In vivo T-cell depletion enhances production of anti-GALalpha1,3GAL natural antibodies in alpha1,3-galactosyltransferase-deficient mice.

In vivo T-cell depletion enhances production of anti-GALalpha1,3GAL natural antibodies in alpha1,3-galactosyltransferase-deficient mice.
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体内 T 细胞耗竭可增强 α1,3-半乳糖基转移酶缺陷小鼠体内抗 GALα1,3GAL 天然抗体的产生。

DOI:
10.1097/00007890-200003150-00041
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发表时间:
2000
期刊:
影响因子:
6.2
通讯作者:
Sykes,M
Sykes,M
中科院分区:
医学2区
文献类型:
--
作者:
Ohdan,H;Yang,YG;Swenson,KG;Thall,AD;Sykes,M

文献摘要

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Background.It hasbeen reported that T-cell depletion by in vivo treatment with monoclonal antibodies results in polyclonal B-cell activation. However, its effects on B cells responding to Galα1, 3Gal (Gal) epitopes remain unknown.Methods.α1, 3-Galactosyltransferase-deficient (GalT-/-) mice were treated with depleting anti-CD4 and CD8 monoclonal antibodies. The kinetics of anti-Gal natural antibodies (NAb) and total immunoglobulin levels in their sera were evaluated. The frequencies of anti-Gal NAb-producing cells were determined in the various tissues of GalT-/-mice by enzyme-linked immunospot assay.Results.In vivo T-cell depletion led to significant increases in both anti-Gal IgM and total IgM levels in sera of GalT-/-mice, but did not influence either anti-Gal IgG or total IgG levels. An increased frequency of anti-Gal and total IgM-producing cells was observed in the spleens and bone marrow of T-cell-depleted GalT-/-mice but not in peritoneal cavity cells.Conclusion.In vivo T-cell depletion facilitates anti-Gal IgM production, suggesting that T cells deliver inhibitory signals to B cells responding to Gal.