CD2-ACTIVATED T CELL LYMPHOKINE PRODUCTION

激活的T淋巴细胞的功能在很大程度上是 由T细胞激活后分泌的淋巴因子通过以下途径之一介导 几种跨膜受体包括TCR/CD3和CD2。而当 TCR/CD3途径激活是抗原特异性T细胞的基础 应答，CD2介导的激活是抗原非依赖性的基础 增殖，包括自身免疫T细胞的激活。特别是， 造血祖细胞增殖可通过 自身调节CD2激活的T细胞。监管机构的产生 (抑制性)T淋巴细胞亚群在正常循环时出现-- DR+CD58+祖细胞诱导自体CD4+CD2+T细胞增殖 细胞。通过CD2途径激活T细胞似乎也能产生 抑制T细胞淋巴因子，特别是肿瘤坏死因子-α (TNFpha)和较小程度的干扰素-伽马(INFGamma)。因此，研究 CD2途径在T细胞活化中的重要作用 了解造血功能的调节。来研究这样的假设 抑制性淋巴因子调节干细胞增殖，克隆 刺激因子(CSF)和细胞因子由CD2激活，并由 自动激活的T细胞将被识别出来。此外，T细胞 对α/CD2刺激反应而分泌淋巴因子的亚群将 被指认出来。如果偏好基因转录的特异性抑制 确认细胞因子，如TNFAlpha，然后是T细胞特异性分子 调节TNFAlpha基因转录的机制将是 特色化的。这项研究对扩大我们的认识很重要。 自身调节的造血动态平衡，受体特异性T细胞 激活，并在表征骨髓移植植入。

The functional repertoire of activated T lymphocytes is in large part mediated by lymphokine secretion following T cell activation via one of several transmembrane receptors including TCR/CD3 and CD2. While activation via the TCR/CD3 pathway is the basis for antigen specific T cell responses, CD2 mediated activation underlies antigen independent proliferation, including autoimmune T cell activation. In particular, hematopoietic progenitor cell proliferation can be directly regulated by autoregulatory CD2 activated T cells. Generation of a regulatory (suppressive) T lymphocyte subset occurs when normal cycling HLA-- DR+CD58+progenitor cells induce proliferation of autologous CD4+CD2+T cells. Activation of T cells via the CD2 pathway also appears to generate suppressive T cell lymphokines, specifically tumor necrosis factor-alpha (TNFalpha) and to a lesser extent interferon-gamma (INFgamma). Thus study of the CD2 pathway of T cell activation is of paramount importance in understanding regulation of hematopoiesis. To study the hypothesis that suppressive lymphokines regulate stem cell proliferation, the colony stimulating factors (CSFs) and cytokines produced by CD2 activated, and by auto-activated T cells will be identified. Additionally, the T cell subsets which secrete lymphokines in response to alpha/CD2 stimulation will be identified. If preferential gene transcription of specific suppressive cytokines, e.g. TNFAlpha is confirmed, then the T cell specific molecular mechanisms regulating the transcription of the TNFAlpha gene will be characterized. This research is important in expanding our understanding of autoregulatory hematopoietic homeostasis, receptor-specific T cell activation, and in characterizing bone marrow transplant engraftment.