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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.
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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.
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