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

Abstract
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 either bcl-2 levels in the resting cells or to the decrease in bcl-2 expression following slg engagement. We discuss the Implications of these findings for our understanding of PCD in B cells.

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