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ISSN 打印: 1040-8401
ISSN 在线: 2162-6472

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DOI: 10.1615/CritRevImmunol.2013006959
pages 165-182

Transcription Factors and Th17 Cell Development in Experimental Autoimmune Encephalomyelitis

Guobing Chen
Gene Expression and Epigenomics Laboratory, Department of Genome Biology, The John Curtin School of Medical Research, Australian National University, Canberra, 2600 Australia; Laboratory of Molecular Biology and Immunology, National Institute on Aging
M. Frances Shannon
Gene Expression and Epigenomics Laboratory, Department of Genome Biology, The John Curtin School of Medical Research, Australian National University, Canberra, 2600 Australia; University of Canberra, Canberra, ACT 2601, Australia

ABSTRACT

Experimental autoimmune encephalomyelitis (EAE), a widely studied animal model of human central nervous system demyelinating diseases such as multiple sclerosis, is a T-cell-mediated autoimmune disease involving effector T helper (Th) subsets such as Th and Th7. Recently, Th7 cells have been shown to play a major role in many autoimmune and other inflammatory diseases. The development of Th subsets is controlled by a complex network of cytokines and signaling and transcription molecules that act to augment the development of one cell type while restricting the development of other lineages. Here, we review the transcription factors (TFs) that are required for Th17 cell development in EAE and classify them into three types: major or essential such as RORγt and STAT3, an array of helper factors that work in combination with or regulate the expression of the major factors, and regulatory TFs that attenuate the expression of Th17 genes. The plasticity of the Th17 cell lineage is also discussed in relation to the interaction of TFs that play a major role in the development of other Th or regulatory T cell (Treg) lineages such as T-bet and Foxp3 with the Th17 TFs.


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