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Role of fibrosarcoma-induced CD11b+ myeloid cells and tumor necrosis factor-α in B cell responses.

Abstract
The role of B cells in the anti-tumor immune response remains controversial. An increase in the number of B cells in the peripheral blood of some tumor patients has been associated with poor immunotherapy efficacy. However, the mechanism leading to the generation of these cells is not well-described. Using a fibrosarcoma model, we show that intraperitoneal administration of a xenogeneic antigen in tumor-bearing mice evokes large increases in antigen-specific serum immunoglobulin formation compared to tumor-naïve mice. An inability of tumor-bearing mice to induce enhanced antibody production after myeloid cell depletion suggests the antibody responses are CD11b+ myeloid cell-dependent. In vitro, CD11b+ myeloid cells promoted B cell proliferation, activation, and survival. High levels of tumor necrosis factor (TNF)-α were produced by CD11b+ cells, and TNF-α blockade inhibited B cell responses. CD11b+ cells appear to be important promoters of B cell responses and targeting B cells may increase the efficacy of immunotherapy in tumor-bearing hosts.
AuthorsZibing Wang, Yuqing Liu, Ling Peng, Brian Till, Yuwei Liao, Shumin Yuan, Xiang Yan, Lin Chen, Qiang Fu, Zhihai Qin
JournalOncogene (Oncogene) Vol. 41 Issue 10 Pg. 1434-1444 (03 2022) ISSN: 1476-5594 [Electronic] England
PMID35034094 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright© 2022. The Author(s), under exclusive licence to Springer Nature Limited.
Chemical References
  • CD11b Antigen
  • Tumor Necrosis Factor-alpha
Topics
  • Animals
  • CD11b Antigen
  • Fibrosarcoma (pathology)
  • Humans
  • Immunotherapy
  • Mice
  • Mice, Inbred C57BL
  • Myeloid Cells (pathology)
  • Tumor Necrosis Factor-alpha (physiology)

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