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葡萄球菌肠毒素和中毒性休克综合征毒素-1等超抗原诱导牛外周血单个核细胞的增殖反应及细胞因子产生

Proliferative response and cytokine production of bovine peripheral blood mononuclear cells induced by the superantigens staphylococcal enterotoxins and toxic shock syndrome toxin-1.

作者信息

Yokomizo Y, Mori Y, Shimoji Y, Shimizu S, Sentsui H, Kodama M, Igarashi H

机构信息

National Institute of Animal Health, Ibaraki, Japan.

出版信息

J Vet Med Sci. 1995 Apr;57(2):299-305. doi: 10.1292/jvms.57.299.

Abstract

The potential of staphylococcal enterotoxin A (SEA), B (SEB), C(SEC) and toxic shock syndrome toxin-1 (TSST-1) to act as superantigens by inducing polyclonal T-cell mitogenesis and cytokine production was tested on bovine peripheral blood mononuclear cells (PBMC). These four toxins were capable of inducing strong proliferative response of PBMC from calves over a broad dosage range (1 pg/ml to 1 microgram/ml) in vitro. The toxin-activated blast cells consisted of both CD4+ T-cells and CD8+ T-cells, but the T-cell proliferation depended upon the presence of monocytes. Treatment of monocytes with monoclonal antibody to major histocompatibility complex class II antigens substantially inhibited the toxin-induced T-cell proliferative response, but paraformaldehyde-fixation did not abrogate the accessory function. SEA, SEB, SEC and TSST-1, all induced the in vitro release of interleukin-2, interferon gamma and tumor necrosis factor alpha in a dose dependent manner. The results indicate that SEA, SEB, SEC and TSST-1 are capable of acting as superantigens by stimulating bovine T-cells as shown in the human and murine systems. The possible implications of these toxins in the immunopathogenesis of bovine mastitis caused by the infection with Staphylococcus aureus are discussed.

摘要

利用牛外周血单个核细胞(PBMC)测试了葡萄球菌肠毒素A(SEA)、B(SEB)、C(SEC)和中毒性休克综合征毒素-1(TSST-1)作为超抗原诱导多克隆T细胞有丝分裂和细胞因子产生的潜力。这四种毒素能够在体外宽剂量范围(1 pg/ml至1微克/ml)内诱导犊牛PBMC产生强烈的增殖反应。毒素激活的母细胞由CD4 + T细胞和CD8 + T细胞组成,但T细胞增殖依赖于单核细胞的存在。用针对主要组织相容性复合体II类抗原的单克隆抗体处理单核细胞可显著抑制毒素诱导的T细胞增殖反应,但多聚甲醛固定并未消除其辅助功能。SEA、SEB、SEC和TSST-1均以剂量依赖性方式诱导白细胞介素-2、干扰素γ和肿瘤坏死因子α在体外释放。结果表明,SEA、SEB、SEC和TSST-1能够像在人和小鼠系统中那样通过刺激牛T细胞而作为超抗原发挥作用。讨论了这些毒素在由金黄色葡萄球菌感染引起的牛乳腺炎免疫发病机制中的可能意义。

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