Antitumor effector B cells directly kill tumor cells via the Fas/FasL pathway and are regulated by IL‐10. Issue 4 (21st January 2015)

• Record Type: Journal Article
• Authors: Tao, Huimin; Lu, Lin; Xia, Yang; Dai, Fu; Wang, Yi; Bao, Yangyi; Lundy, Steven K.; Ito, Fumito; Pan, Qin; Zhang, Xiaolian; Zheng, Fang; Shu, Guoshun; Fang, Bingmu; Jiang, Jinhong; Xia, Jianchuang; Huang, Shiang; Li, Qiao; Chang, Alfred E.
• Is Part Of: European journal of immunology. Volume 45:Issue 4(2015:Apr.)
• Page Start: 999
• Page End: 1009
• Publication Date: 2015-01-21
• Subjects: Immunology -- Periodicals; 616.079
• DOI: 10.1002/eji.201444625
• Languages: English
• ISSNs: 0014-2980

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>We have previously reported that adoptive transfer of tumor‐draining lymph node (TDLN) B cells confers tumor regression in a spontaneous pulmonary metastasis mouse model of breast cancer. In this study, we identified IL‐10‐producing cells within these B cells, and found that IL‐10 removal, either by using IL‐10^−/− TDLN B cells or by systemic neutralization of IL‐10, significantly augmented the therapeutic efficacy of adoptively transferred TDLN B cells. Depletion of IL‐10 in B‐cell adoptive transfers significantly increased CTLs and B‐cell activity of PBMCs and splenic cells in the recipient. Activated TDLN B cells express Fas ligand, which was further enhanced by coculture of these TDLN B cells with 4T1 tumor cells. Effector B cells killed tumor cells directly in vitro in an antigen specific and Fas ligand‐dependent manner. Trafficking of TDLN B cells in vivo suggested that they were recruited to the tumor and lung as well as secondary lymphoid organs. These findings further define the biological function of antitumor effector B cells, which may offer alternative cellular therapies to cancer.</p> </abstract>