期刊
JOURNAL OF IMMUNOLOGY
卷 181, 期 5, 页码 3575-3585出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.5.3575
关键词
-
类别
资金
- National Institutes of Health [HL81151, GM61031, A1058228, HL34303]
- Human Frontier Science Program [LT-00606-2002]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL034303, R01HL068864, R01HL081151] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI058228, R56AI058228] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM061031] Funding Source: NIH RePORTER
Interaction between apoptotic cells and phagocytes through phosphatidylserine recognition structures results in the production of TGF-beta, which has been shown to play pivotal roles in the anti-inflammatory and anti-immunogenic responses to apoptotic cell clearance. Using 3T3-T beta RII and RAWT beta RII cells in which a truncated dominant-negative TGF-beta receptor 11 was stably transfected to avoid autofeedback induction of TGF-beta, we investigate the mechanisms by which TGF-beta was produced through PSRS engagement. We show, in the present study, that TGF-beta was regulated at both transcriptional and translational steps. P38 MAPK, ERK, and JNK were involved in TGF-beta transcription, whereas translation required activation of Rho GTPase, PI3K, Akt, and mammalian target of rapamycin with subsequent phosphorylation of translation initiation factor eukaryotic initiation factor 4E. Strikingly, these induction pathways for TGF-beta production were different from those initiated in the same cells responding to LIPS or PMA.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据