Xiaoming Liu1,2, Xuechao Jiang1,2, Ronghua Liu1,2, Luman Wang1,2, Tingting Qian1,2, Yijie Zheng1,2, Yuting Deng1,2, Enyu Huang1,2, Fengkai Xu3, Ji-Yang Wang1,2, Yiwei Chu1,2. 1. Department of Immunology, Key Laboratory of Medical Molecular Virology of MOE/MOH, School of Basic Medical Sciences, Fudan University, Shanghai, China. 2. Biotherapy Research Center, Fudan University, Shanghai, China. 3. Department of Thoracic Surgery, The Affiliated Zhongshan Hospital of Fudan University, Shanghai, China.
Abstract
UNLABELLED: Increasing evidence in recent years has suggested that B cells act as a crucial regulator in autoimmune diseases. However, little is known about their role in autoimmune hepatitis (AIH) and the underlying regulatory mechanisms. In this study, we show that B cells ameliorated experimental AIH (EAH) by suppressing CD4+ T-cell responses and that CD11b expression on B cells was required for the regulatory function of B cells. In vitro studies reveal that the suppressive function of CD11b was mediated by the impairment of T-cell antigen receptor (TCR) signaling transduction and the promotion of TCR down-regulation. Moreover, we show that the increased CD11b expression on B cells was interleukin (IL)-10 dependent and that additional IL-10 stimulation promoted CD11b expression on B cells, thereby enhancing B-cell regulatory effects. CONCLUSION: These findings reveal a previously unrecognized role for CD11b in B-cell regulatory function and its protective effect on EAH.
UNLABELLED: Increasing evidence in recent years has suggested that B cells act as a crucial regulator in autoimmune diseases. However, little is known about their role in autoimmune hepatitis (AIH) and the underlying regulatory mechanisms. In this study, we show that B cells ameliorated experimental AIH (EAH) by suppressing CD4+ T-cell responses and that CD11b expression on B cells was required for the regulatory function of B cells. In vitro studies reveal that the suppressive function of CD11b was mediated by the impairment of T-cell antigen receptor (TCR) signaling transduction and the promotion of TCR down-regulation. Moreover, we show that the increased CD11b expression on B cells was interleukin (IL)-10 dependent and that additional IL-10 stimulation promoted CD11b expression on B cells, thereby enhancing B-cell regulatory effects. CONCLUSION: These findings reveal a previously unrecognized role for CD11b in B-cell regulatory function and its protective effect on EAH.
Authors: Janelle M Korf; Pedram Honarpisheh; Eric C Mohan; Anik Banerjee; Maria P Blasco-Conesa; Parisa Honarpisheh; Gary U Guzman; Romeesa Khan; Bhanu P Ganesh; Amy L Hazen; Juneyoung Lee; Aditya Kumar; Louise D McCullough; Anjali Chauhan Journal: J Immunol Date: 2022-06-22 Impact factor: 5.426
Authors: Luuk van Hooren; Alessandra Vaccaro; Mohanraj Ramachandran; Konstantinos Vazaios; Sylwia Libard; Tiarne van de Walle; Maria Georganaki; Hua Huang; Ilkka Pietilä; Joey Lau; Maria H Ulvmar; Mikael C I Karlsson; Maria Zetterling; Sara M Mangsbo; Asgeir S Jakola; Thomas Olsson Bontell; Anja Smits; Magnus Essand; Anna Dimberg Journal: Nat Commun Date: 2021-07-05 Impact factor: 14.919