DeMartini J C, MacHugh N D, Naessens J, Teale A J
International Laboratory for Research on Animal Diseases, Nairobi, Kenya.
Vet Immunol Immunopathol. 1993 Jan;35(3-4):253-73. doi: 10.1016/0165-2427(93)90038-6.
The expression of major histocompatibility complex class II (MHC II) non-polymorphic antigens detected by four monoclonal antibodies was investigated in Theileria parva-infected and non-infected cloned lymphoid cell lines, bulk cultures, and in peripheral blood mononuclear cells (PBMC) and lymph node cells (LNC) of experimentally infected calves. Compared with non-infected cell lines, both immunofluorescence microscopy and flow cytofluorometry analysis of infected lines of alpha beta T-cell, gamma delta T-cell and B-cell origin revealed high expression of MHC II MHC molecules. After T. parva infection in vitro, three alloreactive T cell clones, three interleukin-2 (IL-2)-dependent cell lines and a concanavalin A (Con A)-stimulated bulk culture all had an increase both in the proportion of MHC II+ cells and in their mean fluorescence intensity. Radioimmunoprecipitation of class II molecules biosynthesized in infected and non-infected cells revealed that they were constitutively produced in infected cells, and were a slightly larger relative mass than the MHC II molecules of uninfected cells. In a study of the serial expression of MHC II antigens in PBMC and LNC of six calves inoculated with a lethal dose of T.parva, MHC II expression by non-parasitized cells peaked at Days 7 (LNC) or 9 (PBMC) following inoculation and, subsequently, MHC II non-expressing parasitized lymphocytes progressively outnumbered MHC II-expressing parasitized cells. In two calves studied in detail, MHC II expression in PBMC and LNC generally, and in T cells particularly, increased during the course of the disease. Finally, among LNC sorted for MHC II expression at 11 and 17 days after parasite inoculation, the proportion of parasitized cells increased markedly in MHC II non-expressing populations and was reduced or increased only slightly in MHC II-expressing populations. These findings indicate that: (1) enhanced MHC II antigen expression by parasitized lymphocytes may be important in the pathogenesis of the lymphoproliferation that characterizes T. parva infection; (2) the in vivo preponderance of MHC II non-expressing over MHC II-expressing T. parva-infected cells may reflect host-mediated destruction or antigenic modulation of parasitized MHC II-expressing cells.
利用四种单克隆抗体对主要组织相容性复合体II类（MHC II）非多态性抗原的表达情况进行了研究，研究对象包括感染和未感染泰勒虫的克隆淋巴细胞系、大量培养物，以及实验感染小牛的外周血单核细胞（PBMC）和淋巴结细胞（LNC）。与未感染的细胞系相比，对αβT细胞、γδT细胞和B细胞来源的感染细胞系进行免疫荧光显微镜检查和流式细胞荧光分析均显示，MHC II类分子表达较高。体外感染泰勒虫后，三个同种异体反应性T细胞克隆、三个白细胞介素2（IL-2）依赖细胞系以及一个经刀豆蛋白A（Con A）刺激的大量培养物中，MHC II +细胞比例及其平均荧光强度均增加。对感染和未感染细胞中生物合成的II类分子进行放射免疫沉淀分析显示，它们在感染细胞中组成性产生，相对质量比未感染细胞的MHC II分子略大。在一项对六头接种致死剂量泰勒虫的小牛的PBMC和LNC中MHC II抗原连续表达情况的研究中，未被寄生细胞的MHC II表达在接种后第7天（LNC）或第9天（PBMC）达到峰值，随后，不表达MHC II的被寄生淋巴细胞数量逐渐超过表达MHC II的被寄生细胞。在详细研究的两头小牛中，PBMC和LNC中的MHC II表达，尤其是T细胞中的表达，在疾病过程中普遍增加。最后，在寄生虫接种后第11天和第17天对MHC II表达进行分选的LNC中，不表达MHC II的群体中被寄生细胞的比例显著增加，而在表达MHC II的群体中仅略有减少或增加。这些发现表明：（1）被寄生淋巴细胞增强的MHC II抗原表达可能在以泰勒虫感染为特征的淋巴细胞增殖的发病机制中起重要作用；（2）在体内，不表达MHC II的泰勒虫感染细胞比表达MHC II的细胞占优势，这可能反映了宿主介导的对表达MHC II的被寄生细胞的破坏或抗原调节。
