RT Journal Article
SR Electronic
T1 CXCL13 as a Novel Immune Checkpoint for Regulatory B Cells and Its Role in Tumor Metastasis
JF The Journal of Immunology
JO J. Immunol.
FD American Association of Immunologists
SP 2425
OP 2435
DO 10.4049/jimmunol.2100341
VO 208
IS 10
A1 Ren, Jun
A1 Lan, Tianxia
A1 Liu, Ting
A1 Liu, Yu
A1 Shao, Bin
A1 Men, Ke
A1 Ma, Yu
A1 Liang, Xiao
A1 Wei, Yu-quan
A1 Luo, Min
A1 Wei, Xia-wei
YR 2022
UL http://www.jimmunol.org/content/208/10/2425.abstract
AB CXCL13 contributes to tumor metastasis by recruiting regulatory B cells.Recruited regulatory B cells affect both innate and adaptive immunity.Lack of CXCL13 increases the efficacy of chemotherapy and PD-1 blockade.Tumor metastasis is the primary cause of mortality in patients with cancer. Several chemokines are identified as important mediators of tumor growth and/or metastasis. The level of CXCL13 has been reported to be elevated in serum or tumor tissues in patients, which mainly functions to attract B cells and follicular B helper T cells. However, the role of CXCL13 in cancer growth and metastasis is not fully explored. In the current study, we found that CXCL13 is not a strong mediator to directly promote tumor growth; however, the mice deficient in CXCL13 had far fewer pulmonary metastatic foci than did the wild-type mice in experimental pulmonary metastatic models. In addition, Cxcl13−/− mice also had fewer IL-10–producing B cells (CD45+CD19+IL-10+) in the metastatic tumor immune microenvironment than those of wild-type C57BL/6 mice, resulting in an enhanced antitumor immunity. Notably, CXCL13 deficiency further improved the efficacy of a traditional chemotherapeutic drug (cyclophosphamide), as well as that of anti–programmed death receptor-1 immunotherapy. These results suggested that CXCL13 has an important role in regulating IL-10–producing B cells in tumor metastasis and might be a promising target for improving therapeutic efficiency and stimulating tumor immunity in future cancer therapy.