The immune system protects against infection, yet it can sometimes harm the host. Immunopathology studies hypersensitivity responses. The term "sensitised" originates from the idea that those who were previously exposed to an antigen later showed notable responses to it.

Hypersensitivity responses can be caused through endogenous self-antigens or exogenous antigens. Immune reactions for endogenous or self-antigens impacts in autoimmune disorders. On the other hand, immune response may take variety of forms against exogenous antigens such as microbial and non-microbial (i.e. medications, foods, pollens, chemicals and dust) components. Some of the most common reactions to exogenous antigens create the type of disease known as allergy which includes range of symptoms ranging from itching, rash, fever, asthma and anaphylaxis.

Hypersensitivity often develops when an inequity happens among the effector mechanisms and the regulator systems that typically operate to limit such reactions. The course of hypersensitivity I responses is related to the inheritance of certain genes. HLA genes and several non-HLA genes have been related in various infection specific situations.

Immunological reactions including particular T-cells or IgG antibodies might also generate hypersensitive responses. While these effectors support of the immune reaction normally participate in defending against infection, respond to noninfectious antigens to create acute or persistent hypersensitivity responses.

Due to the complicated features, it is difficult to offer a thorough explanation of all areas of immunology in this single article. The objective of this article is to offer a general concept regarding the main components and properties of hypersensitive reaction.

Gell and Coombs in 1963 divided the identified hypersensitive responses in four kinds based on the mechanism of action. Type I hypersensitivity responses are acute allergic reactions (i.e. anaphylaxis), where type II entails antibody mediated cytotoxic response to particular tissues.

Antibody-antigen complexes produce many tissue damages in type III hypersensitivity responses. Sensitized T helper cells cause delayed type IV hypersensitivity. In some autoimmune illnesses, immune reactions stimulate the endocrine system.

Type I hypersensitivity is produced by IgE antibody and resulting in anaphylactic reactions to insect venoms, drugs, and foods. These allergic reactions are systemic or local because allergens induce IgE antibody production. Type I hypersensitivity is caused by an antigen cross-link to a basophil or mast cell's membrane-bound IgE antibody. During an anaphylactic reaction, histamine is released and causes potential tissue damage within the body.

Type I hypersensitivity

Antibodies linked to cell antigens cause type II hypersensitivity responses. Antibodies stimulate complement-dependent lysis, damaging tissue. In a cytotoxic response, the antibody binds to the cell membrane antigen to induce complement-mediated cell lysis. Antigens can be "self" (autoimmune reactions) or "non-self". IgM/IgG mediate cytotoxic responses. Newborn Rh-incompatibility is a good example of cytotoxic reactions. Blood transfusion responses, Good pasture's syndrome, and autoimmune diseases are others.

Type II hypersensitivity

The development of antigen-antibody complexes promotes type III hypersensitivity. IgG and IgM bind antigen and deposit (immune) antigen-antibody complexes. This complex promotes the complement system, which influences PMN chemotaxis and initiation. PMNs then release enzymes that damage tissue into the cell. Serum sickness is one of the most common forms of type III hypersensitivity response in the human body.

Type III hypersensitivity

Initial descriptions of delayed or type IV hypersensitivity focused on the duration of the responses, which took 12 to 24 hours to develop and persisted for two to three days. T-lymphocytes initiate cell-mediated responses, which are then mediated by effector T-cells and macrophages. This reaction contains the antigens bound to the lymphocyte surface. Lymphocytes that have been pre-sensitized can generate cytokines, which can cause cell damage. Many chronic illnesses, such as tuberculosis, have delayed type hypersensitivity.

Type IV cell-mediated (delayed hypersensitivity)

Extreme sensitivity to food, insect stings, spores, and medications is not uncommon. Recent clinical research such as HLA tetramers and microarray techniques are anticipated to have clinical applications for hypersensitive reaction, which is a positive development.