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子宫内开始的CD4 T细胞慢性体内耗竭会抑制肠道B细胞分化。

Chronic in vivo depletion of CD4 T cells begun in utero inhibits gut B cell differentiation.

作者信息

Tolaymat N, Weber S P, Cowdery J S

机构信息

Department of Pediatrics, University of Iowa College of Medicine, Iowa City 52242.

出版信息

Clin Immunol Immunopathol. 1990 Jul;56(1):97-107. doi: 10.1016/0090-1229(90)90173-n.

DOI:10.1016/0090-1229(90)90173-n
PMID:1972673
Abstract

We studied the role of CD4 T cells on the ontogeny of mucosal IgA compartment. We treated C57 BL/6 mice, beginning in utero and for 4 weeks thereafter, with anti-CD4 monoclonal antibody. Mice were evaluated at 1, 3, and 5 weeks after stopping the treatment. At 1 week, anti-CD4-treated mice had no detectable CD4 T cells in spleen or Peyer's patches. These CD4-depleted mice demonstrated a 40% reduction of surface Peyer's patch IgA+ B cells and a marked decrease in jejunal IgA secretion. By 5 weeks, CD4 T cells were detectable in spleen and Peyer's patch and the number of surface IgA+ B cells in Peyer's patch was increased, but they remained less than the control levels. Jejunal IgA secretion recovered to the control level by 5 weeks. LPS induced normal levels of in vitro IgM secretion by Peyer's patch B cells in anti-CD4-treated mice; thus, treatment with anti-CD4 does not nonspecifically inhibit the gut B cell compartment. This study demonstrates that CD4 T cell depletion begun in utero significantly inhibits the differentiation of mucosal B cells to IgA-secreting cells and partially inhibits switching to IgA+ B cells in Peyer's patch.

摘要

我们研究了CD4 T细胞在黏膜IgA区室个体发育中的作用。我们从子宫内开始并在其后4周对C57 BL/6小鼠用抗CD4单克隆抗体进行处理。在停止治疗后1周、3周和5周对小鼠进行评估。在1周时,用抗CD4处理的小鼠在脾脏或派伊尔结中未检测到CD4 T细胞。这些CD4耗竭的小鼠表面派伊尔结IgA+B细胞减少了40%,空肠IgA分泌显著减少。到5周时,在脾脏和派伊尔结中可检测到CD4 T细胞,派伊尔结中表面IgA+B细胞的数量增加,但仍低于对照水平。空肠IgA分泌在5周时恢复到对照水平。脂多糖在体外诱导用抗CD4处理的小鼠派伊尔结B细胞分泌正常水平的IgM;因此,用抗CD4处理不会非特异性地抑制肠道B细胞区室。这项研究表明,从子宫内开始的CD4 T细胞耗竭显著抑制黏膜B细胞向分泌IgA细胞的分化,并部分抑制派伊尔结中向IgA+B细胞的转换。

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