C57BL/6 小鼠的 B 细胞反应缺陷与巨噬细胞介导的杀伤美洲利什曼原虫的能力丧失相关。
A deficiency in the B cell response of C57BL/6 mice correlates with loss of macrophage-mediated killing of Leishmania amazonensis.
机构信息
Department of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, IA 50011-1250, USA.
出版信息
Int J Parasitol. 2010 Feb;40(2):157-61. doi: 10.1016/j.ijpara.2009.11.010. Epub 2009 Dec 11.
Abstract
Infection of C3HeB/FeJ and C57BL/6 mice with Leishmania major stimulates a healing cell-mediated immune response, while Leishmania amazonensis infection leads to chronic disease. Here we show C3HeB/FeJ mice co-infected with both species of Leishmania heal, while co-infected C57BL/6 mice do not. Using an in vitro killing assay we determined B cells from infected C57BL/6 mice are ineffective in promoting parasite killing compared with B cells from infected C3HeB/FeJ mice. Furthermore, infected C57BL/6 mice produce less antigen-specific antibodies compared with infected C3HeB/FeJ mice. These findings suggest B cells play a required role in the cell-mediated immune response against L. amazonensis.
摘要
C3HeB/FeJ 小鼠和 C57BL/6 小鼠感染利什曼原虫后会引发治愈性的细胞免疫应答，而感染莱什曼原虫则会导致慢性疾病。在这里，我们发现同时感染这两种利什曼原虫的 C3HeB/FeJ 小鼠能够被治愈，而同时感染的 C57BL/6 小鼠则不能。通过体外杀伤试验，我们发现与感染 C3HeB/FeJ 小鼠的 B 细胞相比，感染 C57BL/6 小鼠的 B 细胞在促进寄生虫杀伤方面效果不佳。此外，与感染 C3HeB/FeJ 小鼠相比，感染 C57BL/6 小鼠产生的抗原特异性抗体较少。这些发现表明 B 细胞在针对莱什曼原虫的细胞免疫应答中发挥了必需的作用。
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