The identification and characteristics of IL-22-producing T cells in acute graft-versus-host disease following allogeneic bone marrow transplantation

The identification and characteristics of IL-22-producing T cells in acute graft-versus-host disease following allogeneic bone marrow transplantation
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同种异体骨髓移植后急性移植物抗宿主病中产生 IL-22 的 T 细胞的鉴定和特征。

DOI:
10.1016/j.imbio.2013.05.005
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发表时间:
2013-12-01
期刊:
影响因子:
2.8
通讯作者:
Xu, Kailin
Xu, Kailin
中科院分区:
医学4区
文献类型:
--
作者:
Zhao, Kai;Zhao, Dongmei;Xu, Kailin

文献摘要

被引文献

相似文献

移植物抗宿主病(GVHD)是异基因骨髓移植的主要障碍,其中涉及同种异体反应性供者T细胞分泌的多种促炎细胞因子。IL-22作为IL-10家族成员在GVHD中的作用仍有争议,产生IL-22的细胞的性质也不清楚。我们在此证明了参与GVHD的CD 4(+)T细胞而不是CD 8(+)T细胞是供体来源的IL-22的主要细胞来源。Th 1和Th 17细胞不仅表达经典的细胞因子IFN-γ或IL-17,而且还参与了GVHD中IL-22的分泌。Th 22细胞以独立分泌IL-22为特征,占产生IL-22的CD 4(+)T细胞的近一半。产生IL-22的CD 4(+)T细胞的频率随GVHD的发展呈动态变化。最后,我们观察到GVHD小鼠产生IL-22的CD 4(+)T细胞携带CD 62 L-CD 44(高/低)表面标记。总之,我们阐明了供者来源的产生IL-22的CD 4(+)T细胞的特性,这可能对进一步研究GVHD的发病机制具有潜在的意义。(C)2013 Elsevier GmbH. All rights reserved.
Graft-versus-host disease (GVHD) remains the major obstacle for allogeneic bone marrow transplantation, in which many proinflammatory cytokines secreted by alloreactive donor T cells are involved. Role of IL-22 as a member of IL-10 family in GVHD is still disputed and the properties of IL-22-producing cells are unclear. We demonstrated here that CD4(+) T cells but not CD8(+) T cells involved in GVHD were the main cellular source of donor-derived IL-22. Th1 and Th17 cells were detected not only express classical cytokine IFN-gamma or IL-17, but also contributed to IL-22 secretion in GVHD. Th22 cells characterized by the independent secretion of IL-22 were identified and occupied almost half percentage of IL-22-producing CD4(+) T cells. The frequency of IL-22-producing CD4(+) T cells showed dynamic changes with the development of GVHD. Finally, we observed that IL-22-producing CD4(+) T cells in GVHD mouse carried CD62L-CD44(high/low) surface markers. In conclusion, we illuminate the characteristics of donor-derived IL-22-producing CD4(+) T cells, which may have potent implication for further study of pathogenesis of GVHD. (C) 2013 Elsevier GmbH. All rights reserved.