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.
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Authors | Zibing Wang, Yuqing Liu, Ling Peng, Brian Till, Yuwei Liao, Shumin Yuan, Xiang Yan, Lin Chen, Qiang Fu, Zhihai Qin |
Journal | Oncogene
(Oncogene)
Vol. 41
Issue 10
Pg. 1434-1444
(03 2022)
ISSN: 1476-5594 [Electronic] England |
PMID | 35034094
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2022. The Author(s), under exclusive licence to Springer Nature Limited. |
Chemical References |
- CD11b Antigen
- Tumor Necrosis Factor-alpha
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Topics |
- Animals
- CD11b Antigen
- Fibrosarcoma
(pathology)
- Humans
- Immunotherapy
- Mice
- Mice, Inbred C57BL
- Myeloid Cells
(pathology)
- Tumor Necrosis Factor-alpha
(physiology)
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