Arthus Reaction

Maurice Arthus (1862-1945) combines Koch's and Richet's discovery of the delayed hypersensitivity reaction. From Paris he travels to Switzerland where he injects rabbits with horse serum containing anti-toxin antibodies. The cognate antigen, toxin, injected a few days later subcutaneously will induce the now well known Arthus-phenomenon: the antigen attracts antibody to the site of injection leading to local formation of immune-complexes, which precipitate in vessel walls of the microcirculation thus inducing local inflammation. With the indirect Arthus-phenomenon used more frequently for experiments it is the antibody that becomes injected locally followed by systemic administration of antigen, but such procedure leads to identical tissue damage. Polymorphonuclear leukocytes bearing E-selectins (adhesion molecules) do not roll on endothelial cells anymore and infiltrate the tissue traversing endothelial cell gaps. Jointly, intercellular and vascular cell adhesion molecules-1, ICAM, VCAM, endeavor to the Arthus reaction by further regulating leukocyte accumulation and proinflammatory cytokine production; P-selecting glycoprotein ligand-1 (PSGL-1) induces chemokine secretion at inflamed sites. Ensuing complement activation destroys the tissue. Neutrophil peptides help DNA-containing immune complexes to enhance the synthesis rate of interferon alpha, a billion molecules in a 12-hour period, brought about by plasmacytoid dendritic cells.

Inject antigen into the skin of an animal which already has made antibody upon prior antigen exposure: vasculitis is the consequence.

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