转化生长因子-β：天生具有双重性。

Transforming growth factor-beta: innately bipolar.

作者信息

Wahl Sharon M

机构信息

Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH), Bethesda, MD 20892-4352, USA.

出版信息

Curr Opin Immunol. 2007 Feb;19(1):55-62. doi: 10.1016/j.coi.2006.11.008. Epub 2006 Nov 28.

DOI:10.1016/j.coi.2006.11.008

PMID:17137775

Abstract

Widely heralded for depressing ongoing immune responses, renewed interest in the proficiency by which transforming growth factor beta (TGF-beta) not only engages but also might drive an over-reactive innate response highlights its bipolar nature. Although coordination of the development and function of Treg, in addition to direct inhibition of cellular activation, are prominent pathways by which TGF-beta controls adaptive immunity, paradoxically TGF-beta appears instrumental in initiation of host responses to invasion through recruitment and activation of immune cells and persuasion of Th17 lineage commitment. Nevertheless, true to its manic-depressive behavior, new evidence links TGF-beta with depression of innate cells, including NK cells, and by way of a potential bridge between mast cells and Treg. Disruption of the tenuous balance between these opposing actions of TGF-beta underlies immunopathogenicity.

摘要

转化生长因子β（TGF-β）不仅能抑制持续的免疫反应，还可能引发过度活跃的先天反应，这一能力重新引发了人们对它的兴趣，凸显了其双重性质。尽管TGF-β除了直接抑制细胞活化外，还能协调调节性T细胞（Treg）的发育和功能，这是TGF-β控制适应性免疫的重要途径，但矛盾的是，TGF-β似乎通过招募和激活免疫细胞以及促使Th17细胞系分化，在宿主对入侵的反应启动中发挥作用。然而，与其躁郁行为相符的是，新证据表明TGF-β与先天细胞（包括自然杀伤细胞）的抑制有关，并且通过肥大细胞和Treg之间的潜在桥梁发挥作用。TGF-β这些相反作用之间脆弱平衡的破坏是免疫致病性的基础。