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10.1189/jlb.3A0114-012RR http://scihub22266oqcxt.onion/10.1189/jlb.3A0114-012RR C4197561!4197561 !25085111     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25085111 &cmd=llinks): Failed to open stream: HTTP request failed! 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Liver metastases induce reversible hepatic B cell dysfunction mediated by Gr-1+CD11b+ myeloid cells |pdf=|usr=}}{{25085111 }} gab.com Text Liver metastases induce reversible hepatic B cell dysfunction mediated by Gr-1+CD11b+ myeloid cells JO: J Leukoc Biol http://www.kidney.de/pget.php?&tw=1&pmid=25085111 #FOAvip LM escape immune surveillance, in part, as a result of the expansion of CD11b+MC, which alter the intrahepatic microenvironment to promote tumor tolerance. HBC make up a significant proportion of liver lymphocytes and appear to delay tumor progression; however, their significance in the setting of LM is poorly defined. Therefore, we characterized HBC and HBC/CD11b+MC interactions using a murine model of LM. Tumor-bearing livers showed a trend toward elevated absolute numbers of CD19+ HBC. A significant increase in the frequency of IgM(lo)IgD(hi) mature HBC was observed in mice with LM compared with normal mice. HBC derived from tumor-bearing mice demonstrated increased proliferation in response to TLR and BCR stimulation ex vivo compared with HBC from normal livers. HBC from tumor-bearing livers exhibited significant down-regulation of CD80 and were impaired in inducing CD4(+) T cell proliferation ex vivo. We implicated hepatic CD11b+MC as mediators of CD80 down-modulation on HBC ex vivo via a CD11b-dependent mechanism that required cell-to-cell contact and STAT3 activity. Therefore, CD11b+MC may compromise the ability of HBC to promote T cell activation in the setting of LM as a result of diminished expression of CD80. Cross-talk between CD11b+MC and HBC may be an important component of LM-induced immunosuppression. Twit Text FOAVip Liver metastases induce reversible hepatic B cell dysfunction mediated by Gr-1+CD11b+ myeloid cells ????J Leukoc Biol http://www.kidney.de/pget.php?&tw=1&pmid=25085111 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25085111 #FOAvip English Wikipedia <ref>{{Cite pmid|25085111 }}</ref> Liver metastases induce reversible hepatic B cell dysfunction mediated by Gr-1+CD11b+ myeloid cells #MMPMID25085111 Thorn M ; Point GR ; Burga RA ; Nguyen CT ; Joseph Espat N ; Katz SC J Leukoc Biol 2014[Nov]; 96 (5 ): 883-94 PMID25085111 show ga LM escape immune surveillance, in part, as a result of the expansion of CD11b+MC, which alter the intrahepatic microenvironment to promote tumor tolerance. HBC make up a significant proportion of liver lymphocytes and appear to delay tumor progression; however, their significance in the setting of LM is poorly defined. Therefore, we characterized HBC and HBC/CD11b+MC interactions using a murine model of LM. Tumor-bearing livers showed a trend toward elevated absolute numbers of CD19+ HBC. A significant increase in the frequency of IgM(lo)IgD(hi) mature HBC was observed in mice with LM compared with normal mice. HBC derived from tumor-bearing mice demonstrated increased proliferation in response to TLR and BCR stimulation ex vivo compared with HBC from normal livers. HBC from tumor-bearing livers exhibited significant down-regulation of CD80 and were impaired in inducing CD4(+) T cell proliferation ex vivo. We implicated hepatic CD11b+MC as mediators of CD80 down-modulation on HBC ex vivo via a CD11b-dependent mechanism that required cell-to-cell contact and STAT3 activity. Therefore, CD11b+MC may compromise the ability of HBC to promote T cell activation in the setting of LM as a result of diminished expression of CD80. Cross-talk between CD11b+MC and HBC may be an important component of LM-induced immunosuppression. |Adoptive Transfer [MESH] |Animals [MESH] |B-Lymphocyte Subsets/*immunology/metabolism [MESH] |B7-1 Antigen/metabolism [MESH] |B7-2 Antigen/metabolism [MESH] |CD11b Antigen/*metabolism [MESH] |Cell Line, Tumor [MESH] |Disease Models, Animal [MESH] |Down-Regulation [MESH] |Liver Neoplasms/diagnosis/*immunology/metabolism/secondary [MESH] |Luminescent Measurements/methods [MESH] |Lymphocyte Activation/immunology [MESH] |Male [MESH] |Mice [MESH] |Molecular Imaging/methods [MESH] |Myeloid Cells/*immunology/*metabolism [MESH] |Neoplasm Metastasis [MESH] |Receptors, Cell Surface/*metabolism [MESH] |T-Lymphocyte Subsets/immunology/metabolism [MESH]Liver metastases induce reversible hepatic B cell dysfunction mediated(epmc).pdf DeepDyve Pubget Overpricing