期刊
EXPERIMENTAL AND MOLECULAR MEDICINE
卷 41, 期 10, 页码 707-716出版社
SPRINGERNATURE
DOI: 10.3858/emm.2009.41.10.077
关键词
graft rejection; interleukin-17; neutrophils; T-lymphocytes, regulatory
资金
- Clinical Research Institute (CRI)
- Seoul National University Hospital [0620082780]
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.
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