Cutting Edge: Acute and Chronic Exposure of Immature B Cells to Antigen Leads to Impaired Homing and SHIP1-Dependent Reduction in Stromal Cell-Derived Factor-1 Responsiveness
An encounter of B cells with cognate self Ags in the periphery can lead to anergy, a condition characterized by altered anatomical localization, shortened life span, and refractility to Ag stimulation. We recently reported that an immature B cell encounter with cognate self-Ag in the bone marrow can...
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| Veröffentlicht in: | Journal of Immunology 2007-03, Vol.178 (6), p.3353-3357 |
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| creator | Brauweiler, Anne Merrell, Kevin Gauld, Stephen B Cambier, John C |
| description | An encounter of B cells with cognate self Ags in the periphery can lead to anergy, a condition characterized by altered anatomical localization, shortened life span, and refractility to Ag stimulation. We recently reported that an immature B cell encounter with cognate self-Ag in the bone marrow can also lead to anergy. In this study we show that anergic as well as acutely Ag-stimulated immature B cells are defective in stromal cell-derived factor-1 (SDF-1)-induced calcium mobilization and migration and do not localize to bone marrow following adoptive transfer. This hyporesponsiveness does not involve CXCR4 modulation. However, BCR signal-mediated hyporesponsiveness to SDF-1 is associated with phosphorylation of the 5-inositol phosphatase SHIP1 and requires SHIP1 expression. Therefore, an encounter with cognate Ag may, by preventing SDF-1-induced phosphatidylinositol 3,4,5-triphosphate accumulation, trigger premature emigration of immature B cells from bone marrow. |
| doi_str_mv | 10.4049/jimmunol.178.6.3353 |
| format | Article |
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We recently reported that an immature B cell encounter with cognate self-Ag in the bone marrow can also lead to anergy. In this study we show that anergic as well as acutely Ag-stimulated immature B cells are defective in stromal cell-derived factor-1 (SDF-1)-induced calcium mobilization and migration and do not localize to bone marrow following adoptive transfer. This hyporesponsiveness does not involve CXCR4 modulation. However, BCR signal-mediated hyporesponsiveness to SDF-1 is associated with phosphorylation of the 5-inositol phosphatase SHIP1 and requires SHIP1 expression. 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We recently reported that an immature B cell encounter with cognate self-Ag in the bone marrow can also lead to anergy. In this study we show that anergic as well as acutely Ag-stimulated immature B cells are defective in stromal cell-derived factor-1 (SDF-1)-induced calcium mobilization and migration and do not localize to bone marrow following adoptive transfer. This hyporesponsiveness does not involve CXCR4 modulation. However, BCR signal-mediated hyporesponsiveness to SDF-1 is associated with phosphorylation of the 5-inositol phosphatase SHIP1 and requires SHIP1 expression. Therefore, an encounter with cognate Ag may, by preventing SDF-1-induced phosphatidylinositol 3,4,5-triphosphate accumulation, trigger premature emigration of immature B cells from bone marrow.</description><subject>Adoptive Transfer</subject><subject>Animals</subject><subject>Antigens - immunology</subject><subject>B-Lymphocytes - immunology</subject><subject>Bone Marrow - immunology</subject><subject>Calcium Signaling - immunology</subject><subject>Cell Movement - immunology</subject><subject>Chemokine CXCL12</subject><subject>Chemokines, CXC - immunology</subject><subject>Clonal Anergy - immunology</subject><subject>Inositol Polyphosphate 5-Phosphatases</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Phosphatidylinositol Phosphates - immunology</subject><subject>Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases</subject><subject>Phosphoric Monoester Hydrolases - immunology</subject><subject>Phosphorylation</subject><subject>Protein Processing, Post-Translational - immunology</subject><subject>Receptors, Antigen, B-Cell - immunology</subject><subject>Receptors, CXCR4 - immunology</subject><issn>0022-1767</issn><issn>1550-6606</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcGO0zAURSMEYsrAFyAhr2CVYseJnbDrhA6tVAnEwNpynZfWo9gOtkPhp_hGnGkR7Fj56encI-vdLHtJ8LLEZfP2XhszWTcsCa-XbElpRR9lC1JVOGcMs8fZAuOiyAln_Cp7FsI9xpjhonyaXRFOaVMWfJH9aqcYtT2gdXeAd2ilpghI2g61R--sVmj9Y3Rh8oBcj7bGyDjPN6iFYQgoOrSyUR_Aoh3I7mGxNaPUHjq0cWYWz7K7zfYTyd_DCLYDG9Fn6CYVtbNIW3QXvTNyeFAmxuvvKXwrVXQ-JwkNo7MhLS2E8Dx70sshwIvLe519vV1_aTf57uOHbbva5arkPOaSdbhRhO47XDJWVw1jIIE2BFilOCuB1zXHilX7putLSXi1p_W-JljRnvWNotfZ67N39O7bBCEKo4NKH5QW3BQExwWtcMH_C5KG4brATQLpGVTeheChF6PXRvqfgmAx9yn-9ClSn4KJuc-UenXRT3sD3d_MpcAEvDkDR304ntLdRUi3HBJOxOl0-kf1G546rIo</recordid><startdate>20070315</startdate><enddate>20070315</enddate><creator>Brauweiler, Anne</creator><creator>Merrell, Kevin</creator><creator>Gauld, Stephen B</creator><creator>Cambier, John C</creator><general>Am Assoc Immnol</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20070315</creationdate><title>Cutting Edge: Acute and Chronic Exposure of Immature B Cells to Antigen Leads to Impaired Homing and SHIP1-Dependent Reduction in Stromal Cell-Derived Factor-1 Responsiveness</title><author>Brauweiler, Anne ; Merrell, Kevin ; Gauld, Stephen B ; Cambier, John C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c477t-a6d09c13bd046685966eae391e65c764e78870c65b9df4a175b38b810c3f6f9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adoptive Transfer</topic><topic>Animals</topic><topic>Antigens - immunology</topic><topic>B-Lymphocytes - immunology</topic><topic>Bone Marrow - immunology</topic><topic>Calcium Signaling - immunology</topic><topic>Cell Movement - immunology</topic><topic>Chemokine CXCL12</topic><topic>Chemokines, CXC - immunology</topic><topic>Clonal Anergy - immunology</topic><topic>Inositol Polyphosphate 5-Phosphatases</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Phosphatidylinositol Phosphates - immunology</topic><topic>Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases</topic><topic>Phosphoric Monoester Hydrolases - immunology</topic><topic>Phosphorylation</topic><topic>Protein Processing, Post-Translational - immunology</topic><topic>Receptors, Antigen, B-Cell - immunology</topic><topic>Receptors, CXCR4 - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brauweiler, Anne</creatorcontrib><creatorcontrib>Merrell, Kevin</creatorcontrib><creatorcontrib>Gauld, Stephen B</creatorcontrib><creatorcontrib>Cambier, John C</creatorcontrib><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><jtitle>Journal of Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brauweiler, Anne</au><au>Merrell, Kevin</au><au>Gauld, Stephen B</au><au>Cambier, John C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cutting Edge: Acute and Chronic Exposure of Immature B Cells to Antigen Leads to Impaired Homing and SHIP1-Dependent Reduction in Stromal Cell-Derived Factor-1 Responsiveness</atitle><jtitle>Journal of Immunology</jtitle><addtitle>J Immunol</addtitle><date>2007-03-15</date><risdate>2007</risdate><volume>178</volume><issue>6</issue><spage>3353</spage><epage>3357</epage><pages>3353-3357</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><eissn>1365-2567</eissn><abstract>An encounter of B cells with cognate self Ags in the periphery can lead to anergy, a condition characterized by altered anatomical localization, shortened life span, and refractility to Ag stimulation. We recently reported that an immature B cell encounter with cognate self-Ag in the bone marrow can also lead to anergy. In this study we show that anergic as well as acutely Ag-stimulated immature B cells are defective in stromal cell-derived factor-1 (SDF-1)-induced calcium mobilization and migration and do not localize to bone marrow following adoptive transfer. This hyporesponsiveness does not involve CXCR4 modulation. However, BCR signal-mediated hyporesponsiveness to SDF-1 is associated with phosphorylation of the 5-inositol phosphatase SHIP1 and requires SHIP1 expression. Therefore, an encounter with cognate Ag may, by preventing SDF-1-induced phosphatidylinositol 3,4,5-triphosphate accumulation, trigger premature emigration of immature B cells from bone marrow.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>17339427</pmid><doi>10.4049/jimmunol.178.6.3353</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adoptive Transfer Animals Antigens - immunology B-Lymphocytes - immunology Bone Marrow - immunology Calcium Signaling - immunology Cell Movement - immunology Chemokine CXCL12 Chemokines, CXC - immunology Clonal Anergy - immunology Inositol Polyphosphate 5-Phosphatases Mice Mice, Transgenic Phosphatidylinositol Phosphates - immunology Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases Phosphoric Monoester Hydrolases - immunology Phosphorylation Protein Processing, Post-Translational - immunology Receptors, Antigen, B-Cell - immunology Receptors, CXCR4 - immunology |
| title | Cutting Edge: Acute and Chronic Exposure of Immature B Cells to Antigen Leads to Impaired Homing and SHIP1-Dependent Reduction in Stromal Cell-Derived Factor-1 Responsiveness |
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