Hypersensitivity

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Slide 1 : Hypersensitive Reaction
Slide 2 : Introduction The immune response involves mobilization of a battery effector molecules to remove Ag the effector molecules induce a localized inflammatory response that eliminates Ag without extensive damage of host’s tissue Under certain circumstances this inflammatory response can have deleterious effects, resulting in significant tissue damage or even death This inappropriate immune response is termed hypersensitivity or allergy The word hypersensitivity implies an increased response, the response is not always heightened but may, instead, be an inappropriate immune response to an antigen
Slide 3 : Hypersensitive reactions may develop in the course of either HI or CMI response The hypersensitivity reaction may be immediate hypersensitivity if it occurs within the humoral branch & initiated by Ab or Ag-Ab complexes because the symptoms are manifested within minutes or hours after a sensitized recipient encounters antigen Delayed-type hypersensitivity (DTH) is so named in recognition of the delay of symptoms until days after exposure Several forms of hypersensitive reaction can be distinguished and classified according to the immune responses and the effector mechanisms responsible for cell and tissue injury
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Slide 5 : Gell and Coombs Classification Gell and Coombs proposed a classification scheme in which hypersensitive reactions are divided into 4 types: Three types of hypersensitivity occur within the humoral branch and are mediated by antibody or antigen-antibody complexes: IgE-mediated (type I) antibody-mediated (type II) immune complex–mediated (type III) A fourth type of hypersensitivity depends on reactions within the cell-mediated branch termed delayed-type hypersensitivity, or DTH (type IV) Each type involves distinct mechanisms, cells, and mediator molecules
Slide 6 : Type I hypersensitivity reaction induced by antigens referred to as allergens exhibits all the hallmarks of normal humoral response an allergen induces a humoral Ab response resulting in the generation of antibody-secreting plasma cells and memory cells secretion of IgE by plasma cells makes it d/t from normal humoral response The IgE binds to Fc receptors on the surface of tissue mast cells and blood basophils Mast cells and basophils coated by IgE are said to be sensitized A later exposure to the same allergen cross-links the membrane-bound IgE on sensitized mast cells and basophils, causing degranulation of these cells
Slide 7 : The pharmacologically active mediators released from the granules act on the surrounding tissues The principal effects—vasodilation and smooth-muscle contraction—may be either systemic or localized, depending on the extent of mediator release:- Components of Type I Reactions ALLERGENS IgE IgE receptors Mast cells and Basophils
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Slide 9 : Pharmacologic Agents that mediate Type I reaction The clinical manifestations of type I hypersensitive reactions are related to the biological effects of the mediators released during mast-cell or basophil degranulation These mediators are pharmacologically active agents that act on local tissues as well as on populations of secondary effector cells: Eosinophils, neutrophils, T lymphocytes, monocytes and platelets The mediators thus serve as an amplifying terminal effector mechanism much as the complement system serves as an amplifier and effector of an antigen-antibody interaction
Slide 10 : When generated in response to parasitic infection, these mediators initiate beneficial defense processes, including vasodilatation and increased vascular permeability, which brings an influx of plasma and inflammatory cells to attack the pathogen mediator release induced by allergens, results in unnecessary increases in vascular permeability and inflammation whose detrimental effects far outweigh any beneficial effect
Slide 11 : The mediators The mediators can be classified as: primary or secondary Primary mediators are produced before degranulation and are stored in the granules Secondary mediators are synthesized either after target-cell activation or are released by the breakdown of membrane phospholipids during the degranulation process differing manifestations of type I hypersensitivity in different species or different tissues partly reflect variations in the primary and secondary mediators present
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Slide 13 : Clinical Manifestations of Type I reaction systemic or localized range from life-threatening conditions, such as systemic anaphylaxis and asthma, to hay fever and eczema, which are merely annoying Systemic Anaphylaxis a shock-like and often fatal state whose onset occurs within minutes of a type I hypersensitivity reaction induced in a variety of experimental animals and occasionally in humans wide range of antigens trigger this reaction in susceptible humans: venom from bee wasp hornet ant stings drugs (penicillin, insulin &antitoxins) seafood nuts
Slide 14 : If not treated quickly, these reactions can be fatal. Epinephrine is the drug of choice for systemic anaphylactic reactions - counteracts the effects of mediators - improves cardiac output - blocking further degranulation
Slide 15 : Localized anaphylaxis The reaction is limited to a specific target tissue or organ, often involving epithelial surfaces at the site of allergen entry The tendency to manifest localized anaphylactic reactions is inherited and is called atopy Atopic allergies, which afflict at least 20% of the population in developed countries, include a wide range of IgE-mediated disorders, including allergic rhinitis (hay fever), asthma, atopic dermatitis (eczema), and food allergies
Slide 16 : Regulation of Type I reactions level of the IgE response induced by an antigen (i.e., its allergenicity) depends on antigen dose mode of antigen presentation genetic constitution the relative levels of the TH1 and TH2 subsets also are key to the regulation of type I hypersensitive responses TH1 reduce the response TH2 cells enhance it
Slide 17 : Controlling Hypersensitivity reaction (Type I) to avoid contact with known allergens Immunotherapy repeated injections of increasing doses of allergens (hyposensitization) Use of drugs that block release of allergic mediators by interfering with various biochemical steps in mast-cell activation and degranulation
Slide 18 : Antibody-Mediated Cytotoxic (Type II) hypersensitivity reaction
Slide 19 : Type II hypersensitive reactions involve antibody-mediated destruction of cells Ab can activate the complement system creating pores in the membrane of a foreign cell or it can mediate cell destruction by antibody dependent cell-mediated cytotoxicity (ADCC) In this process, cytotoxic cells with Fc receptors bind to the Fc region of Abs on target cells and promote killing of the cells Antibody bound to a foreign cell also can serve as an opsonin enabling phagocytic cells with Fc or C3b receptors to bind and phagocytose the antibody-coated cell
Slide 20 : Type II hypersensitivity reaction Transfusion Reactions Hemolytic Disease of the Newborn develops when maternal IgG antibodies specific for fetal blood-group Ags cross the placenta and destroy fetal RBCs consequences can be minor, serious, or lethal severe hemolytic disease of the newborn, called erythroblastosis fetalis, most commonly develops when an Rh+ fetus expresses an Rh antigen on its blood cells that the Rh– mother does not express
Slide 21 : Drug-Induced Hemolytic Anemia certain antibiotics (e.g., penicillin, cephalosporin, and streptomycin) can adsorb nonspecifically to proteins on RBC membranes, forming a complex similar to a hapten-carrier complex such drug-protein complexes induce formation of antibodies, which then bind to the adsorbed drug on red blood cells complement mediated lysis and thus progressive anemia when the drug is withdrawn, the hemolytic anemia disappears
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Slide 25 : Immune Complex–Mediated (Type III) Hypersensitivity
Slide 26 : The reaction of antibody with antigen generates immune complexes and this complexing of antibodies with antigen facilitates the clearance of antigen by phagocytic cells However, large amounts of immune complexes can lead to tissue-damaging type III hypersensitive reactions magnitude depends on : the quantity of immune complexes distribution within the body The rxn could be localized if the complexes are deposited in tissue very near to site of Ag entry when the complexes are formed in the blood, a reaction develop wherever the complexes are deposited
Slide 27 : Complex deposition is frequently observed on blood-vessel walls, in the synovial membrane of joints, on the glomerular basement membrane of the kidney, and on the choroid plexus of the brain. The deposition of these complexes initiates a reaction that results in the recruitment of neutrophils to the site. The tissue is injured as a consequence of granular release from the neutrophil Type III hypersensitive reactions develop when immune complexes activate the complement system’s array of immune effector molecules
Slide 28 : The C3a, C4a, and C5a complement split products are anaphylatoxins that cause localized mast-cell degranulation and consequent increase in local vascular permeability. C3a, C5a, and C5b67 are also chemotactic factors for neutrophils, which can accumulate in large numbers at the site of immune-complex deposition. Larger immune complexes are deposited on the basement membrane of blood vessel walls or kidney glomeruli, whereas smaller complexes may pass through the basement membrane and be deposited in the subepithelium. The type of lesion that results depends on the site of deposition of the complexes.
Slide 29 : Much of the tissue damage in type III reactions stems from release of lytic enzymes by neutrophils as they attempt to phagocytose immune complexes. The C3b complement component acts as an opsonin, coating immune complexes. A neutrophil binds to a C3b-coated immune complex by means of the type I complement receptor, which is specific for C3b. Because the complex is deposited on the base mentmembrane surface, phagocytosis is impeded, so that lytic enzymes are released during the unsuccessful attempts of the neutrophil to ingest the adhering immune complex.
Slide 30 : Further activation of the membrane-attack mechanism of the complement system can also contribute to the destruction of tissue. In addition, the activation of complement can induce aggregation of platelets, and the resulting release of clotting factors can lead to formation of microthrombi Manifestations of Type III hypersensitivity reactions Localized Injection of an antigen intradermally or subcutaneously into an animal that has high levels of circulating antibody specific for that antigen leads to formation of localized immune complexes, which mediate an acute Arthus reaction within 4–8 h
Slide 31 : Generalized Type III Reactions When large amounts of antigen enter the bloodstream and bind to antibody, circulating immune complexes can form If antigen is in excess, small complexes form; because these are not easily cleared by the phagocytic cells, they can cause tissue-damaging type III reactions at various sites Historically, generalized type III reactions were often observed after the administration of antitoxins containing foreign serum, such as horse antitetanus or antidiphtheria serum
Slide 32 : In such cases, the recipient of a foreign antiserum develops antibodies specific for the foreign serum proteins; these antibodies then form circulating immune complexes with the foreign serum antigens Typically, within days or weeks after exposure to foreign serum antigens, an individual begins to manifest a combination of symptoms that are called serum sickness These symptoms include: Fever, weakness, generalized vasculitis (rashes) with edema and erythema, Lymphadenopathy, arthritis and sometimes glomerulonephritis
Slide 33 : Manifestations of serum sickness depend on the - quantity of immune complexes formed - overall size of the complexes, which determine the site of their deposition The sites of deposition vary but, in general, complexes accumulate in tissues where filtration of plasma occurs this explains the high incidence of : glomerulonephritis (complex deposition in the kidney) vasculitis (deposition in the arteries) arthritis (deposition in the synovial joints) caused by serum sickness
Slide 34 : formation of circulating immune complexes contributes to the pathogenesis of a number of conditions other than serum sickness: Autoimmune Diseases Systemic lupus erythematosus Rheumatoid arthritis Goodpasture’s syndrome Drug Reactions Allergies to penicillin and sulfonamides Infectious Diseases Poststreptococcal glomerulonephritis Meningitis Hepatitis Mononucleosis Malaria Trypanosomiasis
Slide 35 : Type IV or Delayed-Type Hypersensitivity (DTH)
Slide 36 : When some subpopulations of activated TH cells encounter certain types of antigens, they secrete cytokines that induce a localized inflammatory reaction called delayed-type hypersensitivity (DTH). The reaction is characterized by large influxes of nonspecific inflammatory cells, in particular, macrophages. The development of the DTH response begins with an initial sensitization phase of 1–2 weeks after primary contact with an antigen. During this period, TH cells are activated and clonally expanded
Slide 37 : A subsequent exposure to the antigen induces the effector phase of the DTH response. In the effector phase, TH1 cells secrete a variety of cytokines that recruit and activate macrophages and other nonspecific inflammatory cells. A DTH response normally does not become apparent until an average of 24 h after the second contact with the antigen; the response generally peaks 48–72 h after second contact. The delayed onset of this response reflects the time required for the cytokines to induce localized influxes of macrophages and their activation
Slide 38 : Macrophages are the principal effector cells of the DTH response Cytokines elaborated by TH1 cells induce blood monocytes to adhere to vascular endothelial cells and migrate from the blood into the surrounding tissues. During this process the monocytes differentiate into activated macrophages Activated macrophages exhibit increased levels of phagocytosis and an increased ability to kill microorganisms through various cytotoxic mediators. In addition, activated macrophages express increased levels of class II MHC molecules and cell-adhesion molecules and therefore function more effectively as antigen-presenting cells.
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