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Title:
Regulatory B cells contribute to the impaired antitumor immunity in ovarian cancer patients | Tumor Biology
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Multiple factors in the tumor microenvironment were found to inhibit antitumor adaptive immune responses, allowing tumor persistence and growth. In this study, ascites from ovarian cancer patients were collected. We observed that a population of interleukin-10+ B (IL-10+ B) cells was preferentially enriched in the ascites. This population was associated with naive B cell phenotype or IgM or class-switched memory B cell phenotypes. The frequencies of IL-10+ B cells were negatively correlated with the frequencies of interferon gamma-producing (IFN-g+) CD8+ T cells and were positively correlated with the frequencies of Foxp3+ CD4+ T cells. To examine whether increased IL-10+ B cells in ascites could directly result in increased suppression of IFN-g production by CD8+ T cells, we cocultured CD8+ T cells with autologous blood B cells or ascitic B cells and found that CD8+ T cells cocultured with ascitic B cells demonstrated significantly suppressed IFN-g production. This suppression was in part mediated by IL-10 as well as low CD80/CD86 expression, since depletion of IL-10 and stimulation of CD28 partially reverted IL-10+ B cell-mediated suppression. Together, these data demonstrated an additional regulatory mechanism in the tumor microenvironment, which utilizes IL-10+ B cells.
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pubmed, cells, article, google, scholar, cas, cell, cancer, central, regulatory, ovarian, immunol, tumor, wei, httpwwwncbinlmnihgovpubmed, liaocheng, immunity, patients, shandong, privacy, cookies, content, antitumor, access, tumorinfiltrating, lymphocytes, human, hospital, china, function, data, information, publish, research, search, xin, jin, tian, microenvironment, nature, httpwwwhubmedorgdisplaycgiuids, author, peoples, log, journal, impaired, december, yangqiu, zhang, inhibit,
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artid=3636159&tool=pmcentrez&rendertype=abstract month download article/chapter anti-pd-l1 antibody mpdl3280a low cd80/cd86 expression cd27+ memory b-cells ovarian carcinoma-infiltrating regulatory antigen-specific cd4+ helper cells inhibit tumor-infiltrating atypical cd27āmemory phenotype human tumor-infiltrating lymphocytes cd20+ tumor-infiltrating lymphocytes attenuates anti-hiv cd8+ /article/s1074761314002301/fulltext nature publishing group macmillan publishers limited suppress hiv-1-specific full article pdf privacy choices/manage cookies related subjects tumor-infiltrating lymphocytes van den eynde article wei ovarian cancer patients hiv disease progression cell tim-3 expression advanced ovarian cancer ovarian cancer outcomes class-switched memory sci transl med allowing tumor persistence anti-tumor response additional regulatory mechanism tumor-evoked regulatory european economic area pilot results leading converting resting cd4+ tlr9 ligand induces 1007/s13277-015-4538-0 keywords gov/pubmed/17916463 gov/pubmed/1445813 gov/pubmed/7600302 gov/pubmed/16585599 gov/pubmed/20014885 gov/pubmed/21149607 gov/pubmed/23396472 gov/pubmed/23434518 cd4+ cd25+ regulatory conditions privacy policy shared melanoma antigens cell populations revealed
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headline:Regulatory B cells contribute to the impaired antitumor immunity in ovarian cancer patients
description:Multiple factors in the tumor microenvironment were found to inhibit antitumor adaptive immune responses, allowing tumor persistence and growth. In this study, ascites from ovarian cancer patients were collected. We observed that a population of interleukin-10+ B (IL-10+ B) cells was preferentially enriched in the ascites. This population was associated with naive B cell phenotype or IgM or class-switched memory B cell phenotypes. The frequencies of IL-10+ B cells were negatively correlated with the frequencies of interferon gamma-producing (IFN-g+) CD8+ T cells and were positively correlated with the frequencies of Foxp3+ CD4+ T cells. To examine whether increased IL-10+ B cells in ascites could directly result in increased suppression of IFN-g production by CD8+ T cells, we cocultured CD8+ T cells with autologous blood B cells or ascitic B cells and found that CD8+ T cells cocultured with ascitic B cells demonstrated significantly suppressed IFN-g production. This suppression was in part mediated by IL-10 as well as low CD80/CD86 expression, since depletion of IL-10 and stimulation of CD28 partially reverted IL-10+ B cell-mediated suppression. Together, these data demonstrated an additional regulatory mechanism in the tumor microenvironment, which utilizes IL-10+ B cells.
datePublished:2015-12-05T00:00:00Z
dateModified:2015-12-05T00:00:00Z
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Ovarian cancer
Cancer Research
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headline:Regulatory B cells contribute to the impaired antitumor immunity in ovarian cancer patients
description:Multiple factors in the tumor microenvironment were found to inhibit antitumor adaptive immune responses, allowing tumor persistence and growth. In this study, ascites from ovarian cancer patients were collected. We observed that a population of interleukin-10+ B (IL-10+ B) cells was preferentially enriched in the ascites. This population was associated with naive B cell phenotype or IgM or class-switched memory B cell phenotypes. The frequencies of IL-10+ B cells were negatively correlated with the frequencies of interferon gamma-producing (IFN-g+) CD8+ T cells and were positively correlated with the frequencies of Foxp3+ CD4+ T cells. To examine whether increased IL-10+ B cells in ascites could directly result in increased suppression of IFN-g production by CD8+ T cells, we cocultured CD8+ T cells with autologous blood B cells or ascitic B cells and found that CD8+ T cells cocultured with ascitic B cells demonstrated significantly suppressed IFN-g production. This suppression was in part mediated by IL-10 as well as low CD80/CD86 expression, since depletion of IL-10 and stimulation of CD28 partially reverted IL-10+ B cell-mediated suppression. Together, these data demonstrated an additional regulatory mechanism in the tumor microenvironment, which utilizes IL-10+ B cells.
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Cancer Research
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