Table 1.
Current research about the interactions of B cells influencing tumor clinical outcomes, using scRNA-seq or cell-cell communication analysis.
| Tumor type | Interactions | Outcomes | Reference |
|---|---|---|---|
| Non-small cell lung cancer (NSCLC), malignant pleural effusion (MPE) | In MPE, Bregs interact primarily with CD4+ T cells (including Th1/17, Treg and Tfh), but not CD8+ T cells. | Bregs in MPE show great cell proliferation signaling and are related to poor clinical outcomes. | (95) |
| Colorectal Cancer (CRC) | Compared to non-tumor tissues - Enhanced interactions between non-immune cells (including MKI67+ goblet cells, DEFA5+DEFA6+ metaplastic paneth cells, colonocytes, and fibroblasts) and immune cells (including B cells, T cells and myeloid cells) in tumor tissues. - Altered interaction pathways between B cells and T cells. |
- B, plasma and non-immune cells in tumor tissues exert important roles in shaping tumor microenvironment. - Proliferative B-cell signatures are enriched in tumors that respond to immunotherapy. |
(96) |
| CRC | Compared to non-tumor tissues - Enhanced interactions between myeloid cells and lymphocytes (including B cells, plasma cells and T cells) in tumor tissue. - Enhanced interactions between B cells and T cells through CD48-CD244. - B cells tend to interact with SIGLEC10+ T cells and inhibit T cell activation. - Enhanced interactions between IgA+ IGLC2+ plasma cells and multiple types of T cells. - CCL8+ IGLC2+ plasma cells and cycling B cells interacte with CCR5+ T cells in CRC and recruit CCR5+ T cells to the tumor foci. - Attenuated interactions between epithelial cells and B cells, but the SIRPA-CD47 and NRG1-ERBB3 pathways are enhanced. These are associated with immune escape and epithelial-mesenchymal transition (EMT)-associated metastasis. Compared to early stage tumor tissue - Enhanced interaction of B cells with other immune cells in advanced tumor tissue. - IgA+IGLC2+ plasma cells, which are associated with poor prognosis, have significant interactions with myeloid cells and cytotoxic T cells. |
- B cells and myeloid cells are predominantly responsible for immunoregulatory functions in CRC rather than CD4+ regulatory T cells. - B cells in early CRC tumors exhibit pre-B like tumor suppressors, while B cells in advanced CRC tumors tend to develop into plasma cells. - B cells in CRC may contribute to tumor progression. |
(97) |
| CRC | B cells, MKI67+ T cells and dysfunctional T cells, interact with tumor-associated macrophages (TAMs), which are enriched by preoperative chemotherapy, through HLA-F-LILRB2 and HLA-DPB1-NRG1 pathways in the cell niche of primary tumors. | - Less-activated B cells are more prevalent in the tumor microenvironment of treatment-naïve tumors. - B cell activation is observed in tumors treated with preoperative chemotherapy. |
(98) |
| Nasopharyngeal Carcinoma (NPC) | - The three exhausted T cell populations in TME (HAVCR2+, TOX+, and LAG3+ T cells) preferentially interact with memory B cells, innate-like B cells, unactivated B cells, and IFN-induced B cells, but not with plasma cells, naive B cells, and double-negative B cells. - Among them, B cells interact with HAVCR2+ and TOX+ exhausted T cell populations mainly through the CXCL13-CXCR5 axis. |
- A higher abundance of B cells is correlated with a better clinical prognosis in NPC patients. - A higher percentage of double-negative B cells is predictive of worse survival rate in NPC patients. |
(99) |
| Esophageal squamous cell carcinoma (ESCC) | Attenuated interactions between tumor cells and B cells compared to interactions between tumor cells and other immune cells in TME. | The specific cellular communication potentially shapes the unique TME in ESCC. | (100) |
| Ovarian Cancer | - Tumor-infiltrating B cells (B-TILs) interact with CD4+CXCL13 T cells as well as dysfunctional CD8+GZMB T cells through CXCR5-CXCL13, which is a possible mechanism for recruiting B cells into the tumor microenvironment. - B-TILs interact with endothelial cells via CCR7-CCL21, suggesting another possible mechanism for recruiting B cells into the tumor microenvironment. |
Stromal cells and T cells participate in the recruitment of B cells in tumor and stromal compartments of ovarian cancer. | (101) |
| Lymphoma | - Malignant B cells receive suppressive signals from all four major T cell subsets (T helper, T toxic, Tfh, Treg) through CD80/CD86-CD28 and CD80/CD86-CTLA. - Malignant B cells interact with T helper cells and Tregs through BCMA-BAFF, BAFF-R-BAFF, and CD40-CD40LG. - Malignant B cells interact with Tfh cells through IL4-IL4R, IL4-IL13RA1 and IL21-IL21R. |
- B cells modulate the frequency of various lymphoma-infiltrated T cell subsets to shape the microenvironment. - Malignant B cells are heterogenous among lymphoma patients with different proliferative activity. This is associated with lymphoma-specific transcriptional features. |
(102) |
| Head and neck squamous cell carcinoma (HNSCC), caused by environmental carcinogens or human papilloma virus (HPV) | - B cells interact with CD4+ T cells in both HPV- and HPV+ TME. Besides, the spatial distance between B cells and CD4+ T cells is closer, which reflects the probability of interaction. - Interactions between GC B cells and TFH are only in HPV+ TME. |
B cells in germinal center are observed in HPV+ tumor microenvironment, and correlate positively with the overall survival in HNSCC. | (103) |