Howell C D, Yoder T D, Vierling J M
University of Colorado School of Medicine, Denver.
Cell Immunol. 1991 Jan;132(1):256-68. doi: 10.1016/0008-8749(91)90024-6.
Murine chronic graft-vs-host disease (CGBHD) to minor histocompatibility antigens (B10.D2----BALB/c) is characterized by inflammatory destruction of intrahepatic bile ducts, scleroderma-like skin lesions, and lymphoid involution. Spleen cells isolated from this model proliferate poorly when stimulated with mitogens. Previous reports indicate defective lymphocyte proliferation in this model is the result of active suppression induced by the graft-vs-host reaction in the spleen and is mediated by Thy 1.2-, sIg-, plastic nonadherent, splenic natural suppressor (NS) cells. To determine whether the intense CGVHD in the liver is associated with induction of suppression, we compared the suppressor activity of hepatic and splenic mononuclear inflammatory cells isolated concurrently during murine CGVHD. Both hepatic and splenic MC suppressed the proliferation of mitogen-stimulated normal spleen cells in a non-MHC, non-Mls restricted manner. T cells contributed to the suppressor activity of both populations. However, the suppressor activity of hepatic MC was mediated largely by a macrophage-enriched population of MC while that of splenic MC was mediated largely by NS cells.
小鼠针对次要组织相容性抗原（B10.D2→BALB/c）的慢性移植物抗宿主病（CGBHD）的特征为肝内胆管的炎性破坏、硬皮病样皮肤病变和淋巴组织萎缩。从该模型分离出的脾细胞在受到丝裂原刺激时增殖能力较差。先前的报告表明，该模型中淋巴细胞增殖缺陷是由脾脏中的移植物抗宿主反应诱导的主动抑制所致，且由Thy 1.2⁻、sIg⁻、塑料非黏附性脾自然抑制（NS）细胞介导。为了确定肝脏中强烈的CGVHD是否与抑制的诱导有关，我们比较了在小鼠CGVHD期间同时分离的肝和脾单核炎性细胞的抑制活性。肝和脾的单核细胞均以非MHC、非Mls限制的方式抑制丝裂原刺激的正常脾细胞的增殖。T细胞对这两种细胞群体的抑制活性均有贡献。然而，肝单核细胞的抑制活性主要由富含巨噬细胞的单核细胞群体介导，而脾单核细胞的抑制活性主要由NS细胞介导。
