Mouse parvovirus infection potentiates allogeneic skin graft rejection and induces syngeneic graft rejection
Mouse parvovirus infection potentiates allogeneic skin graft rejection and induces syngeneic graft rejection
复制标题
DOI：
10.1097/00007890-199806150-00005
复制
发表时间：
1998-06-15
期刊：
影响因子：
6.2
通讯作者：
Smith, AL
中科院分区：
文献类型：
--
作者：
McKisic, M;Macy, JD;Smith, AL
背景。最近发现的自主小鼠细小病毒命名为小鼠细小病毒-1 （MPV-1）在成年BALB/c小鼠中持续存在至少9周，感染淋巴组织，干扰克隆T细胞增殖的能力，并表现出免疫调节特性。基于这些发现，本研究进一步研究了MPV-1在体内和体外对T细胞介导的免疫反应的免疫调节作用。为了评估MPV-1感染对CD8(+) T细胞介导的免疫应答的影响，我们采用同种异体BALB/c皮肤移植后感染BALB/c- h2 （dm2）小鼠。MPV-1增强异体皮肤移植的排斥反应。这种增强不是原位杂交确定的病毒感染移植物细胞或血管成分的结果，而是由T细胞介导的。然而，移植物致敏感染小鼠的同种抗原反应淋巴细胞的增殖能力减弱。MPV-1还能诱导异体皮肤移植物的排斥反应，这些感染的移植物致敏小鼠的T细胞能裂解异体P815靶细胞。这些结果表明，MPV-1感染皮肤移植小鼠可能会破坏正常的外周耐受机制，并为研究病毒诱导的自身免疫提供了一个独特的模型。
Background. The recently identified autonomous mouse parvovirus designated mouse parvovirus-1 (MPV-1) persists in adult BALB/c mice for at least 9 weeks, infects lymphoid tissues, interferes with the ability of cloned T cells to proliferate, and exhibits immunomodulatory properties. As a consequence of these findings, the present studies were undertaken to characterize further the immunomodulatory effects of MPV-1 on T cell-mediated immune responses in vivo and in vitro.Methods. To evaluate the effect of MPV-1 infection on CD8(+) T cell-mediated responses, BALB/c-H2(dm2) mice were infected after transplantation of allogeneic BALB/c skin.Results. MPV-1 potentiated the rejection of allogeneic skin grafts. This potentiation was not a result of virus infecting the cellular or vascular component of the graft as determined by in situ hybridization, but was mediated by T cells. However, the proliferative capacity of alloantigen-reactive lymphocytes from graft-sensitized infected mice was diminished. MPV-1 also induced the rejection of syngeneic skin grafts, and T cells from these infected graft-sensitized mice lysed syngeneic P815 target cells.Conclusions. These results suggest that MPV-1 infection of skin-grafted mice may disrupt normal mechanisms of peripheral tolerance and provide a unique model to study virus-induced autoimmunity.