THE XID DEFECT DETERMINES AN IMPROVED CLINICAL COURSE OF MURINE LEISHMANIASIS IN SUSCEPTIBLE MICE
THE XID DEFECT DETERMINES AN IMPROVED CLINICAL COURSE OF MURINE LEISHMANIASIS IN SUSCEPTIBLE MICE
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DOI：
10.1093/intimm/6.8.1117
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发表时间：
1994-08-01
影响因子：
4.4
通讯作者：
ROLLINGHOFF, M
中科院分区：
文献类型：
--
作者：
HOERAUF, A;SOLBACH, W;ROLLINGHOFF, M
研究了B细胞缺陷型BALB B.Xid小鼠感染利什曼原虫的过程。与BALB/c对照组相比，感染BALB.Xid小鼠的病变发展明显较慢，淋巴器官中的寄生虫负荷降低了10- 30倍。与BALB/c对照小鼠相比，BALB.Xid小鼠中的B细胞免疫应答（通过抗利什曼抗体产生和淋巴器官中的B细胞数量进行定量）仍显著较低。与疾病发展一致，当在体外用利什曼原虫抗原刺激时，来自感染BALB.Xid小鼠淋巴结的CD 4（+）T细胞产生的IFN-γ是BALB/c小鼠相应T细胞的6- 10倍。来自BALB/c小鼠的淋巴结和腹腔的B细胞可以被诱导产生比来自B细胞缺陷型BALB.Xid小鼠的相应细胞多3- 8倍的IL-10。因此，数据表明，Xid突变允许T（h）1细胞的发展，该细胞赋予对L.少校此外，数据表明，B细胞有助于对L。通过使T-h细胞网络向T（h）2表型倾斜，在BALB/c小鼠中主要感染。由于BALB/c和BALB.Xid小鼠之间B细胞衍生的IL-10产生的差异在腹膜B细胞中更为突出，因此数据支持T细胞应答的偏斜可能主要由B1细胞亚群介导的观点。
The course of Leishmania major infection in B cell-defective BALB.Xid mice was investigated. Infected BALB.Xid mice showed a significantly slower lesion development compared with BALB/c controls accompanied by a 10- to 30-fold lower parasite burden in lymphatic organs. The B cell immune response, as quantified by anti-leishmanial antibody production and B cell numbers in lymphatic organs, remained significantly lower in BALB.Xid mice as compared with BALB/c control mice. In accordance with disease development, CD4(+) T cells from lymph nodes of infected BALB.Xid mice produced 6- to 10-fold more IFN-gamma than the respective T cells of BALB/c mice, when stimulated with leishmanial antigen in vitro. B cells from lymph nodes and the peritoneal cavities of BALB/c mice could be induced to produce 3- to 8-fold more IL-10 than the respective cells from B cell-defective BALB.Xid mice. The data thus indicate that the Xid mutation allows for the development of T(h)1 cells which confer resistance to infection with L. major. Moreover, the data suggest that B cells contribute to susceptibility to L. major infection in BALB/c mice by skewing the T-h cell network towards a T(h)2 phenotype. Since the difference in B cell-derived IL-10 production between BALB/c and BALB.Xid mice was more prominent in peritoneal B cells, the data support the notion that the skewing of the T cell response may be predominantly mediated by the B1 cell subset.