The role of human T-lymphocyte-monocyte contact in inflammation and tissue destruction

Abstract

Contact-mediated signaling of monocytes by human stimulated T lymphocytes (T_L) is a potent proinflammatory mechanism that triggers massive upregulation of the proinflammatory cytokines IL-1 and tumor necrosis factor-α. These two cytokines play an important part in chronic destructive diseases, including rheumatoid arthritis. To date this cell–cell contact appears to be a major endogenous mechanism to display such an activity in monocyte-macrophages. Since T_L and monocyte-macrophages play a pivotal part in the pathogenesis of chronic inflammatory diseases, we investigated the possible ligands and counter-ligands involved in this cell–cell interaction. We also characterized an inhibitory molecule interfering in this process, apolipoprotein A-I. This review aims to summarize the state of the art and importance of contact-mediated monocyte activation by stimulated T_L in cytokine production in rheumatoid arthritis and mechanisms that might control it.