Hypersensitivity Flashcards
hypersensitivity
over-reactions of the immune system to harmless environmental antigens. 4 types based on the location of the target antigen and whether the immune response is mediated by antibodies or immune cells.
type 1 or immediate hypersensitivity
mediated by IgE. commonly called allergies or atopic disorders. normal response to multicellular parasites but directed to innocuous antigens with structural similarities. clinical manifestations depend on the route of entry of the antigen and the location of the responding cells
hygiene hypothesis
excessive hygiene reduces childhood exposures to microorganisms. vaccination reduces immune system experience with natural infection. overuse of antibiotics reduces immune system experience and ability to discriminate self from foreign. immune system perception of foreign danger is affected
characteristics of allergens
low weight, highly soluble and stabile proteins. contain peptides that can be presented by MHC class II. effective at activating Th2-type cytokines, especially IL-4 (stimulates IgE response)
initial sensitization to allergen
first exposure to allergen has antigen activation of Th2 cells and stimulation of IgE class switching in B cells. IgE binds to the FCR1 receptors on the mast cells.
subsequent exposures to allergens
mast cell degranulation. vasoactive amines, and lipid mediators give immediate hypersensitivity reaction. cytokines give late phase reaction
effects of mast cell mediators
SRS-A (slow releasing substance of anaphylaxis)-mixture of leukotrienes produced during response. Serotonin-affects vascular permeability. TNF stimulates expression of adhesion molecules on endothelial cells
what do the mediators lead to?
influx of inflammatory cells! reciprocally regulated. TGFB, IL-3 lead to increased basophils and decreased eosinophils, which are stimulated by IL-5 and GM-CSF.
granulocyte response
promotes expulsion of parasites by peristalsis and mucus. also makes cationic granule proteins to kill parasites, and enzymes to remodel tissue.
responses to subcutaneous allergen
localized swelling (urticaria). deeper swelling is angiodema. mechanism in skin testing for allergies is done through RAST assay for allergen specific IgE.
responses to inhaled allergen
Allergic rhinitis. if the eyes are affected, allergic conjunctivitis
allergic asthma
Th2 cells that produce IL-13. airway constriction and mucus. chronic asthma can occur in the absence of allergens: hyper-responsive to other irritants in air such as smoke
reactions to adsorbed allergen
food allergies. widely disseminated causing urticaria. smooth muscle contraction induces vomiting and diarrhea.
responses to systemic allergen
systemic anaphylaxis. most severe form of a type 1 reaction: antigens include drugs, serum, venom, and peanuts. treat with epinephrine. promotes tight junctions, relaxes bronchial smooth muscle, stimulates the heart
transfer of IgE and antigen in pregnancy
child more rish for allergy if mother is atopic. IgE complexed with allergen in amniotic fluid could be ingested by fetus
treatment for type 1 hypersensitivity
avoid allergen. treat symptoms with antihistamines, corticosteroids, etc. desensitize through controlled exposure leading to IgA and IgG blocking of IgE. vaccines, omalizumab
type II hypersensitivity
mediated by IgG. antibodies bind to a cell associated antigen or cell surface receptor and fix complement. EX: drug binds to surfaces of new RBCs creating new epitopes, and RBCs are lysed. platelets can also be lysed
when does hemolytic disease of the newborn occur?
every pregnancy after the first one where a RhD- mother had an RhD+ fetus. the mother now has the IgG against RhD+, and passes them to the baby
hyperacute graft rejection
may occur when transplant recipients have antibodies that react with donor ABO or HLA class I antigens
type III hypersensitivity
large quantities of soluble antigens and their antibodies develop and form large latticed immune complexes. isotype, valency, charge, and ability to fix complement determine IC pathogenicity. latticed immune complexes are pathologically capable of depositing systemically in any of a variety of tissue sites
arthus reaction
localized. PMNs attracted to site produce lysosomal enzymes causing tissue damage.
serum sickness
occurs after the development of antibody to antigen, about 7-10 days. may occur after large amounts of a foreign protein such as antisera for snake bite, mouse antibodies as therapeutics, streptokinase.
Type IV hypersensitivity reactions
mediated by antigen specific effector T cells. require greater amounts of allergen than Ig-mediated hypersensitivity
delayed type hypersensitivty
antigen introduced and processed by antigen presenting cells. Th1 effector cell recognizes antigen and releases cytokines which act on vascular endothelium. leads to recruitment of T cells, phagocytes, etc. in 24-72 hours
contact hypersensitivity
CD4+ t cells activate other immune cells while CD8+ T cells kill chemical reacted cells that display foreign antigen.
transplant rejection
when a kidney is transplanted, the recipient’s T cells attack the transplant.
Graft versus host disease
when hematopoietic cells are transplanted, the T cell in the transplant attack the recipient’s tissues
treatment of type II, III, IV hypersensitivity reactions
avoid antigen. reduce impact of immune response with anti-inflamm and steroids. reduce general immune response. induce regulation of response and block effector mechanisms of allergic response
