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暴露于结核分枝杆菌脂质的B-1a细胞和B-1b细胞都会分化为分泌IgM抗体的细胞。

Both B-1a and B-1b cells exposed to Mycobacterium tuberculosis lipids differentiate into IgM antibody-secreting cells.

作者信息

Ordoñez Ciara, Savage Hannah P, Tarajia Musharaf, Rivera René, Weeks-Galindo Cheyenne, Sambrano Dilcia, Riley Lee, Fernandez Patricia L, Baumgarth Nicole, Goodridge Amador

机构信息

Tuberculosis Biomarker Research Unit, Centro de Biología Molecular y Celular de Enfermedades-Instituto de Investigaciones Científicas y Servicios de Alta Tecnología (INDICASAT-AIP), CIUDAD DEL SABER, Clayton, Panama.

Department of Biotechnology, Acharya Nargajuna University, Guntur, India.

出版信息

Immunology. 2018 Feb 18;154(4):613-23. doi: 10.1111/imm.12909.

DOI:10.1111/imm.12909
PMID:29455451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6050208/
Abstract

Tuberculosis is an infectious disease caused by Mycobacterium tuberculosis. The cellular immune response to mycobacteria has been characterized extensively, but the antibody response remains underexplored. The present study aimed to examine whether host or bacterial phospholipids induce secretion of IgM, and specifically anti-phospholipid IgM, antibodies by B cells and to identify the responsible B-cell subset. Here we show that peritoneal B cells responded to lipid antigens by secreting IgM antibodies. Specifically, stimulation with M. tuberculosis H37Rv total lipids resulted in significant induction of total and anti-phosphatidylcholine IgM. Similarly, IgM antibody production increased significantly with stimulation by whole Mycobacterium bovis bacillus Calmette-Guérin. The B-1 subset was the dominant source of IgM antibodies after exposure to cardiolipin. Both CD5 B-1a and CD5 B-1b cell subsets secreted total IgM antibodies after exposure to M. tuberculosis H37Rv total lipids in vitro. Overall, our results suggest that the poly-reactive B-1 cell repertoire contributes to non-specific anti-phospholipid IgM antibody secretion in response to M. tuberculosis lipids.

摘要

结核病是由结核分枝杆菌引起的一种传染病。对分枝杆菌的细胞免疫反应已得到广泛研究,但抗体反应仍未得到充分探索。本研究旨在检测宿主或细菌磷脂是否能诱导B细胞分泌IgM,特别是抗磷脂IgM抗体,并确定相关的B细胞亚群。在此我们表明,腹膜B细胞通过分泌IgM抗体对脂质抗原作出反应。具体而言,用结核分枝杆菌H37Rv总脂质刺激可显著诱导总IgM和抗磷脂酰胆碱IgM。同样,用完整的卡介苗刺激可显著增加IgM抗体的产生。B-1亚群是接触心磷脂后IgM抗体的主要来源。在体外接触结核分枝杆菌H37Rv总脂质后,CD5 B-1a和CD5 B-1b细胞亚群均分泌总IgM抗体。总体而言,我们的结果表明,多反应性B-1细胞库有助于响应结核分枝杆菌脂质分泌非特异性抗磷脂IgM抗体。

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