Rosat J P, MacDonald H R, Louis J A
WHO Immunology Research and Training Center, University of Lausanne, Switzerland.
J Immunol. 1993 Jan 15;150(2):550-5.
To assess the importance of gamma delta + T lymphocyte responses in experimental murine cutaneous leishmaniasis, the expression of gamma delta + TCR on the surface of lymphocytes in spleen and draining lymph nodes of mice infected with Leishmania major was examined. In both susceptible BALB/c and resistant CBA/J mice, an increase in gamma delta + T cells was observed after s.c. infection. Whereas in chronically infected BALB/c mice, these cells can represent up to 35% of the CD3+ cells in the spleen, in CBA/J mice the percentage of gamma delta + T cells returns to a lower level after resolution of lesions. Further experiments, in which the disease outcome was modified in susceptible BALB/c and in resistant CBA/J mice by chemotherapy or immunointervention, have confirmed that a correlation existed between the multiplication of the parasites and the expansion of gamma delta + T cells in the spleen. Interestingly, in BALB/c mice infected for 4 mo, these gamma delta + T cells represent 80% of the activated blast population and a large proportion of them express the alpha-chain of the CD8 molecule. In an attempt to assess a potential role for the gamma delta + T cells in the control of infection with L. major, the effect of injection of mAb against gamma delta TCR on the course of infection was studied. In both BALB/c and CBA/J mice, blocking of the gamma delta TCR resulted in the development of larger lesions that contained increased numbers of parasites. This treatment significantly delayed the healing of cutaneous lesions in otherwise resistant CBA/J mice. Taken together these results indicate that gamma delta + T cells are expanded during experimental infection of mice with L. major and could be involved in host defense against this parasite.
为评估γδ + T淋巴细胞反应在实验性小鼠皮肤利什曼病中的重要性,检测了感染硕大利什曼原虫的小鼠脾脏和引流淋巴结中淋巴细胞表面γδ + TCR的表达。在易感的BALB/c小鼠和抗性的CBA/J小鼠中,皮下感染后均观察到γδ + T细胞增加。在慢性感染的BALB/c小鼠中,这些细胞可占脾脏中CD3 + 细胞的35%,而在CBA/J小鼠中,病变消退后γδ + T细胞的百分比恢复到较低水平。进一步的实验通过化疗或免疫干预改变了易感BALB/c小鼠和抗性CBA/J小鼠的疾病结局,证实了寄生虫增殖与脾脏中γδ + T细胞扩增之间存在相关性。有趣的是,在感染4个月的BALB/c小鼠中,这些γδ + T细胞占活化母细胞群体的80%,其中很大一部分表达CD8分子的α链。为了评估γδ + T细胞在控制硕大利什曼原虫感染中的潜在作用,研究了注射抗γδ TCR单克隆抗体对感染过程的影响。在BALB/c小鼠和CBA/J小鼠中,阻断γδ TCR均导致病变增大,寄生虫数量增加。这种治疗显著延迟了原本具有抗性 的CBA/J小鼠皮肤病变的愈合。综合这些结果表明,γδ + T细胞在小鼠感染硕大利什曼原虫的实验过程中扩增,并可能参与宿主对该寄生虫的防御。