Antibody‐Mediated (Humoral) Immunity (AMI).Introduction to Controlling Microbial Growth.Introduction to Prokaryotes, Eukaryotes.Ultimately, tissue injury occurs.Ĭlinical examples: Contact dermatitis, rheumatoid arthritis, mantoux test.
This cytokines recruits and activates phagocytes, as well as inducing local inflammation. T-cell mediated cytotoxicity (mediated by CD8+ T cells) - in this reaction, T-cytotoxic cell specific for autoantigen on host cells may directly kill these cells.ĭelayed type hypersensitivity ĪPC or tissue antigen (autoantigen) activate/sensitize CD4+ and CD8+ T cells, causing them to secrete cytokines.Delayed type hypersenstivity (mediated by CD4+ and CD8+T cells).This is also called the T-cell mediated hypersensitivity. Systemic lupus erythematosus, post-streptococcal vasculitis, post-streptococcal glomerulonephritis This may also activate the complement system or become target of phagocytes, causing damage to the vessel wall and ultimately the organ itself (the kidney). In some people, in relation to post-streptococcal endocarditis, the antibodies that is formed against streptococcus forms immune-complex that is deposited in vascular membrane, especially the glomerulus. This is also called immune-complex mediated hypersensitivty. In some cases, antibodies are formed after infection, such as in post-streptococcal endocarditis, in which antibodies used against streptococcus becomes cross reactive also against endocardium (rheumatic fever). Autoantibodies act as ligands for receptors (in Grave's disease)Īutoantibodies are formed as a result of failure of tolerance (central and peripheral tolerance).Autoantibodies against self antigens function as opsonin for phagocytes.IgM and IgG against self-antigens (autoantibodies) of the extracellular matrix or cell surface triggers the classical pathway of complement activation.There are a few ways in which antibody can cause hypersensitivity reaction, including: This type of hypersensitivity is also called antibody mediated hypersensitivity. Other mediators, especially cytokines recruit other inflammatory cells to the site of reaction.These mediators cause vasodilation, increased vasopermeability, tissue damage and smooth muscle contraction.Subsequent exposure to allergen results in degranulation of the mast cell, releasing its mediators, namely cytokines, vasoactive amines and eicosanoids - prostaglandin and leukotrines).The mast cell is 'sensitized' against the allergen. These IgE is bound to the Fc receptor on mast cell.In the first exposure to an allergen, IgE is produced, presumably under the stimulation of T-Helper type 2.An atopic patient may not undergo allergic reaction if not exposed to a particular allergen.Ītopic eczema. This type of reaction is also indiscriminately called immediate hypersensitivity or allergy or atopy, even though the term atopy is usually used for describing genetic propensity to develop this hypersensitive reaction, in which person with this propensity is called atopic. There is a strong genetic basis in developing hypersensitivity. The effect may range from discomfort, organ damaging to fatality. Allergic reaction may be localised (asthma) or systemic (anaphylactic shock).Īutoimmunity is a pathological reaction in which the immune system directly or indirectly targets and damages own cells. Response time is the time at which the reaction develops after contact with an allergen.
The time lag before developing an allergic reaction is called the refractory period. Simple low molecular weight substances are only partial antigens ( hapten), become a complete antigen in the body after binding with internal protein. Allergens are substances usually protein in nature. It includes allergy and autoimmunity.Īllergy is a pathological reaction of the immune system to external antigens - allergens, which exist normally in the environment (pollens, molds, animals, foods, insect stings, etc.). Hypersensitivity is an undesirable reaction produced by normal immune system.