Physiological cell death in B lymphocytes: I. Differential susceptibility of WEHI-231 sublines to anti-Ig induced physiological cell death and lack of correlation with bcl-2 expression.

Physiological cell death in B lymphocytes: I. Differential susceptibility of WEHI-231 sublines to anti-Ig induced physiological cell death and lack of correlation with bcl-2 expression.
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B淋巴细胞中的生理性细胞死亡:I.WEHI-231亚系对抗Ig诱导的生理性细胞死亡的不同敏感性以及与bcl-2表达缺乏相关性。

DOI:
10.1093/intimm/6.1.121
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发表时间:
1994
影响因子:
4.4
通讯作者:
Quintáns,J
Quintáns,J
中科院分区:
医学3区
文献类型:
--
作者:
Gottschalk,AR;McShan,CL;Merino,R;Nuñez,G;Quintáns,J

文献摘要

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WEHI-231是一种小鼠淋巴瘤,通常被认为代表未成熟的B细胞。SLG在WEHI-231上的交联会导致生长停滞,最终导致生理性细胞死亡(PCD)。我们用流式细胞术对WEHI-231的三个亚系进行了鉴定,并比较了它们与SLG交联剂的反应。所有亚系均表达一系列共同的B细胞表面标志(Ig M、Ig D、FcγR、ICAM-1和CD45),但I-A−表达不同。尽管这些亚系之间的表型plc相似,但antl-IgM只在两个亚系中引起凋亡体,尽管它抑制了所有三个亚系的生长。Ant1-Ig M诱导的生长停滞可被脂多糖和Th2型克隆逆转,且不依赖Fc、γR的参与。与antl-IgM不同的是,antL-LGD既不会引起生长停滞,也不会引起细胞凋零。为了进一步比较亚系对PCD的敏感性,我们通过超微结构、[~3H]胸腺释放、碘化丙啶排斥和DNA掺入等方法研究了它们对抗-IgM的反应。根据所有这些实验标准,WEHI-231亚系中有两个亚系对PCD敏感,而第三个亚系对抗-IgM表现出显著的抗性,但不能辐射或Th1诱导的PCD。这种对PCD的不同敏感性既与静息细胞中的bcl2水平无关,也与SLG参与后bcl2表达的减少无关。我们讨论了这些发现对于我们理解B细胞中的PCD的意义。
WEHI-231 is a murine lymphoma generally considered to represent an Immature B cell. Cross-linking of slg on WEHI-231 leads to growth arrest and eventually physiological cell death (PCD). We characterized three sublines of WEHI-231 by flow cytometry and compared their responses with slg cross-linking. All sublines had Identical expression of a series of common B cell surface markers (IgM, IgD, FCγR, ICAM-1, and CD45), but one was I-A−. Despite the phenotyplc similarities between these sublines, antl-IgM caused aptotosls in only two sublines, although it inhibited growth in all three. The growth arrest induced by antl-IgM was reversible by lipopolysaccharide and Th2 clones and independent of FcγR engagement. Antl-lgD, unlike antl-IgM, Induced neither growth arrest nor apoptosls. To further compare the sublines' susceptibility to PCD, we investigated their responses to antl-IgM by ultrastructural morphology, [3H]thymldlne release, propidium Iodide exclusion, and incorporation into DNA. By all these experimental criteria, two of the WEHI-231 sublines were susceptible to PCD while the third demonstrated remarkable resistance to antl-IgM, but not irradiation or Th1-induced PCD. This differential susceptibility to PCD did not correlate with eitherbcl-2 levels in the resting cells or to the decrease inbcl-2 expression following slg engagement. We discuss the Implications of these findings for our understanding of PCD in B cells.