Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9110977 | Cytokine | 2005 | 7 Pages |
Abstract
The suppressor activity of splenic macrophages induced by Mycobacterium intracellulare infection (MI-MÏs) against T cell concanavalin A (Con A) mitogenesis is mediated by MI-MÏ's mediators, such as reactive nitrogen intermediates (RNIs), phosphatidylserine, free fatty acids, prostaglandin E2 and to a minor extent TGF-β. Here, we have compared the roles of RNIs and TGF-β in the expression of MI-MÏ's suppressor activity against Con A mitogenesis and anti-CD3 monoclonal antibody (mAb)- and anti-CD28 mAb-induced mitogenesis (TCR signal-induced mitogenesis) of the target T cells, and have found the following. First, NG-monomethyl-l-arginine (NMMA) inhibited MI-MÏ's suppressor activity against TCR signal-induced mitogenesis as well as Con A mitogenesis. Second, anti-TGF-β mAb weakly restored the MI-MÏ-mediated suppression only in the case of Con A mitogenesis, under limited conditions, such as very low cell densities of MI-MÏs. Third, the blocking effects of NMMA plus anti-TGF-β mAb were somewhat more prominent in the case of Con A mitogenesis than in the case of TCR signal-induced mitogenesis. Fourth, Con A- or TCR signal-stimulated MI-MÏs secreted significant amounts of the latent TGF-β but not the active one. These findings indicate that RNIs, but not TGF-β, play important roles in the MI-MÏ-mediated suppression of TCR signal-induced mitogenesis, as well as Con A mitogenesis, of the target T cells.
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Authors
Toshiaki Shimizu, Shanshan Cai, Haruaki Tomioka,