LEISHMANIA-MAJOR - ANALYSIS OF LYMPHOCYTE AND MACROPHAGE CELLULAR PHENOTYPES DURING INFECTION OF SUSCEPTIBLE AND RESISTANT MICE
LEISHMANIA-MAJOR - ANALYSIS OF LYMPHOCYTE AND MACROPHAGE CELLULAR PHENOTYPES DURING INFECTION OF SUSCEPTIBLE AND RESISTANT MICE
复制标题
DOI：
10.1016/0014-4894(88)90130-0
复制
发表时间：
1988-04-01
影响因子：
2.1
通讯作者：
LOCKSLEY, RM
中科院分区：
文献类型：
--
作者：
HEINZEL, FP;SADICK, MD;LOCKSLEY, RM
将对利什曼原虫具有遗传易感性的BALB/c小鼠和具有抗性的C57BL/6小鼠感染利什曼原虫主要型，对引流淋巴结和皮肤病变中应答细胞的表型进行分析。早在1周时，BALB/c小鼠淋巴结中L3T4⁺细胞数量相较于Lyt - 2⁺细胞显著增加（P < 0.005）。在C57BL/6小鼠中，L3T4⁺和Lyt - 2⁺细胞的增加相当，导致L3T4/Lyt - 2比值比BALB/c小鼠低三倍。两种品系的T细胞亚群均被激活，使其白细胞介素 - 2受体（IL2R）表达高于静息值，尽管在感染1周和3周时，BALB/c小鼠引流淋巴结中活化的L3T4⁺细胞数量比C57BL/6小鼠多（P = 0.02）。尽管两种品系中均存在活化的L3T4⁺细胞，但在感染过程中巨噬细胞在免疫重要表面分子的表达上存在差异。BALB/c小鼠的组织巨噬细胞在疾病晚期为IgG1/G2b Fc受体（FcR）⁺和Ia⁻，而C57BL/6小鼠的巨噬细胞在愈合过程中变为FcR⁻和Ia⁺。用单克隆抗体GK1.5处理以暂时清除L3T4⁺细胞的BALB/c小鼠对后续感染产生抗性，并形成了FcR⁻和Ia⁺的巨噬细胞表型。巨噬细胞表型的这些差异与利什曼原虫主要型感染过程中的易感性密切相关，并可能在小鼠利什曼病的病理生理学中起作用。
Genetically susceptible BALB/c and resistant C57BL/6 mice were infected with Leishmania major and the phenotypes of the responding cells in the draining lymph nodes and cutaneous lesions were analyzed. As early as 1 week, significantly increased numbers of L3T4+ cells as compared to Lyt-22 cells were present in BALB/c mice lymph nodes (P < 0.005). Increases in L3T4+ and Lyt-2+ cells were comparable in C57BL/6 mice, resulting in threefold lower L3T4/Lyt-2 ratio than in BALB/c mice. T cell subsets were activated in both strains to express interleukin-2 receptor (IL2R) above resting values, although greater numbers of activated L3T4+ cells were present in the draining lymph nodes from BALB/c at 1 and 3 weeks of infection than in C57BL/6 (P = 0.02). Despite the presence of activated L3T4+ cells in both strains, macrophages differed in the expression of immunologically important surface molecules during infection. Tissue macrophages from BALB/c mice were IgG1/G2b Fc receptor (FcR)+ and Ia- late in disease, whereas macrophages in C57BL/6 became FcR- and Ia+ during healing. BALB/c mice, treated with monoclonal antibody GK1.5 to transiently deplete L3T4+ cells, became resistant to subsequent infection and developed a macrophage phenotype that was FcR- and Ia+. These differences in macrophage phenotype were closed linked to susceptibility during infection with L. major and may play a role in the pathophysiology of murine leishmaniasis.