Cross R J, Roszman T L
Department of Microbiology and Immunology, University of Kentucky, Albert B. Chandler Medical Center, Lexington 40536-0084.
J Neuroimmunol. 1988 Aug;19(1-2):33-45. doi: 10.1016/0165-5728(88)90033-1.
We have previously shown that depletion of central nervous system (CNS) catecholamines by injecting the neurotoxin 6-hydroxydopamine (6-OHDA) into the cisterna magna of C57B1/6 mice markedly impairs the humoral immune response to sheep red blood cells. This work extends these observations by showing that 6-OHDA treatment also inhibits the humoral antibody response to the T-cell-dependent antigen trinitrophenyl-keyhole limpet hemocyanin, but does not affect the response to the T-independent antigen trinitrophenyl-lipopolysaccharide. This treatment also impairs humoral responsiveness at peripheral lymphoid sites in addition to inhibiting natural killer cell activity. However, 6-OHDA treatment in vivo does not affect in vitro mixed lymphocyte responsiveness, mitogen-induced lymphocyte activation or antigen presentation by macrophages.
我们之前已经表明,通过向C57B1/6小鼠的脑池中注射神经毒素6-羟基多巴胺(6-OHDA)来耗尽中枢神经系统(CNS)中的儿茶酚胺,会显著损害对绵羊红细胞的体液免疫反应。这项工作通过表明6-OHDA处理也抑制对T细胞依赖性抗原三硝基苯基-钥孔血蓝蛋白的体液抗体反应,但不影响对T细胞非依赖性抗原三硝基苯基-脂多糖的反应,扩展了这些观察结果。这种处理除了抑制自然杀伤细胞活性外,还损害外周淋巴部位的体液反应性。然而,体内6-OHDA处理并不影响体外混合淋巴细胞反应性、丝裂原诱导的淋巴细胞活化或巨噬细胞的抗原呈递。