| First Author | Hoyer KK | Year | 2009 |
| Journal | Blood | Volume | 113 |
| Issue | 2 | Pages | 389-95 |
| PubMed ID | 18815283 | Mgi Jnum | J:144257 |
| Mgi Id | MGI:3830561 | Doi | 10.1182/blood-2008-04-153346 |
| Citation | Hoyer KK, et al. (2009) Distinct roles of helper T-cell subsets in a systemic autoimmune disease. Blood 113(2):389-95 |
| abstractText | 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-gamma (IFN-gamma) 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-gamma, delays the development of AIHA. Further, CD4(+) T cells from IL-2/IFN-gamma-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. |
