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Involvement of gamma interferon in antibody enhancement by adjuvants.

机译:γ干扰素参与佐剂增强抗体的过程。

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In a previous study the adjuvant action of a monophosphoryl lipid A, a nontoxic derivative of endotoxic lipopolysaccharide (LPS), was found to be negated by a monoclonal anti-gamma interferon (anti-IFN-gamma) antibody. The present investigation centered on three other adjuvants of diverse microbial origins, testing for their capacity to affect the release of IFN-gamma as an explanation for their antibody-enhancing action. The adjuvant action of each of the three, a wild-type LPS, synthetic poly(A)-poly(U) complexes, and a synthetic muramyl dipeptide, n-acetylmuramyl-L-alanyl-D-glutaminyl-n-butyl ester (murabutide), was transferable by adjuvant-stimulated T cells to normal spleen cells on coculture. Supernatant fluids from these T cells contained increased levels of IFN-gamma. Addition of a monoclonal anti-IFN-gamma antibody to adjuvant-stimulated spleen cell cultures reduced the adjuvant action by approximately one-half. Removal of natural killer cells from spleen cell populations prior to culture with antigen had no effect on the enhancement induced by LPS and monophosphoryl lipid A. It was concluded that the enhancement induced by the adjuvants LPS, poly(A)-poly(U), and murabutide is mediated in part by their action on T cells resulting in release of IFN-gamma suggesting activation of a common transmembrane signal.
机译:在先前的研究中,发现单磷酰脂质A(一种内毒素性脂多糖(LPS)的无毒衍生物)的佐剂作用被单克隆抗γ干扰素(anti-IFN-γ)抗体所抵消。本研究集中在其他三种来自多种微生物的佐剂上,测试其影响IFN-γ释放的能力,以此来说明其增强抗体的作用。这三种野生型LPS,合成的Poly(A)-poly(U)配合物和合成的ram基二肽,n-乙酰基村m基-L-丙氨酰基-D-谷氨酰胺基-正丁酯( murabutide)可在联合培养时被佐剂刺激的T细胞转移至正常脾细胞。来自这些T细胞的上清液含有增加水平的IFN-γ。向佐剂刺激的脾细胞培养物中添加单克隆抗IFN-γ抗体可将佐剂作用降低约一半。在用抗原培养之前从脾细胞群中去除自然杀伤细胞对LPS和单磷酰脂质A诱导的增强没有影响。结论是,佐剂LPS,poly(A)-poly(U), murabutide部分受其对T细胞的作用所介导,导致IFN-γ的释放,提示共同跨膜信号的激活。

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