Green K A, Noelle R J, Durell B G, Green W R
Department of Microbiology and Immunology, Dartmouth Medical School and Norris Cotton Cancer Center, Lebanon, New Hampshire 03756, USA.
J Virol. 2001 Apr;75(8):3581-9. doi: 10.1128/JVI.75.8.3581-3589.2001.
Genetically susceptible C57BL/6 (B6) mice that are infected with the LP-BM5 isolate of murine retroviruses develop profound splenomegaly, lymphadenopathy, hypergammaglobulinemia, terminal B-cell lymphomas, and an immunodeficiency state bearing many similarities to the pathologies seen in AIDS. Because of these similarities, this syndrome has been called murine AIDS (MAIDS). We have previously shown that CD154 (CD40 ligand)-CD40 molecular interactions are required both for the initiation and progression of MAIDS. Thus, in vivo anti-CD154 monoclonal antibody (MAb) treatment inhibited MAIDS symptoms in LP-BM5-infected wild-type mice when either a short course of anti-CD154 MAb treatment was started on the day of infection or a course was initiated 3 to 4 weeks after LP-BM5 administration, after disease was established. Here, we further characterize this required CD154-CD40 interaction by a series of adoptive transfer experiments designed to elucidate which cellular subsets must express CD154 or CD40 for LP-BM5 to induce MAIDS. Specifically with regard to CD154 expression, MAIDS-insusceptible B6 nude mice reconstituted with highly purified CD4+ T cells from wild-type, but not from CD154 knockout, B6 donors displayed clear MAIDS after LP-BM5 infection. In contrast, nude B6 recipients that received CD8+ T cells from wild-type B6 donors did not develop MAIDS after LP-BM5 infection. B6 CD40 knockout mice, which are also relatively resistant to LP-BM5-induced MAIDS, became susceptible to LP-BM5-induced disease after reconstitution with highly purified wild-type B cells but not after receiving purified wild-type dendritic cells (DC) or a combined CD40+ population composed of DC and macrophages obtained from B6 SCID mouse donors. Based on these and other experiments, we thus conclude that the cellular basis for the requirement for CD154-CD40 interactions for MAIDS induction and progression can be accounted for by CD154 expression on CD4+ T cells and CD40 expression on B cells.
感染鼠逆转录病毒LP - BM5分离株的遗传易感C57BL/6(B6)小鼠会出现严重的脾肿大、淋巴结病、高球蛋白血症、终末期B细胞淋巴瘤以及一种免疫缺陷状态,该状态与艾滋病中所见的病理情况有许多相似之处。由于这些相似性,这种综合征被称为鼠艾滋病(MAIDS)。我们之前已经表明,CD154(CD40配体)- CD40分子相互作用对于MAIDS的起始和进展都是必需的。因此,在体内,当在感染当天开始短期抗CD154单克隆抗体(MAb)治疗,或者在LP - BM5给药3至4周后疾病确立时开始一个疗程的治疗,抗CD154 MAb治疗可抑制LP - BM5感染的野生型小鼠的MAIDS症状。在此,我们通过一系列过继转移实验进一步表征这种必需的CD154 - CD40相互作用,这些实验旨在阐明LP - BM5诱导MAIDS时哪些细胞亚群必须表达CD154或CD40。具体就CD154表达而言,用来自野生型而非CD154基因敲除的B6供体的高度纯化的CD4 + T细胞重建的对MAIDS不敏感的B6裸鼠在感染LP - BM5后表现出明显的MAIDS。相比之下,接受来自野生型B6供体的CD8 + T细胞的裸鼠B6受体在感染LP - BM5后未发生MAIDS。同样对LP - BM5诱导的MAIDS相对抗性的B6 CD40基因敲除小鼠,在用高度纯化的野生型B细胞重建后变得易患LP - BM5诱导的疾病,但在接受纯化的野生型树突状细胞(DC)或从B6 SCID小鼠供体获得的由DC和巨噬细胞组成的CD40 +混合群体后则不然。基于这些及其他实验,我们因此得出结论,MAIDS诱导和进展所需的CD154 - CD40相互作用的细胞基础可以由CD4 + T细胞上的CD154表达和B细胞上的CD40表达来解释。