Grenningloh Roland, Kang Bok Yun, Ho I-Cheng
Department of Medicine, Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA 02115, USA.
J Exp Med. 2005 Feb 21;201(4):615-26. doi: 10.1084/jem.20041330.
To mount an effective type 1 immune response, type 1 T helper (Th1) cells must produce inflammatory cytokines and simultaneously suppress the expression of antiinflammatory cytokines. How these two processes are coordinately regulated at the molecular level is still unclear. In this paper, we show that the proto-oncogene E26 transformation-specific-1 (Ets-1) is necessary for T-bet to promote interferon-gamma production and that Ets-1 is essential for mounting effective Th1 inflammatory responses in vivo. In addition, Ets-1-deficient Th1 cells also produce a very high level of interleukin 10. Thus, Ets-1 plays a crucial and unique role in the reciprocal regulation of inflammatory and antiinflammatory Th responses.
为了启动有效的1型免疫反应,1型辅助性T(Th1)细胞必须产生炎性细胞因子,同时抑制抗炎性细胞因子的表达。这两个过程在分子水平上是如何协同调节的仍不清楚。在本文中,我们表明原癌基因E26转化特异性-1(Ets-1)是T-bet促进γ干扰素产生所必需的,并且Ets-1对于在体内启动有效的Th1炎性反应至关重要。此外,缺乏Ets-1的Th1细胞还会产生非常高水平的白细胞介素10。因此,Ets-1在炎性和抗炎性Th反应的相互调节中发挥着关键且独特的作用。