Journal
NATURE IMMUNOLOGY
Volume 11, Issue 1, Pages 36-40Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1802
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Funding
- US National Institutes of Health
- Crohn's and Colitis Foundation of America
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Chronic reactivity of CD4(+) T cells to autoantigens and to components of the commensal flora drive destructive inflammation in a variety of mouse models of autoimmunity. Insight gained using these models is empowering translational research into human disease. Immunologists are trying to assign disease culpability to one of the ever-growing number of T helper (T-H) cell subsets. Although recent discovery of the interleukin 17-producing T-H-17 lineage appeared to supplant the pre-eminence of T(H)1 cells in promoting autoimmunity, the newest data defy simple paradigms. Here we speculate on the respective contributions to autoimmunity made by an increasingly complex list of T-H subsets and argue that the T(H)1 phenotype may be staging a comeback.
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