Table 2.
Targets of Bregs in tumor microenvironment to regulate antitumor responses.
| Targets | Cancer types | Mechanisms | References |
|---|---|---|---|
| Effector T cells | Breast, ovarian, cervical, colorectal, prostate, gastric cancer; glioma, glioblastoma, melanoma, hepatocellular carcinoma | Inhibit proliferation and cytokine production of effector T cells | (30, 36–43, 76–79), |
| Regulatory T cells | Gastric, breast cancer; tongue squamous cell carcinoma | Convert CD4+ T cells into Tregs | (31, 37, 46, 80), |
| MDSCs | 4T1 adenocarcinoma cells and B16F10 melanoma | Educate MDSCs to fully evoke regulatory and prometastatic functions of MDSCs | (81) |
| NK cells | Mouse EL-4 tumor | Secrete IL-10 to inhibit IFN-γ production and tumor elimination by NK cells | (60) |
| Multiple myeloma | Abolish NK cell-mediated lysis of multiple myeloma cells | (45) | |
| Effector B cells | Head and neck squamous cell carcinoma | Secrete adenosine to dampen BKT phosphorylation and Ca2+ influx in effector B cells | (47) |
| Monocytes/macrophages | Lymphoma | Secrete IL-10 to suppress mAb-mediated monocyte activation and effector function, resulting in reduced lymphoma depletion | (44) |
| Breg-tumor cross-regulation | Hepatocellular carcinoma | Bregs directly interacted with liver cancer cells to enhance cancer growth and invasiveness. | (48) |
| Multiple myeloma | Multiple myeloma cells inhibited apoptosis of Bregs. | (45) | |
| Breast cancer | Breast cancer cells produced metabolites of the 5-lipoxygenase pathway to generate Bregs, leading to cancer escape eventually. | (82) | |
| B16-F10 melanoma | Bregs were restrictedly accumulated in TDLN, which promoted tumor growth after adoptive transfer. | (32) |
Treg, regulatory T cell; MDSC, myeloid-derived suppressor cell; NK, natural killer; BKT, Bruton’s tyrosine kinase; TDLN, tumor-draining lymph node.