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单核细胞增生李斯特菌活细胞与死细胞诱导巨噬细胞白细胞介素-1产生的差异。

Difference in the induction of macrophage interleukin-1 production between viable and killed cells of Listeria monocytogenes.

作者信息

Mitsuyama M, Igarashi K, Kawamura I, Ohmori T, Nomoto K

机构信息

Department of Bacteriology, Niigata University School of Medicine, Japan.

出版信息

Infect Immun. 1990 May;58(5):1254-60. doi: 10.1128/iai.58.5.1254-1260.1990.

Abstract

T-cell-mediated immunity to Listeria monocytogenes in mice, as determined by delayed-type hypersensitivity and acquired resistance, was induced by immunization with viable bacteria but not with killed bacteria, even when killed cells were injected in a high dose or repeatedly. T cells obtained from mice immunized with viable L. monocytogenes were readily stimulated with killed-bacterial antigens, resulting in T-cell proliferation in vitro and expression of a delayed footpad reaction in vivo. After immunization with killed-bacterial vaccine, T-cell responsiveness to interleukin 2 (IL-2) never developed but a lower level of responsiveness to IL-1 appeared later than with T cells from mice immunized with viable bacteria. When IL-1 production by macrophages was examined in vitro, viable L. monocytogenes stimulated a high level of IL-1 release while killed bacteria did not. Avirulent strains which were ineffective in the induction of T-cell mediated immunity were incapable of inducing IL-1 production as well. The impaired ability of killed bacteria to stimulate IL-1 production was confirmed by the level of IL-1 mRNA expression. These results suggested that the ineffectiveness of killed L. monocytogenes vaccine is not due to loss or lack of antigenic epitopes but may be ascribed to insufficient induction of IL-1 production in the initial stage of the immune response in vivo.

摘要

通过迟发型超敏反应和获得性抵抗力所测定的小鼠对单核细胞增生李斯特菌的T细胞介导免疫,是由用活细菌免疫诱导产生的,而用死细菌免疫则不能诱导产生,即使死细胞以高剂量注射或反复注射也不行。从用活的单核细胞增生李斯特菌免疫的小鼠获得的T细胞,很容易被死细菌抗原刺激,导致体外T细胞增殖和体内足垫迟发反应的表达。在用死细菌疫苗免疫后,T细胞对白介素2(IL-2)的反应性从未产生,但对IL-1的反应性水平比用活细菌免疫的小鼠的T细胞出现得晚。当在体外检测巨噬细胞产生IL-1的情况时,活的单核细胞增生李斯特菌刺激高水平的IL-1释放,而死细菌则不能。在诱导T细胞介导免疫方面无效的无毒菌株也不能诱导IL-1的产生。通过IL-1 mRNA表达水平证实了死细菌刺激IL-1产生的能力受损。这些结果表明,死的单核细胞增生李斯特菌疫苗无效不是由于抗原表位的丧失或缺乏,而是可能归因于体内免疫反应初始阶段IL-1产生的诱导不足。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd4a/258617/3964deef65a9/iai00053-0136-a.jpg

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