期刊
CLINICAL AND EXPERIMENTAL IMMUNOLOGY
卷 159, 期 2, 页码 137-147出版社
WILEY
DOI: 10.1111/j.1365-2249.2009.04040.x
关键词
suppression; Th1; Th2; Th17; Treg
类别
资金
- UK Medical Research Council
- Wellcome Trust
- UK Multiple Sclerosis Society
- Research Councils UK
- MRC
- BBSRC
- National Institute for Health Research (NIHR)
- Biomedical Research Centre
- King's College London
- King's College Hospital NHS Foundation Trust
- MRC [G0801924] Funding Source: UKRI
- Medical Research Council [G9900991B, G0801924] Funding Source: researchfish
P>CD4+ T cells display considerable flexibility in their effector functions, allowing them to tackle most effectively the range of pathogenic infections with which we are challenged. The classical T helper (Th) 1 and Th2 subsets have been joined recently by the Th17 lineage. If not controlled, the potent effector functions (chiefly cytokine production) of which these different cells are capable can lead to (sometimes fatal) autoimmune and allergic inflammation. The primary cell population tasked with providing this control appears to be CD4+ regulatory T (T-reg) cells expressing the forkhead box P3 (FoxP3) transcription factor. Here we consider the comparative capacity of FoxP3+ T-regs to influence the polarization, expansion and effector function of Th1, Th2 and Th17 cells in vitro and in vivo as well as in relation to human disease. This remains a particularly challenging series of interactions to understand, especially given our evolving understanding of T-reg and T effector interrelationships, as well as recent insights into functional plasticity that cast doubt upon the wisdom of a strict categorization of T effector cells based on cytokine production.
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