当前位置： SCI文献检索 > CELLULAR IMMUNOLOGY期刊下所有文献 > Anti-Fas antibody induces different types of cell death in the human histiocytic cell line, U937, and the human B cell line, B104: the role of single-strand DNA breaks and poly (ADP-ribosyl)ation in cell death.

Anti-Fas antibody induces different types of cell death in the human histiocytic cell line, U937, and the human B cell line, B104: the role of single-strand DNA breaks and poly (ADP-ribosyl)ation in cell death.

Abstract：

:We investigated the anti-Fas antibody-induced cell death in two different types of human cell lines, U937 and B104. IFN-gamma increased the surface expression of Fas antigen and susceptibility to anti-Fas Ab-induced cell death of B104 and U937 cells. Anti-Fas Ab-induced death of U937 and B104 cells required neither a Ca2+ influx nor macromolecular synthesis. U937 cells treated with anti-Fas Ab represented apoptosis with DNA fragmentation, whereas anti-Fas Ab-treated B104 cells did not. Single-strand DNA breaks, however, appeared in the B104 cells. Zinc ions prevented DNA fragmentation and the morphological features of apoptosis in anti-Fas Ab-treated U937 cells, but did not inhibit cell death. However, zinc ions, when used in combination with the poly(ADP-ribosyl)ation inhibitors, inhibited anti-Fas Ab-induced U937 cell death. The inhibitors by themselves did not inhibit anti-Fas Ab-induced U937 cell death, but did inhibit anti-Fas Ab-induced B104 cell death. A substantial decrease in NAD pools was observed in anti-Fas Ab-treated B104 and U937 cells in parallel with the increase of DNA strand breaks before cell death became apparent. These results suggest the involvement of single-strand DNA breaks and poly(ADP-ribosyl)ation in the mechanisms of anti-Fas Ab-induced U937 and B104 cell death.

journal_name

Cell Immunol

journal_title

Cellular immunology

authors

Sumimoto S,Ishigami T,Horiguchi Y,Yonehara S,Kanazashi S,Heike T,Katamura K,Mayumi M

doi

10.1006/cimm.1994.1016

subject

Has Abstract

pub_date

1994-01-01 00:00:00

pages

184-93

issue

1

eissn

0008-8749

issn

1090-2163

pii

S0008874984710161

journal_volume

153

pub_type

杂志文章

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