hypersensetivity

·         It is an exaggerated response of immune system that leads to the damage of the tissue and cells, and is shown by an individual on a second contact with the antigen.

·         Coombs and Gell classified the hypersensitivity reactions in four classes of reactions

Type I hypersensitivity:

·         The type I hypersensitivity is also known as allergic reaction. It is induced by antigens which are referred to as allergens.

·         Allergens are specifically non parasitic antigens capable of stimulating type I hypersensitivity responses.

·         The type I hypersensitivity reactions are IgE mediated reactions.

·         The reaction is stimulated by IgE to high affinity IgE-specific Fc receptors expressed on the mast cells and the basophil cells

·         When activated by the antigens (allergens) the IgE antibodies stimulates the mast cells and basophil cells to release primary mediators: vasoactive amines, stored in the granules (degranulation)

·         The chief mediators are the proteases, heparin and histamines etc..

·         The mediators are responsible for all the normal consequences of an acute inflammatory reaction. I.e. granulocyte chemotaxis, vascular permeability and all sorts of the consequences of inflammations.

·         The type I hypersensitivity is further classified as :

Ø  Anaphylaxis: this type of the type I hypersensitivity is highly rapid, life threatening, severe and are spread to whole body, they are caused due to the re-exposure of the individual to the antigen (allergens)

Ø  Atopy: if the tendency to develop allergic reactions is inherited genetically, they are called the atopic hypersensitivity reactions.

Type II hypersensitivity:

·         The type II hypersensitivity reactions cause the destruction of the host cells and tissues; by lysis or toxic mediators, hence they are also called as cytotoxic or cytolytic reactions.

·         It is an IgM and IgG mediated response.

·         It is caused by the binding of the antibodies to the cell or tissue antigens.

·         They (IgG and IgM) cause cell destruction by Fc-mediated mechanisms, either directly or indirectly activating the complement via the classical pathway.

·         Example of the hypersensitivity class ii reaction is the hypersensitivity shown by an individual who has been transfused blood of blood group other than that of the individual.

·         The antibodies attach to the cell membrane component, leading to complement fixation; this activates the complement chain and leads to either lysis or oposonization of the cell.

·         Lysis of target cell is analogous to that of cytotoxic T cells and involves the release of cytoplasmic granules, containing perforin and granzymes that activates the event leading to the apoptosis.

Type III hypersensitivity:

·         It is mediated by immune complexes of IgG antibodies with soluble antigens.

·         The circulating immunity complexes may accumulate at various tissue sites, where they activate complement and subsequently cause tissue cell lysis.

·         Normally these complements are phagocytized by the monocyte-macrophage system.

Type IV hypersensitivity:

·         Commonly it is known as delayed type of hypersensitivity.

·         Only class of hypersensitivity that is triggered by antigen-specific T cells. (cell mediated immunity reactions)

·         This is mediated by T-cell dependent effector mechanisms involving T_H cells.

·         This reaction has nothing to do with the antibodies.