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10.1016/j.cellimm.2017.02.002

http://scihub22266oqcxt.onion/10.1016/j.cellimm.2017.02.002
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C5383205!5383205!28238361
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suck abstract from ncbi

pmid28238361      Cell+Immunol 2017 ; 314 (ä): 54-62
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  • Macrophage regulation of B cell proliferation #MMPMID28238361
  • Goldman N; Valiuskyte K; Londregan J; Swider A; Somerville J; Riggs JE
  • Cell Immunol 2017[Apr]; 314 (ä): 54-62 PMID28238361show ga
  • Unlike organized lymphoid tissue, the tumor microenvironment (TME) often includes a high proportion of immunosuppressive macrophages. We model the TME by culturing peritoneal cavity (PerC) cells that naturally have a high macrophage to lymphocyte ratio. Prior studies revealed that, following TCR ligation, PerC T cell proliferation is suppressed due to IFN?-triggered inducible nitric oxide synthase expression. In this study we assessed the ability of PerC B cells to respond to surrogate activating signals in the presence of high numbers of macrophages. Surface IgM (BCR) ligation led to cyclooxygenase-mediated, and TLR-4 ligation to IL10-mediated, suppression of PerC B cell proliferation. In contrast, PerC B cells had a robust response to CD40 ligation, which could overcome the suppression generated by the BCR or TLR-4 response. However, the CD40 response was suppressed by concurrent TCR ligation. These results reveal the challenges of promoting B and T cell responses in macrophage-rich conditions that model the TME.
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