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抗原呈递细胞参与霍乱毒素B亚单位对体外抗体应答的增强作用。

Involvement of antigen-presenting cells in the enhancement of the in vitro antibody responses by cholera toxin B subunit.

作者信息

Hirabayashi Y, Tamura S I, Shimada K, Kurata T

机构信息

Department of Pathology, National Institute of Health, Tokyo, Japan.

出版信息

Immunology. 1992 Mar;75(3):493-8.

PMID:1374056
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1384745/
Abstract

The enhancing effect of cholera toxin B subunit (CTB) on primary antibody responses to keyhole limpet haemocyanin (KLH) and the cellular basis of the effect were investigated, using in vitro cultures of mouse spleen cells. CTB (1-100 ng/ml) enhanced anti-KLH IgM, IgG and IgA antibody responses in a dose-dependent manner, when added to the cultures with KLH. This immunoenhancement was antigen specific, but not due to either polyclonal activation of the spleen cells or antigenic cross-reactivity between CTB and KLH. CTB did not affect the kinetics of the anti-KLH antibody responses. Early (Days 0-1) addition of CTB to the cultures enhanced the anti-KLH antibody production, whereas late (Days 5-7) addition of CTB did not. Addition of CTB with KLH to splenic adherent cells (SAC) resulted in a dose-dependent enhancement of the anti-KLH antibody responses, when the SAC were reconstituted with unimmunized non-adherent cells. Moreover, CTB enhanced IL-1 secretion from SAC incubated with KLH. These results suggest that CTB enhances the primary anti-KLH antibody responses in vitro by acting on early events in the responses, and that antigen-presenting cells play a major role in the enhancement.

摘要

利用小鼠脾细胞的体外培养,研究了霍乱毒素B亚基(CTB)对钥孔戚血蓝蛋白(KLH)初次抗体反应的增强作用及其作用的细胞基础。当与KLH一起加入培养物中时,CTB(1-100 ng/ml)以剂量依赖的方式增强了抗KLH IgM、IgG和IgA抗体反应。这种免疫增强是抗原特异性的,但既不是由于脾细胞的多克隆激活,也不是由于CTB与KLH之间的抗原交叉反应。CTB不影响抗KLH抗体反应的动力学。在培养物中早期(第0-1天)加入CTB可增强抗KLH抗体的产生,而晚期(第5-7天)加入CTB则无此作用。当用未免疫的非贴壁细胞重建脾贴壁细胞(SAC)时,将CTB与KLH一起加入SAC会导致抗KLH抗体反应呈剂量依赖性增强。此外,CTB增强了与KLH一起孵育的SAC中IL-1的分泌。这些结果表明,CTB通过作用于反应的早期事件在体外增强了初次抗KLH抗体反应,并且抗原呈递细胞在这种增强中起主要作用。

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Infect Immun. 1997 Apr;65(4):1445-54. doi: 10.1128/iai.65.4.1445-1454.1997.
3
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