Eicosanoids and aspirin in immune cell function

✍ Scribed by J. Martyn Bailey

• Publisher: John Wiley and Sons
• Year: 1985
• Tongue: English
• Weight: 746 KB
• Volume: 3
• Category: Article
• ISSN: 0265-9247
• DOI: 10.1002/bies.950030205

✦ Synopsis

Abstract

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.