Quantitative analysis of the influenza virus-specific CD4+ T cell memory in the absence of B cells and Ig.
Quantitative analysis of the influenza virus-specific CD4+ T cell memory in the absence of B cells and Ig.
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DOI：
10.4049/jimmunol.157.7.2947
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发表时间：
1996-10
影响因子：
4.4
通讯作者：
David J. Topham;R. Tripp;A. Hamilton-Easton;S. Sarawar;P. Doherty
中科院分区：
文献类型：
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作者：
David J. Topham;R. Tripp;A. Hamilton-Easton;S. Sarawar;P. Doherty
B淋巴细胞及其Ig产物在病毒特异性CD4+T细胞的发育和维持中的作用已经被分析在Ig Mu基因(Mu MT)纯合的小鼠中。这些小鼠缺乏成熟的B220+B细胞，不分泌Ig，但能产生正常的CD8+细胞毒性T淋巴细胞反应，并且很容易将HKx31甲型流感病毒从受感染的呼吸道中清除出去。对病毒特异性的CD4+T细胞的序贯极限稀释分析表明，Mu MT和C57BL/6(B6)小鼠在感染后7天至6个月的引流淋巴结和/或脾中产生IL-2的T辅助细胞前体细胞的频率基本相似。免疫球蛋白或B细胞的抗原提呈和处理机制显然不是产生病毒特异性T辅助细胞前体所必需的，滤泡树突状细胞上的抗原-免疫球蛋白复合体对于病毒特异性CD4+T细胞记忆的持久性也不是必不可少的。主要区别在于MU MT小鼠的脾比B6对照组小得多，并且在区域纵隔淋巴结中持续可见数量较多的CD4+T细胞。这可能是MU MT CD4+T细胞上淋巴归巢受体(CD62L)异常表达的结果。然而，CD62L的长期表达情况在两组总的和病毒特异性的CD4+T细胞中是相似的。因此，MU MT脾的作用减弱更可能反映生发中心和/或Ig的缺失，而不是CD62L介导的T细胞运输的中断。
The role of B lymphocytes and their Ig product in the development and maintenance of virus-specific CD4+ T cells has been analyzed in mice homozygous for disruption of the Ig mu gene (mu MT). These mice lack mature B220+ B cells and do not secrete Ig, but generate normal CD8+ cytotoxic T lymphocyte responses and have no difficulty clearing the HKx31 influenza A virus from the infected respiratory tract. Sequential limiting dilution analysis of virus-specific CD4+ T cells established that the frequencies of IL-2-producing T helper cell precursors in the draining lymph nodes and/or spleen from 7 days to 6 mo after infection were essentially similar in mu MT and C57BL/6 (B6) mice. Ag presentation and processing mechanisms involving Ig or B cells are apparently not required to generate virus-specific T helper cell precursors, and Ag-Ig complexes on follicular dendritic cells are not essential for the persistence of virus-specific CD4+ T cell memory. The main difference was that the spleens of the mu MT mice were much smaller than those of the B6 controls, and greater numbers of CD4+ T cells were found consistently in the regional mediastinal lymph nodes. This could be the result of abnormal expression of the lymph node homing receptor (CD62L) on the mu MT CD4+ T cells. However, the profiles of CD62L expression over the long term were comparable for both total and virus-specific CD4+ T cells from the two groups. The diminished role of the mu MT spleen is thus more likely to reflect the absence of germinal centers and/or Ig rather than a disruption of CD62L-mediated T cell trafficking.