期刊
SCANDINAVIAN JOURNAL OF IMMUNOLOGY
卷 72, 期 3, 页码 173-184出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1365-3083.2010.02432.x
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资金
- NIH [R01NS045937, R01NS035685, R37NS030843, R01A1044880, P01A1039671, P01NS038037]
- National Multiple Sclerosis Society [RG-2571]
- Boehringer Ingelheim
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI044880, P01AI039671] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS030843, R37NS030843, P01NS038037, R01NS045937, R01NS035685] Funding Source: NIH RePORTER
Many autoimmune diseases are driven by self-reactive T helper cells. Until recently, organ-specific autoimmune diseases were primarily associated with Th1 cells but not Th2 cells. However, the discovery of a number of new effector T-cell subsets, like Th17 and Th9 cells, and regulatory T cells, like Tregs and Tr1 cells, has changed the way we view and understand autoimmunity at cellular and molecular levels. In recent years, IL-17-producing Th17 cells have emerged as major players in autoimmunity. The complicated relationship between Th1 and Th17 cells, as well as the intricate balance between Tregs and Th17 cells, provides a basis for understanding the immunological mechanisms that induce and regulate autoimmunity. Here, we give an overview of the interplay between different effector T-cell subsets and regulatory T-cell subsets, and how they contribute to the development of autoimmunity and tissue inflammation.
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