title: Sequential evolution of IL-17 responses in the early period of allograft rejection.
abstract: In addition to CD4+CD25+Foxp3+ regulatory T (T(reg)) cells which protect against autoimmune tissue injury, IL-17-producing CD4+ T (T(h)17) cells have been recently described and shown to play a crucial role in autoimmune injury. It appears that there is a reciprocal developmental pathway between T(h)17 and T(reg) cells. Although IL-17 is known to be associated with allograft rejection, the cellular source of IL-17 and the nature of T(h)17 in the context of allograft rejection remain unknown. In the current study, the dynamics of T(reg) and IL-17-producing cells after syngeneic and allogeneic transplantation were examined using a wild-type murine cardiac transplantation model. Ly6G+ cells were found to produce IL-17 during the early postoperative period and CD8+ as well as CD4+ T cells were also found to produce IL-17 during alloimmune response. Graft-infiltrating Ly6G+, CD4+, and even CD8+ cells were found to express IL-17 highly compared to those in spleen. Although the frequencies of T(h)17 and T(reg) were found to gradually increase in both syngeneic and allogeneic recipients, T(h)17/T(reg) ratios were significantly higher in recipients with allograft rejection than in syngeneic recipients. In conclusion, IL-17 is produced by neutrophils during the early postoperative period and subsequently by T(h)17 and CD8+ T cells during allograft rejection. T(h)17/T(reg) imbalance is associated with the development of allograft rejection. This study would provide basic information on T(h)17 biology for future investigation in the field of transplantation.
authors: Department of Surgery, Seoul National University College of Medicine, Seoul 110-799, Korea.
authors: Sang Il
authors: SI
authors: Min
authors: Jongwon
authors: J
authors: Ha
authors: Chung-Gyu
authors: CG
authors: Park
authors: Jae Kyung
authors: JK
authors: Won
authors: Yang Jin
authors: YJ
authors: Park
authors: Seung-Kee
authors: SK
authors: Min
authors: Sang Joon
authors: SJ
authors: Kim
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis; D015551:Autoimmunity; D051858:Forkhead Transcription Factors / Q000096:biosynthesis; D006084:Graft Rejection / Q000276:immunology / Q000378:metabolism*; D016027:Heart Transplantation; D020381:Interleukin-17 / Q000276:immunology / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism*; D013997:Time Factors; D014181:Transplantation Immunology
chemical_list: D015703:Antigens, CD; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D020381:Interleukin-17