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播散性组织胞浆菌病小鼠免疫调节因子的细胞起源和靶细胞

Cellular origins and target cells of immunoregulatory factors in mice with disseminated histoplasmosis.

作者信息

Deepe G S, Watson S R, Bullock W E

出版信息

J Immunol. 1984 Apr;132(4):2064-71.

PMID:6230399
Abstract

Disseminated infection with Histoplasma capsulatum stimulates the production of a suppressor factor (SF-H) by spleen cells from C3H/HeJ mice and a helper factor (HF-H) by spleen cells from C57BL/6 mice. In the present study these disparate immunoregulatory factors were analyzed in detail with regard to: a) the surface phenotype of the cells that produce SF-H and HF-H; b) the role of accessory cells in the production of these factors; and c) the surface phenotype of the target cells activated by SF-H and HF-H. Treatment of spleen cells from Histoplasma-infected C3H/HeJ mice with anti-Thy-1.2 plus complement (C) or with anti-Ly-2 plus C or with anti-I-Jk antiserum plus C abolished production of SF-H. Conversely, generation of HF-H by spleen cells from C57BL/6 mice was abrogated by treatment with either anti-Thy-1.2 plus C or with anti-Ly-1 plus C. Thus, a Thy-1.2+, Ly-2+, I-J+ T cell releases SF-H, and a Thy-1.2+, Ly-1+ T cell secretes HF-H. Production of SF-H and HF-H by splenic T cells was reduced markedly by depletion of macrophages (M phi); readdition of 1% syngeneic, plastic-adherent splenocytes from normal or infected mice to M phi-depleted, splenic T cell cultures of either strain restored the capacity to generate immunoregulatory factors. Furthermore, adherent splenocytes from normal or infected mice liberated a factor or factors that enhanced production of both SF-H and HF-H. Kinetic studies demonstrated that activation of normal spleen cells required at least 48 hr of exposure to SF-H or HF-H. Both factors failed to activate splenocytes pretreated with anti-Thy-1.2 plus C. Spleen cells from C3H/HeJ mice depleted of Ly-1+, Ly-2+, or I-J+ cells and exposed to SF-H did not demonstrate suppressor activity, whereas Ly-1-depleted splenocytes from C57BL/6 mice exposed to HF-H failed to exert helper activity. Therefore, the target of SF-H is a Thy-1.2+, Ly-1+2+, I-J+ T cell, and the target of HF-H is a Thy-1.2+, Ly-1+ T cell.

摘要

荚膜组织胞浆菌的播散性感染可刺激C3H/HeJ小鼠脾细胞产生一种抑制因子(SF-H),以及C57BL/6小鼠脾细胞产生一种辅助因子(HF-H)。在本研究中,对这些不同的免疫调节因子进行了详细分析,涉及以下方面:a)产生SF-H和HF-H的细胞的表面表型;b)辅助细胞在这些因子产生中的作用;c)被SF-H和HF-H激活的靶细胞的表面表型。用抗Thy-1.2加补体(C)或抗Ly-2加C或抗I-Jk抗血清加C处理来自感染荚膜组织胞浆菌的C3H/HeJ小鼠的脾细胞,可消除SF-H的产生。相反,用抗Thy-1.2加C或抗Ly-1加C处理可消除C57BL/6小鼠脾细胞产生HF-H。因此,Thy-1.2+、Ly-2+、I-J+ T细胞释放SF-H,而Thy-1.2+、Ly-1+ T细胞分泌HF-H。巨噬细胞(M phi)的清除显著降低了脾T细胞产生SF-H和HF-H的能力;将来自正常或感染小鼠的1%同基因塑料贴壁脾细胞重新添加到M phi清除的任一品系的脾T细胞培养物中,恢复了产生免疫调节因子的能力。此外,来自正常或感染小鼠的贴壁脾细胞释放出一种或多种增强SF-H和HF-H产生的因子。动力学研究表明,正常脾细胞的激活需要至少48小时暴露于SF-H或HF-H。两种因子均不能激活用抗Thy-1.2加C预处理的脾细胞。来自C3H/HeJ小鼠的Ly-1+、Ly-2+或I-J+细胞被清除并暴露于SF-H的脾细胞未表现出抑制活性,而来自C57BL/6小鼠的Ly-1清除的脾细胞暴露于HF-H则未能发挥辅助活性。因此,SF-H的靶细胞是Thy-1.2+、Ly-1+2+、I-J+ T细胞,HF-H的靶细胞是Thy-1.2+、Ly-1+ T细胞。

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