specific IgG diffusing from blood into injection site tissues and combining with soluble antigen to form immune complexes and activating complement |
|
|
Term
| What causes systemic type III reactions? |
|
Definition
| caused by IV administration of large quantities of antigen |
|
|
Term
|
Definition
| results from immune response to non-self material administered into bloodstream as treatment for a variety of illnesses |
|
|
Term
| What causes serum sickness? |
|
Definition
| systemic accumulation of immune complexes and eventual systemic inflammatory responses |
|
|
Term
| What characterizes serum sickness? |
|
Definition
| chills, fever, rash, arthritis, vasculitis, sometimes glomerulonephritis |
|
|
Term
| What are some examplse of serum sickness? |
|
Definition
| immune horse sera injected into patients to treat life-threatening bacterial infections such as diphtheria, tetanus, scarlet fever; monoclonal anti-T cell Ab in large doses to transplant patients to prevent rejection; large injections of bacterial enzyme streptokinase to degrade blood clots in heart attack patients; large IV injections of penicillin, even in people not allergic to pencillin- causes alteration of RBCs, eliciting Ab responses |
|
|
Term
| How else can type III hypersenstivity be caused? |
|
Definition
| continual inhalation of antigens that elicit IgG instead of IgE antibody reponses |
|
|
Term
| What does continued inhalation of antigens do? |
|
Definition
| accumulation of immune complexes in walls of lung alveoli, leading to inflammatory responses |
|
|
Term
| What does inflammation in lungs from continued antigen inhalation lead to? |
|
Definition
| accumulation of fluid, antigen, immune cells that prevent proper lung function |
|
|
Term
| What people are at risk for inhaled antigen diseases of Type III variety? |
|
Definition
| workers exposed daily to same airborne antigens; farmers; bird breeders |
|
|
Term
|
Definition
| type III condition describing constant exposrue to ahy dust and mold spores |
|
|
Term
| What is bird breeder's disease? |
|
Definition
| another common type III hypersensitivity disease of lungs caused by inhalation of avian antigens |
|
|
Term
| What is Type IV hypersensitivity? |
|
Definition
| reactions mediated by antigen specific effector T cells |
|
|
Term
| What is another term for type IV? |
|
Definition
| delayed type hypersensitivity (DTH) |
|
|
Term
| Why are DTH called "delayed?" |
|
Definition
| occur 1-3 days after contact with antigen in stark contrast to Ab mediated hypersensitivites which are usually apparent within minutes of antigen exposure |
|
|
Term
| How much antigen is required in DTH and why? |
|
Definition
| 100-1000 fold larger quantities due to relative inefficiency of antigen processing/presentation |
|
|
Term
| What are the most common antigens eliciting DTH responses? |
|
Definition
| mycobacterial proteins, insect venoms, penadecacatechol (poison ivy), small metal ions |
|
|
Term
| What is the most well studied example of Type IV? |
|
Definition
| tuberculin reaction- clinical test to determine if a person has been infected with Mycobacteria tuberculosis |
|
|
Term
| How do you perform the tuberculin test? |
|
Definition
| small amount of protein from M. tuberculosis is injected subQ |
|
|
Term
| What happens in an individual who has been exposed to TB (they have produced immune response previously)? |
|
Definition
| he/she produces an inflammatory reaction around the site of injection 24-72 hours post-injection |
|
|
Term
| What mediates the inflammatory response in tuberculin test? |
|
Definition
| effector Th1 cells that recognize pepties (presented by MHC class II on macrophages) derived from injected protein; cells produce cytokines that activate and recruit macrophages to the site |
|
|
Term
|
Definition
| term used to describe type IV hypersenstivity reaction produced against penadecacatechol (Pchol) |
|
|
Term
|
Definition
| small, highly reactive lipid-like molecule that is present in the roots and leaves of North American "poison ivy" plant, Rhus toxicodendron |
|
|
Term
| What happens upon initial contact with the poison ivy plant? |
|
Definition
| Pchol penetrates outer layers of skin and indiscriminately forms covalent bonds with extracellular proteins and skin cell surface proteins, forming new antigens that are recognized as non-self;local APCs (macrophages and Langerhans cells) take up new antigens, return to secondary lymphoid tissue, and prsent peptide antigens on MHC class II to naive CD4 cells |
|
|
Term
| What happens as a result of Pchol's ability to penetrate cell membranes and modify intracellular proteins? |
|
Definition
| modified proteins can be processed and presented via MHC class I molecules to naïve CD8 cells as well |
|
|
Term
| What happens in initial contact with poison ivy? |
|
Definition
| production of effector T cells and immunological memory but little if any inflammatory resopnse |
|
|
Term
| What happens in subsequent contact with poison ivy plants? |
|
Definition
| unpleasant rash of skin mediated by antigen-speicfic effector CTLs (kill cells exposed to Pchol) and antigen-specific effector Th1 cells that produce cytokines that activate macrophages and induce inflammation |
|
|
Term
| What is poison ivy an example of ? |
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Definition
| contact sensitivity because contact of allergen with skin is required to initiate allergic response |
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