Xenocostas A, Ghayur T, Setrakian J C, Lapp W S, Osmond D G
Department of Physiology, McGill University, Montreal, Quebec, Canada.
Blood. 1994 Dec 1;84(11):3965-73.
The nature of the effector cell(s) responsible for the depression of B-cell genesis in the bone marrow of mice undergoing systemic graft-versus-host disease (GVHD) has been examined. Donor C57BL/6 (B6) mice were treated in vivo with either a single injection of anti-asialo GM1 antibody (anti-ASGM1) to eliminate naturally occurring (endogenous) ASGM1+ cells or B6xAF1 (B6AF1) lymphoid cells followed by anti-ASGM1 to eliminate both endogenous and "induced" ASGM1+ cells. Lymphoid cells from donor mice after the elimination of endogenous ASGM1+ cells produced severe GVHD and concomitant depression of B-cell genesis when injected into B6AF1 recipients. In contrast, cells from donors depleted of both the endogenous and inducible ASGM1+ populations did not cause GVHD or depletion of B lineage cells in B6AF1 recipients but did depress B-cell genesis in B6C3F1 mice. The "induced" ASGM1+ cells were Thy 1+, but their elimination did not significantly alter either overall T-cell function or specific cytotoxic T-cell (CTL) reactivity against the sensitizing (B6AF1) strain. The results suggest that the effector cell responsible for the depression of B-cell genesis during systemic GVHD can be induced to express ASGM1, is strain-specific and Thy 1+; but is not a conventional CTL.
对在发生系统性移植物抗宿主病（GVHD）的小鼠骨髓中导致B细胞生成受抑制的效应细胞的性质进行了研究。给供体C57BL/6（B6）小鼠体内单次注射抗唾液酸GM1抗体（抗ASGM1）以消除天然存在的（内源性）ASGM1+细胞，或注射B6xAF1（B6AF1）淋巴细胞，随后注射抗ASGM1以消除内源性和“诱导性”ASGM1+细胞。消除内源性ASGM1+细胞后的供体小鼠淋巴细胞注射到B6AF1受体小鼠体内时，会产生严重的GVHD并伴随B细胞生成受抑制。相比之下，内源性和诱导性ASGM1+细胞群体均被耗尽的供体细胞不会在B6AF1受体小鼠中引起GVHD或B谱系细胞耗竭，但会抑制B6C3F1小鼠的B细胞生成。“诱导性”ASGM1+细胞为Thy 1+，但其消除不会显著改变整体T细胞功能或针对致敏（B6AF1）品系的特异性细胞毒性T细胞（CTL）反应性。结果表明，在系统性GVHD期间导致B细胞生成受抑制的效应细胞可被诱导表达ASGM1，具有品系特异性且为Thy 1+；但不是传统的CTL。
