[Immunological aspects of corticotherapy]

The therapeutic effectiveness of corticoids in transplantation, in autoimmune conditions and in numerous diseases in which the pathogenic role of hypersensitivity reactions is invoked, is perfectly established on the empirical basis of clinical cases. The study of the effects of corticoids on the immunological response is on the contrary very fragmentary; it comes up against numerous difficulties, especially against the differences in susceptibility from one species to another. The lymphoid cells have cytoplasmic and nuclear receptors for corticosteroids. The fixation of corticosteroids on lymphocytes inhibits the synthesis of nucleic acids and raises the intracellular level of cyclic AMP. Corticosteroids decrease the mobility of polymorph leukocytes in the presence of a chemotactic stimulus, at high doses, they disturb phagocytosis by marcophages, oppose the degranulation of mast cells and polymorph leukocytes, and the cytotoxic action of sensitised T lymphocytes. In vivo, corticosteroids have little effect on the production of antibodies (primary of secondary response) do not modify the "immunological memory" by through an anti-inflammatory effect, abolish the peripheral manifestations of late hypersentsitivity reactions. Corticosteroids enable the treatment of acute rejection crises in transplantation, they have a symptomatic effect on type I and IV Gel and Cooms hypersensitivity reaction, their activity is less regular in the other phenomena of hypersensitivity.