CD43 expression in a B cell lymphoma, WEHI 231, reduces susceptibility to G(1) arrest and extends survival in culture upon serum depletion

被引:18
作者
Misawa, Y
Nagaoka, H
Kimoto, H
Ishii, Y
Kitamura, K
TsunetsuguYokota, Y
Shibuya, M
Takemori, T
机构
[1] NATL INST HLTH,DEPT IMMUNOL,SHINJUKU KU,TOKYO 162,JAPAN
[2] UNIV TOKYO,INST MED SCI,DEPT GENET,TOKYO,JAPAN
[3] HOECHST JAPAN LTD,CELL BIOL LABS,KAWAGOE,SAITAMA 35011,JAPAN
关键词
B cell; CD43; cell cycle; survival;
D O I
10.1002/eji.1830261106
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
CD43 is a major surface sialoprotein on hemopoietic cells, whose extracellular domain is heavily O-glycosylated. The functional role of CD43 in the hemopoietic system is not fully understood; however, it has been suggested that CD43 may have a role in cell-cell repulsion and in modifying T cell proliferation and activation. CD43 is expressed in immature B cells in the bone marrow, but not by peripheral B cells, except for B-1 B cells and plasma cells. To analyze the biological effect of CD43 in B-lineage cells, we transfected mouse CD43 cDNA into a CD43(-) B cell lymphoma, WEHI 231, and the growth and survival in culture were compared to those of a parental cell line, human CD8 transfectants, and CD43(-) revertants established from CD43(+) clones. We observed that CD43 expression supported cell growth in culture upon serum reduction, whereas growth of CD43(-) cell lines was barely detected under this condition. CD43(-) cell lines accumulated in G(1) phase of the cell cycle, and the numbers of viable cells were greatly reduced during culture upon serum depletion, whereas expression of CD43 reduced the susceptibility to G, arrest and temporarily retarded the apoptotic process? which, in turn, resulted in an increase and maintenance of the number of viable cells in culture. The results suggest that CD43 may have some role in the survival and expansion of B-lineage cells. The biological effect of CD43 was initiated without stimulation by cross-linking and was significantly impaired by replacement of the extracellular domain by the human CD8 extracellular domain. The basis of these regulatory processes is discussed.
引用
收藏
页码:2573 / 2581
页数:9
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