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Th17 Cells and autoimmune encephalomyelitis (EAE/MS) Aranami T; Yamamura TAllergol Int 2008[Jun]; 57 (2): 115-20Multiple sclerosis (MS) is a CD4+ T cell-mediated autoimmune disease affecting the central nervous system. It was largely accepted that Th1 cells driven by IL-12 were pathogenic T cells in human MS and experimental autoimmune encephalomyelitis, an animal model of MS. Recent data have established that IL-17-producing CD4+ T cells, driven by IL-23 and referred to as Th17 cells, play a pivotal role in the pathogenesis of EAE. A combination of TGF-beta and IL-6 induce Th17 cell lineage commitment via expression of transcription factor RORgammat. Th17 cells and induced Foxp3+ T regulatory cells are in reciprocal position in the T cell lineage commitment governed by TGF-beta and IL-6. The vitamin A metabolite retinoic acid is involved in this process via TGF-beta dependent induction of Foxp3. We have demonstrated that human Th17 cells could be identified as CCR2+ CCR5- memory CD4+ T cells. It is becoming clear that IL-23/Th17 axis also plays an important role in the pathogenesis of various human autoimmune diseases including MS. Additionally, accumulating evidences raise a possibility that CCR2 on Th17 cells may be a therapeutic target in MS.|Animals[MESH]|Autoimmune Diseases/*immunology[MESH]|Cell Differentiation[MESH]|Encephalomyelitis, Autoimmune, Experimental/immunology[MESH]|Encephalomyelitis/*immunology[MESH]|Forkhead Transcription Factors/metabolism[MESH]|Humans[MESH]|Interleukins/metabolism[MESH]|Multiple Sclerosis/*immunology[MESH]|Nuclear Receptor Subfamily 1, Group F, Member 3[MESH]|Receptors, CCR2/metabolism[MESH]|Receptors, Retinoic Acid/metabolism[MESH]|Receptors, Thyroid Hormone/metabolism[MESH]|T-Lymphocyte Subsets/*immunology[MESH]|T-Lymphocytes, Helper-Inducer/*immunology[MESH]|Th1 Cells/immunology[MESH]|Transforming Growth Factor beta/metabolism[MESH] |
