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Eicosanoids and aspirin in immune cell function
Author(s) -
Bailey J. Martyn
Publication year - 1985
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.950030205
Subject(s) - lymphokine , diacylglycerol kinase , immune system , microbiology and biotechnology , arachidonic acid , phospholipase a2 , biology , protein kinase c , lipid signaling , phospholipase , biochemistry , chemistry , signal transduction , receptor , immunology , enzyme
Clonal expansion of T‐lymphocyte populations results from interactions of antigenic structures presented in combination with accessory cells (macrophages) and antibody recognition sites on the surface of T cells. The resulting activation of a membrane phospholipase C plays a crucial role in lymphocyte responses by releasing diglyceride and PIP 3 . The released diglyceride activates a cellular protein kinase C while PIP 3 stimulates Ca 2+ influx. Arachidonic acid released by the action of diglyceride lipase serves as substrate for the synthesis of bioactive eicosanoids (prostaglandins and leukotrienes) which in turn modulate cellular adenyl and guanyl cyclases. The eicosanoids serve as both intra‐ and extra‐cellular signals for lymphocytes, regulating the production and expression of lymphokines and mediating the complex interactions between the monocyte‐macrophage components and helper and suppressor T cells. Aspirin and other anti‐inflammatory drugs stimulate mitogenesis by inhibiting production of the negative modulator prostaglandin E 2 in accessory cells and by enhancing the production of the lymphokine 1L‐2 by producer T‐cells.