Macrophage colony‐stimulating factor enhances rituximab‐dependent cellular cytotoxicity by monocytes
Recent studies suggest that monocytes are the dominant effectors by which rituximab induces cell death in B‐cell lymphoma. Because macrophage colony‐stimulating factor (M‐CSF) can enhance the cytotoxicity of monocytes, the authors examined whether this growth factor can enhance their ability to kill...
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| Veröffentlicht in: | Cancer science 2007-09, Vol.98 (9), p.1368-1372 |
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| creator | Shimadoi, Shigeru Takami, Akiyoshi Kondo, Yukio Okumura, Hirokazu Nakao, Shinji |
| description | Recent studies suggest that monocytes are the dominant effectors by which rituximab induces cell death in B‐cell lymphoma. Because macrophage colony‐stimulating factor (M‐CSF) can enhance the cytotoxicity of monocytes, the authors examined whether this growth factor can enhance their ability to kill lymphoma cells in vitro. Monocytes derived from a healthy volunteer were cultured for 48 h in the presence or absence of M‐CSF. Monocytes stimul ated with M‐CSF were significantly more cytotoxic to Daudi B‐cell lymphomas than unstimulated monocytes. Flow cytometry revealed that M‐CSF increased monocyte expression of Fcγ receptors III and I by 1.6‐ and 1.5‐fold, whereas the expression of Fcγ receptor II remained unchanged. These results suggest that pretreatment with M‐CSF can improve the therapeutic efficacy of rituximab against intractable CD20+ lymphoma. (Cancer Sci 2007; 98: 1368–1372) |
| doi_str_mv | 10.1111/j.1349-7006.2007.00544.x |
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Because macrophage colony‐stimulating factor (M‐CSF) can enhance the cytotoxicity of monocytes, the authors examined whether this growth factor can enhance their ability to kill lymphoma cells in vitro. Monocytes derived from a healthy volunteer were cultured for 48 h in the presence or absence of M‐CSF. Monocytes stimul ated with M‐CSF were significantly more cytotoxic to Daudi B‐cell lymphomas than unstimulated monocytes. Flow cytometry revealed that M‐CSF increased monocyte expression of Fcγ receptors III and I by 1.6‐ and 1.5‐fold, whereas the expression of Fcγ receptor II remained unchanged. These results suggest that pretreatment with M‐CSF can improve the therapeutic efficacy of rituximab against intractable CD20+ lymphoma. 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Takami, Akiyoshi ; Kondo, Yukio ; Okumura, Hirokazu ; Nakao, Shinji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6014-84319af9ba87e5cf65dd2aa57b5b78cf6d56bc45f708581b9b53d742e0759e4f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adjuvants, Immunologic - physiology</topic><topic>Antibodies, Blocking - biosynthesis</topic><topic>Antibodies, Blocking - pharmacology</topic><topic>Antibodies, Monoclonal - physiology</topic><topic>Antibodies, Monoclonal - therapeutic use</topic><topic>Antibodies, Monoclonal, Murine-Derived</topic><topic>Antibody-Dependent Cell Cytotoxicity - immunology</topic><topic>Biological and medical sciences</topic><topic>Cell Line, Tumor</topic><topic>Cells, Cultured</topic><topic>Humans</topic><topic>Lymphoma - immunology</topic><topic>Lymphoma - metabolism</topic><topic>Lymphoma - pathology</topic><topic>Lymphoma - therapy</topic><topic>Macrophage Colony-Stimulating Factor - physiology</topic><topic>Medical sciences</topic><topic>Monocytes - immunology</topic><topic>Monocytes - metabolism</topic><topic>Original</topic><topic>Receptors, IgG - biosynthesis</topic><topic>Receptors, IgG - immunology</topic><topic>Rituximab</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shimadoi, Shigeru</creatorcontrib><creatorcontrib>Takami, Akiyoshi</creatorcontrib><creatorcontrib>Kondo, Yukio</creatorcontrib><creatorcontrib>Okumura, Hirokazu</creatorcontrib><creatorcontrib>Nakao, Shinji</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Shimadoi, Shigeru</au><au>Takami, Akiyoshi</au><au>Kondo, Yukio</au><au>Okumura, Hirokazu</au><au>Nakao, Shinji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Macrophage colony‐stimulating factor enhances rituximab‐dependent cellular cytotoxicity by monocytes</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2007-09</date><risdate>2007</risdate><volume>98</volume><issue>9</issue><spage>1368</spage><epage>1372</epage><pages>1368-1372</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Recent studies suggest that monocytes are the dominant effectors by which rituximab induces cell death in B‐cell lymphoma. Because macrophage colony‐stimulating factor (M‐CSF) can enhance the cytotoxicity of monocytes, the authors examined whether this growth factor can enhance their ability to kill lymphoma cells in vitro. Monocytes derived from a healthy volunteer were cultured for 48 h in the presence or absence of M‐CSF. Monocytes stimul ated with M‐CSF were significantly more cytotoxic to Daudi B‐cell lymphomas than unstimulated monocytes. Flow cytometry revealed that M‐CSF increased monocyte expression of Fcγ receptors III and I by 1.6‐ and 1.5‐fold, whereas the expression of Fcγ receptor II remained unchanged. These results suggest that pretreatment with M‐CSF can improve the therapeutic efficacy of rituximab against intractable CD20+ lymphoma. (Cancer Sci 2007; 98: 1368–1372)</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Publishing Asia</pub><pmid>17640305</pmid><doi>10.1111/j.1349-7006.2007.00544.x</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adjuvants, Immunologic - physiology Antibodies, Blocking - biosynthesis Antibodies, Blocking - pharmacology Antibodies, Monoclonal - physiology Antibodies, Monoclonal - therapeutic use Antibodies, Monoclonal, Murine-Derived Antibody-Dependent Cell Cytotoxicity - immunology Biological and medical sciences Cell Line, Tumor Cells, Cultured Humans Lymphoma - immunology Lymphoma - metabolism Lymphoma - pathology Lymphoma - therapy Macrophage Colony-Stimulating Factor - physiology Medical sciences Monocytes - immunology Monocytes - metabolism Original Receptors, IgG - biosynthesis Receptors, IgG - immunology Rituximab Tumors |
| title | Macrophage colony‐stimulating factor enhances rituximab‐dependent cellular cytotoxicity by monocytes |
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