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Gamma Interferon‐Induced Nitric Oxide Production in Mouse CD5 + B1‐Like Cell Line and Its Association with Apoptotic Cell Death
Author(s) -
Koide Naoki,
Sugiyama Tsuyoshi,
Mu Mya Mya,
Mori Isamu,
Yoshida Tomoaki,
Hamano Teruaki,
Yokochi Takashi
Publication year - 2003
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2003.tb03430.x
Subject(s) - biology , apoptosis , programmed cell death , cell culture , microbiology and biotechnology , cytokine , interferon gamma , nitric oxide synthase , nitric oxide , stat protein , cancer research , stat3 , immunology , biochemistry , endocrinology , genetics
The in vitro effect of gamma interferon (IFN‐γ) on nitric oxide (NO) production in a mouse CD5 + B1‐like cell line, TH2.52, was studied. The TH2.52 cell line is the hybridoma line between mouse B lymphoma line and mouse splenic B cells and expresses a series of B1 markers. IFN‐γ induced a marked NO production in TH2.52 cells through the expression of an inducible type of NO synthase (iNOS). IFN‐γ‐induced NO production was triggered by the Janus tyrosine kinase (JAK)/signal transducer and activator of transcription (STAT) pathway since it was inhibited by AG490, a JAK2 inhibitor. The growth of TH2.52 cells significantly was inhibited in the presence of IFN‐γ. A significant number of cells underwent apoptotic cell death, accompanied by the DNA fragmentation, annexin V binding, and caspase 3 activation. N(G)‐monomethyl‐ L ‐arginine, an iNOS inhibitor, prevented IFN‐γ‐induced cell death. Therefore, IFN‐γ‐induced NO production was possible in causing cell death in TH2.52 cells. Further, IFN‐γ‐induced NO production and cell death significantly were prevented by interleukin‐4, a representative Th2 cytokine. The immunological significance of IFN‐γ‐induced NO production in a mouse B1‐like cell line is discussed.