The Swiss 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. Indirect Arthus-phenomenon –> inject antibody then give antigen i.v., this leads to identical tissue damage as direct type.
Polymorphonuclear leukocytes bearing E-selectins (adhesion molecules) cannot roll on endothelial cells hence will 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.