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用抗Ig而非脂多糖(LPS)处理小鼠CD5 - B细胞,可诱导表面CD5表达:两种B细胞活化途径。

Treatment of murine CD5- B cells with anti-Ig, but not LPS, induces surface CD5: two B-cell activation pathways.

作者信息

Cong Y Z, Rabin E, Wortis H H

机构信息

Department of Pathology, Tufts University School of Medicine, Boston, MA 02111.

出版信息

Int Immunol. 1991 May;3(5):467-76. doi: 10.1093/intimm/3.5.467.

DOI:10.1093/intimm/3.5.467
PMID:1716972
Abstract

Anti-Ig stimulated murine B cells express high levels of surface CD5 (ly-1) and increased CD44 while maintaining surface IgD, CD23 and J11d. Sorting of CD5- and CD5+ cells demonstrates that anti-Ig induces CD5 expression rather than the selective expansion of CD5+ cells. Anti Ig plus interleukin-6 (IL-6) induces the CD23, IgD, low ly-5 (B220) (CD45low), J11dhigh phenotype of typical CD5+ peritoneal B cells. In contrast, lipopolysaccharide (LPS)-stimulated B cells have high levels of CD44 but decreased surface IgD, CD23 and J11d and no CD5. Thus LPS and anti-Ig generate activated cells with differing phenotypes. Induced CD5+ cells have increased viability, even in the absence of added exogenous factors, while the viability of CD5- B cells is dependent on factors such as IL-4. We conclude that conventional CD5- B cells can be activated by either of two pathways: one generating CD5+ B cells; the other yielding conventional activated cells. We hypothesize that the first path requires slg cross-linking and corresponds to T-independent (type 2) stimulation, while cognate interaction with helper T cells in the absence of slg cross-linking induces B cells to enter the second path.

摘要

抗Ig刺激的鼠B细胞表达高水平的表面CD5(ly-1)且CD44增加,同时维持表面IgD、CD23和J11d。对CD5 - 和CD5 + 细胞进行分选表明,抗Ig诱导CD5表达而非CD5 + 细胞的选择性扩增。抗Ig加白细胞介素-6(IL-6)诱导典型CD5 + 腹膜B细胞的CD23、IgD、低水平ly-5(B220)(CD45low)、J11dhigh表型。相比之下,脂多糖(LPS)刺激的B细胞具有高水平的CD44,但表面IgD、CD23和J11d减少且无CD5。因此,LPS和抗Ig产生具有不同表型的活化细胞。诱导的CD5 + 细胞即使在没有添加外源性因子的情况下也具有增加的活力,而CD5 - B细胞的活力则依赖于诸如IL-4等因子。我们得出结论,传统的CD5 - B细胞可通过两种途径之一被激活:一种产生CD5 + B细胞;另一种产生传统的活化细胞。我们假设第一条途径需要表面免疫球蛋白(slg)交联,对应于非T细胞依赖性(2型)刺激,而在没有slg交联的情况下与辅助性T细胞的同源相互作用诱导B细胞进入第二条途径。

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