Infiltration and immunosuppressive function of tumor-associated B cells in gastric cancer patients

To investigate the distribution of B cells in both tumor and non-tumor tissues of gastric cancer patients, analyze their phenotypic characteristics and explore the impact on T cell proliferation.

Immunohistochemical staining was utilized to detect the expression of B cell surface marker CD19 in tumor and non-tumor tissues from 33 gastric cancer patients. The expression levels of chemokine receptors and immunoglobulin molecules on B cells in both tumor and non-tumor tissues were measured using flow cytometry. Chemotaxis experiments were conducted to examine the role of the CXCL12-CXCR4 axis in B cell chemotaxis. B cells isolated and purified from both tissue types were co-cultured with autologous peripheral T cells to assess their effect on T cell proliferation.

There were significantly more B cells infiltrated in tumor tissues than those infitrated in the non-tumor tissues of gastric cancer patients (P<0.01), and CXCR4 was highly expressed on tumor-infiltrating B cells compared with B cells derived from non-tumor tissues (P<0.05). The Cancer Genome Atlas (TCGA) analysis indicated that the expression level of CXCL12 in tumor tissues was positively correlated with the expression level of CD19 in gastric cancer patients (r=0.15, P<0.01). And the expression level of CXCL12 in tumor tissues of the gastric cancer patients was also positively correlated with the number of B cells infiltrated in tumor tissues. Chemotaxis experiments confirmed that the CXCL12-CXCR4 axis was involved in promoting B cell chemotaxis (P<0.05). Although B cells in tumor and non-tumor tissues had similar levels of IgM, IgG, and IgA expression, tumor-infiltrating B cells significantly inhibited the proliferation of T cells when compared with B cells derived from non-tumor tissues (P<0.01).

There are more B cells infiltrated in gastric cancer tissues, which may be recruited to tumor tissues through the CXCL12-CXCR4 axis, and then inhibit T cell proliferation to promote the progression of gastric cancer.