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Title 

Carbofuran suppresses T-cell-mediated immune responses by the suppression of T-cell responsiveness, the differential inhibition of cytokine production, and NO production in macrophages

Authors 

Sun Duck JeonJong Seok LimChang Kiu Moon

Publisher 

Elsevier

Issue Date 

2001

Citation 

Toxicology Letters, vol. 119, no. 2, pp. 143-155

Keywords 

carbofurancell-mediated immune responsesdelayed type hypersensitivitysplenocytesmixed lymphocyte reactioncytokinesnitric oxidemacrophages

Abstract 

The effects of carbofuran (2,3-dihydro-2,2-dimethyl-7-benzo-furanol N-methylcarbamate) on the functions of T cells in splenocytes and peritoneal macrophages were examined in view of T-cell-mediated immune response (CMIR) in male C57BL/6 mice. Intraperitoneal administration of carbofuran (0.075, 0.15 and 0.3 mg/kg body weight) resulted in significant suppression of delayed type hypersensitivity (DTH), indicating that it caused the suppression of CMIR. Carbofuran decreased Concanavalin A (Con A)- and alloantigen-induced proliferation, and interleukin (IL)-2 production of splenocytes. In vitro addition of rIL-2 could not completely restore the suppressed T-cell proliferation, and IL-2-induced proliferation of Con A-activated splenocytes was also suppressed, which implied that carbofuran caused defects in IL-2 production and responsiveness of splenocytes to IL-2, leading to the suppression of T-cell proliferation. Con A-induced production of interferon-γ (IFN-γ) was significantly suppressed by carbofuran, while that of IL-4 was not affected. The production of transforming growth factor-β from splenocytes was also significantly inhibited by carbofuran. Judging from these results, carbofuran might directly suppress the cytokine production in T helper 1 (Th1) cells. In addition, IFN-γ-induced production of nitric oxide (NO) in macrophages was also inhibited by carbofuran, which might be one of the important mechanisms of carbofuran-induced CMIR suppression in mice. Collectively, the present study suggests that carbofuran might suppress CMIR through the suppression of T-cell responsiveness, IFN-γ production in Th1 cells, and NO generation in macrophages.

ISSN 

0378-4274

Link 

http://dx.doi.org/10.1016/S0378-4274(00)00307-6

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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