| First Author | Wang W | Year | 1997 |
| Journal | Immunity | Volume | 6 |
| Issue | 2 | Pages | 165-74 |
| PubMed ID | 9047238 | Mgi Jnum | J:38710 |
| Mgi Id | MGI:86092 | Doi | 10.1016/s1074-7613(00)80423-9 |
| Citation | Wang W, et al. (1997) c-Rel is a target of pentoxifylline-mediated inhibition of T lymphocyte activation. Immunity 6(2):165-74 |
| abstractText | The possible clinical use of the methyl xanthine derivative, pentoxifylline (PF), for the treatment of T cell-dependent diseases is being noted with increasing interest. In this paper, we studied the molecular consequences of PF treatment during lymphocyte activation. We found that in T cells, anti-CD3-induced c-Rel expression was blocked by PF, whereas the induction of other NF-kappaB family members was not significantly affected. However, induction of NF-AT, which has the same signaling requirements as c-Rel induction, was not inhibited by PF. Among genes that respond to these transcription factors, IL-2 mRNA induction was suppressed by PF, whereas IL-2R(alpha) chain mRNA induction was not affected. These observations implicated c-Rel as an IL-2 promoter factor, for which experimental support was obtained from transient transfection experiments. In contrast with the observation in T cells, c-Rel induction was not blocked by PF in B cells. The greater selectivity of PF, compared with FK506, at both the molecular and cellular levels may prove advantageous in manipulating T cell responses in vivo. |
