Stasiuk L M, Ghoraishian M, Elson C J, Thompson S J
Department of Pathology and Microbiology, University of Bristol, UK.
Immunology. 1997 Jan;90(1):81-6. doi: 10.1046/j.1365-2567.1997.00121.x.
The development of arthritis induced in mice by intraperitoneal injection of the non-antigenic mineral oil pristane (2,6,10,14-tetramethylpentadecane) was shown to depend on the presence of CD4+ T cells. Initial experiments assessed the influx of lymphoid cells into the peritoneal cavity of CBA/Igb mice after pristane injection. Both CD4+ and CD8+ cell numbers were maximal around 50 days. Other experiments confirmed our original observation that irradiated pristane-treated mice failed to develop arthritis unless they were reconstituted with spleen cells from normal donors. This finding has been extended by showing that the population of transferred splenic lymphoid cells must contain CD4+ T cells, while CD8+ T cells and B cells were not required for reconstitution. Conventionally housed and hsp 65-immunized animals are known to harbour T cells reactive with hsp 65. In addition, hsp 65-immunized mice are resistant to the development of pristane-induced arthritis (PIA). Thus, additional experiments assessed the population of splenic T cells activated and proliferating against mycobacterial 65,000 MW heat shock protein (hsp 65). In cultures of purified splenic T cells derived from both conventional and hsp 65-immunized mice, removal of CD4+ T cells significantly reduced the proliferative response to hsp 65, while removal of CD8+ T cells often enhanced the response. These proliferative responses were also shown to be major histocompatibility complex (MHC) class II restricted. The present findings demonstrate that PIA is CD4+ T-cell mediated, and immunodominant environmental antigens such as hsp 65 activate this population of lymphocytes. The CD4+ hsp 65-reactive population may be pathogenic or protective in PIA, depending upon the route of sensitization.
通过腹腔注射非抗原性矿物油降植烷（2,6,10,14-四甲基十五烷）诱导小鼠发生关节炎，结果表明这一过程依赖于CD4+ T细胞的存在。最初的实验评估了降植烷注射后淋巴细胞流入CBA/Igb小鼠腹腔的情况。CD4+和CD8+细胞数量在大约50天时达到最大值。其他实验证实了我们最初的观察结果，即经照射的降植烷处理小鼠不会发生关节炎，除非用正常供体的脾细胞进行重建。这一发现得到了进一步扩展，表明转移的脾淋巴细胞群体必须包含CD4+ T细胞，而重建并不需要CD8+ T细胞和B细胞。已知常规饲养和经hsp 65免疫的动物体内含有与hsp 65反应的T细胞。此外，经hsp 65免疫的小鼠对降植烷诱导的关节炎（PIA）具有抗性。因此，额外的实验评估了针对分枝杆菌65,000 MW热休克蛋白（hsp 65）活化并增殖的脾T细胞群体。在来自常规饲养和经hsp 65免疫小鼠的纯化脾T细胞培养物中，去除CD4+ T细胞显著降低了对hsp 65的增殖反应，而去除CD8+ T细胞往往会增强这种反应。这些增殖反应也显示为主要组织相容性复合体（MHC）II类限制性。目前的研究结果表明，PIA是由CD4+ T细胞介导的，免疫显性环境抗原如hsp 65可激活这群淋巴细胞。在PIA中，CD4+ hsp 65反应性群体可能具有致病性或保护性，这取决于致敏途径。
