The antigen becomes exogenous (chronic bacterial, viral or parasitic infections) or endogenous autoimmune (non-organ specific: for example, Lupus). It is mediated by soluble immune complexes. In their totality they are of the class of Immunoglobulin G (IgG), although the I Immunoglobulin M (IgM), may also be involved. This resistance can be the pathogenic component of the diseases caused by many microorganisms.Īlso, it develops from 3 to 10 hours after the antigen display (as for example the Arthus reaction). Skin: Systemic Lupus Erythematosus, Arthus reaction.Type 3 Hypersensitivity is also known as Hypersensitivity to immune complexes, including: The treatment includes anti-inflammatory and immunosuppressive agents. The lesion has antibodies, supplements and neutrophils.ĭiagnostic biopsies contain the location of circulating antibodies against the tissues involved and the representation of antibodies and complement in the study (biopsy), using immunofluorescence.

Phagocytes and K cells play a crucial role in this process. The time of reluctance is from minutes to hours, since Type 2 Hypersensitivity is mainly involved by antibodies of the classes Immunoglobulin M (IgM) or Immunoglobulin G (IgG) and its complements. Type 2 Hypersensitivity is also known as Cytotoxic Hypersensitivity is detrimental to a variety of organs and tissues.Īntigens are normally endogenous, however, exogenous chemical derivatives (also known as Haptens), are able to bind significantly to cell membranes, while drastically leading to Type 2 Hypersensitivity.ĭrug-induced hemolytic anemia, granulocytopenia and thrombocytopenia are examples of this type. The mechanism is unclear, but there is a correlation between the appearance of Immunoglobulin G Blockers (IgG) antibodies, and the relief of symptoms. Hyposensitization (Immunotherapy or Desensitization) is another treatment modality that is successful in several allergies, particularly in insect venoms and, to a certain extent, pollen.

Type 3 hypersensitivity