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Blood, 8 January 2009, Vol. 113, No. 2, pp. 389-395. Prepublished online as a Blood First Edition Paper on September 24, 2008; DOI 10.1182/blood-2008-04-153346. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-04-153346v1 113/2/389    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Hoyer, K. K. Articles by Abbas, A. K. Search for Related Content PubMed PubMed Citation Articles by Hoyer, K. K. Articles by Abbas, A. K. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Distinct roles of helper T-cell subsets in a systemic autoimmune disease Katrina K. Hoyer1, Wilson F. Kuswanto1, Eugenio Gallo1, and Abul K. Abbas1 1 Department of Pathology, University of California San Francisco Imbalance of T-helper cell (Th) differentiation and subsequent cytokine dysregulation is implicated in inflammatory and autoimmune diseases. In particular, 2 cytokines produced by different Th cell populations, interferon- (IFN-) and interleukin-17 (IL-17), have been shown to play a critical role in autoimmunity. We have examined the roles of these cytokines in a mouse model of systemic autoimmunity resulting from the deletion of IL-2 in which autoimmune hemolytic anemia (AIHA) is a prominent feature. We demonstrate that, in IL-2–knockout (KO) BALB/c mice, elimination of the Th1 cytokine, IFN-, delays the development of AIHA. Further, CD4+ T cells from IL-2/IFN-–KO mice produce elevated levels of IL-17 compared with wild-type (WT) and IL-2–KO, and these mice eventually develop intestinal inflammation. In contrast, elimination of the Th17 cytokine, IL-17, from IL-2–KO mice fails to suppress early acute AIHA development. These results suggest that in a systemic autoimmune disease with multiple manifestations, Th1 cells drive the early autoantibody response and IL-17–producing cells may be responsible for the more chronic tissue inflammation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. Shi, M. Ramaswamy, B. P. Vistica, C. A. Cox, C. Tan, E. F. Wawrousek, R. M. Siegel, and I. Gery Unlike Th1, Th17 Cells Mediate Sustained Autoimmune Inflammation and Are Highly Resistant to Restimulation-Induced Cell Death J. Immunol., December 1, 2009; 183(11): 7547 - 7556. [Abstract] [Full Text] [PDF] J. Zuber, A. Brodin-Sartorius, N. Lapidus, N. Patey, M. Tosolini, S. Candon, M. Rabant, R. Snanoudj, C. Panterne, E. Thervet, et al. FOXP3-enriched infiltrates associated with better outcome in renal allografts with inflamed fibrosis Nephrol. Dial. Transplant., September 3, 2009; (2009) gfp435v1. [Abstract] [Full Text] [PDF]

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