Disrupted B‐lymphocyte development and survival in interleukin‐2‐deficient mice
Summary Interleukin‐2‐deficient (IL‐2−/−) mice develop a spontaneous, progressive, CD4+ T‐cell‐mediated colitis with an age‐related decrease in the number of B lymphocytes. The aim of this study was to determine the mechanisms of B‐cell loss in IL‐2−/− mice. Serum immunoglobulin G1 (IgG1) levels in...
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| Veröffentlicht in: | Immunology 2001-10, Vol.104 (2), p.127-134 |
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| creator | Schultz, Michael Clarke, Stephen H. Arnold, Larry W. Sartor, R. Balfour Tonkonogy, Susan L. |
| description | Summary
Interleukin‐2‐deficient (IL‐2−/−) mice develop a spontaneous, progressive, CD4+ T‐cell‐mediated colitis with an age‐related decrease in the number of B lymphocytes. The aim of this study was to determine the mechanisms of B‐cell loss in IL‐2−/− mice. Serum immunoglobulin G1 (IgG1) levels in 8‐week‐old IL‐2−/− mice were above normal but then decreased dramatically with advancing age. Between 8 and 11 weeks of age, the number of B‐cell progenitors (B220+ IgM−) in the bone marrow of IL‐2−/− mice was less than half of those in IL‐2+/+ littermates. By 22 weeks of age, very few progenitor cells remained in the bone marrow of most mice, and spleens were almost devoid of B cells. Likewise, B1 cells were not present in the peritoneal cavity of aged IL‐2−/− mice. Flow cytometry analysis of B‐cell differentiation in the bone marrow suggested a progressive loss of B cells from the most mature to the least mature stages, which was not dependent on IL‐2 receptor‐α (IL‐2Rα) expression. B cells transferred from normal animals had similar survival rates in IL‐2−/− and wild‐type mice. We conclude that conventional B cells in older IL‐2−/− mice are lost by attrition owing to a derangement in B‐cell development. Because B1 cells are less dependent on the bone marrow, a separate mechanism for their loss is suggested. |
| doi_str_mv | 10.1046/j.1365-2567.2001.01308.x |
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Interleukin‐2‐deficient (IL‐2−/−) mice develop a spontaneous, progressive, CD4+ T‐cell‐mediated colitis with an age‐related decrease in the number of B lymphocytes. The aim of this study was to determine the mechanisms of B‐cell loss in IL‐2−/− mice. Serum immunoglobulin G1 (IgG1) levels in 8‐week‐old IL‐2−/− mice were above normal but then decreased dramatically with advancing age. Between 8 and 11 weeks of age, the number of B‐cell progenitors (B220+ IgM−) in the bone marrow of IL‐2−/− mice was less than half of those in IL‐2+/+ littermates. By 22 weeks of age, very few progenitor cells remained in the bone marrow of most mice, and spleens were almost devoid of B cells. Likewise, B1 cells were not present in the peritoneal cavity of aged IL‐2−/− mice. Flow cytometry analysis of B‐cell differentiation in the bone marrow suggested a progressive loss of B cells from the most mature to the least mature stages, which was not dependent on IL‐2 receptor‐α (IL‐2Rα) expression. B cells transferred from normal animals had similar survival rates in IL‐2−/− and wild‐type mice. We conclude that conventional B cells in older IL‐2−/− mice are lost by attrition owing to a derangement in B‐cell development. Because B1 cells are less dependent on the bone marrow, a separate mechanism for their loss is suggested.</description><identifier>ISSN: 0019-2805</identifier><identifier>EISSN: 1365-2567</identifier><identifier>DOI: 10.1046/j.1365-2567.2001.01308.x</identifier><identifier>PMID: 11683951</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>AB-1 cells ; Animals ; Ascitic Fluid - immunology ; B-Lymphocytes - immunology ; B-Lymphocytes - pathology ; Bone Marrow Cells - immunology ; Cell Differentiation - immunology ; Cell Survival - immunology ; Flow Cytometry ; Hematopoietic Stem Cells - immunology ; Immunoglobulin G - biosynthesis ; Immunoglobulin G - blood ; Interleukin-2 - deficiency ; Interleukin-2 - immunology ; Mice ; Mice, Inbred C57BL ; Spleen - immunology ; T-Lymphocyte Subsets - immunology</subject><ispartof>Immunology, 2001-10, Vol.104 (2), p.127-134</ispartof><rights>Copyright Blackwell Scientific Publications Ltd. Oct 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5398-9d8548e66262b9794f12c5daafef308090c3d82fefed6ef069cb5b13b80ba6953</citedby><cites>FETCH-LOGICAL-c5398-9d8548e66262b9794f12c5daafef308090c3d82fefed6ef069cb5b13b80ba6953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1365-2567.2001.01308.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1365-2567.2001.01308.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11683951$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schultz, Michael</creatorcontrib><creatorcontrib>Clarke, Stephen H.</creatorcontrib><creatorcontrib>Arnold, Larry W.</creatorcontrib><creatorcontrib>Sartor, R. Balfour</creatorcontrib><creatorcontrib>Tonkonogy, Susan L.</creatorcontrib><title>Disrupted B‐lymphocyte development and survival in interleukin‐2‐deficient mice</title><title>Immunology</title><addtitle>Immunology</addtitle><description>Summary
Interleukin‐2‐deficient (IL‐2−/−) mice develop a spontaneous, progressive, CD4+ T‐cell‐mediated colitis with an age‐related decrease in the number of B lymphocytes. The aim of this study was to determine the mechanisms of B‐cell loss in IL‐2−/− mice. Serum immunoglobulin G1 (IgG1) levels in 8‐week‐old IL‐2−/− mice were above normal but then decreased dramatically with advancing age. Between 8 and 11 weeks of age, the number of B‐cell progenitors (B220+ IgM−) in the bone marrow of IL‐2−/− mice was less than half of those in IL‐2+/+ littermates. By 22 weeks of age, very few progenitor cells remained in the bone marrow of most mice, and spleens were almost devoid of B cells. Likewise, B1 cells were not present in the peritoneal cavity of aged IL‐2−/− mice. Flow cytometry analysis of B‐cell differentiation in the bone marrow suggested a progressive loss of B cells from the most mature to the least mature stages, which was not dependent on IL‐2 receptor‐α (IL‐2Rα) expression. B cells transferred from normal animals had similar survival rates in IL‐2−/− and wild‐type mice. We conclude that conventional B cells in older IL‐2−/− mice are lost by attrition owing to a derangement in B‐cell development. Because B1 cells are less dependent on the bone marrow, a separate mechanism for their loss is suggested.</description><subject>AB-1 cells</subject><subject>Animals</subject><subject>Ascitic Fluid - immunology</subject><subject>B-Lymphocytes - immunology</subject><subject>B-Lymphocytes - pathology</subject><subject>Bone Marrow Cells - immunology</subject><subject>Cell Differentiation - immunology</subject><subject>Cell Survival - immunology</subject><subject>Flow Cytometry</subject><subject>Hematopoietic Stem Cells - immunology</subject><subject>Immunoglobulin G - biosynthesis</subject><subject>Immunoglobulin G - blood</subject><subject>Interleukin-2 - deficiency</subject><subject>Interleukin-2 - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Spleen - immunology</subject><subject>T-Lymphocyte Subsets - immunology</subject><issn>0019-2805</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkctO3DAUhi1EVQboK1QRC3YJvsQee8GCO0ggNrC2EvtEeJobdjIwOx6BZ-RJ6jCjVmLTSrZ8rPP9Rzr6EEoIzgjOxdEiI0zwlHIxzyjGJMOEYZm9bqHZn8Y2msWOSqnEfAfthrDAE8X5d7RDiJBMcTJDj-cu-LEfwCanH2_v9arpnzqzGiCxsIS66xtoh6RobRJGv3TLok5cG88Avobxl2tjiMZroXLGTWzjDOyjb1VRB_ixeffQ4-XFw9l1ent_dXN2cpsazpRMlZU8lyAEFbRUc5VXhBpui6KCKu6DFTbMShp_YAVUWChT8pKwUuKyEIqzPXS4ntv77nmEMOjGBQN1XbTQjUHPKc1zKvJ_gkQSJiURETz4Ai660bdxCU2UyhnOpYyQXEPGdyF4qHTvXVP4lSZYT4L0Qk8e9ORBT4L0pyD9GqM_N_PHsgH7N7gxEoHjNfDialj992B9c3c3Vew3eESh1g</recordid><startdate>200110</startdate><enddate>200110</enddate><creator>Schultz, Michael</creator><creator>Clarke, Stephen H.</creator><creator>Arnold, Larry W.</creator><creator>Sartor, R. Balfour</creator><creator>Tonkonogy, Susan L.</creator><general>Blackwell Science Ltd</general><general>Wiley Subscription Services, Inc</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>7QL</scope><scope>7QR</scope><scope>7T5</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>200110</creationdate><title>Disrupted B‐lymphocyte development and survival in interleukin‐2‐deficient mice</title><author>Schultz, Michael ; Clarke, Stephen H. ; Arnold, Larry W. ; Sartor, R. Balfour ; Tonkonogy, Susan L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5398-9d8548e66262b9794f12c5daafef308090c3d82fefed6ef069cb5b13b80ba6953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>AB-1 cells</topic><topic>Animals</topic><topic>Ascitic Fluid - immunology</topic><topic>B-Lymphocytes - immunology</topic><topic>B-Lymphocytes - pathology</topic><topic>Bone Marrow Cells - immunology</topic><topic>Cell Differentiation - immunology</topic><topic>Cell Survival - immunology</topic><topic>Flow Cytometry</topic><topic>Hematopoietic Stem Cells - immunology</topic><topic>Immunoglobulin G - biosynthesis</topic><topic>Immunoglobulin G - blood</topic><topic>Interleukin-2 - deficiency</topic><topic>Interleukin-2 - immunology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Spleen - immunology</topic><topic>T-Lymphocyte Subsets - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schultz, Michael</creatorcontrib><creatorcontrib>Clarke, Stephen H.</creatorcontrib><creatorcontrib>Arnold, Larry W.</creatorcontrib><creatorcontrib>Sartor, R. Balfour</creatorcontrib><creatorcontrib>Tonkonogy, Susan L.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schultz, Michael</au><au>Clarke, Stephen H.</au><au>Arnold, Larry W.</au><au>Sartor, R. Balfour</au><au>Tonkonogy, Susan L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disrupted B‐lymphocyte development and survival in interleukin‐2‐deficient mice</atitle><jtitle>Immunology</jtitle><addtitle>Immunology</addtitle><date>2001-10</date><risdate>2001</risdate><volume>104</volume><issue>2</issue><spage>127</spage><epage>134</epage><pages>127-134</pages><issn>0019-2805</issn><eissn>1365-2567</eissn><abstract>Summary
Interleukin‐2‐deficient (IL‐2−/−) mice develop a spontaneous, progressive, CD4+ T‐cell‐mediated colitis with an age‐related decrease in the number of B lymphocytes. The aim of this study was to determine the mechanisms of B‐cell loss in IL‐2−/− mice. Serum immunoglobulin G1 (IgG1) levels in 8‐week‐old IL‐2−/− mice were above normal but then decreased dramatically with advancing age. Between 8 and 11 weeks of age, the number of B‐cell progenitors (B220+ IgM−) in the bone marrow of IL‐2−/− mice was less than half of those in IL‐2+/+ littermates. By 22 weeks of age, very few progenitor cells remained in the bone marrow of most mice, and spleens were almost devoid of B cells. Likewise, B1 cells were not present in the peritoneal cavity of aged IL‐2−/− mice. Flow cytometry analysis of B‐cell differentiation in the bone marrow suggested a progressive loss of B cells from the most mature to the least mature stages, which was not dependent on IL‐2 receptor‐α (IL‐2Rα) expression. B cells transferred from normal animals had similar survival rates in IL‐2−/− and wild‐type mice. We conclude that conventional B cells in older IL‐2−/− mice are lost by attrition owing to a derangement in B‐cell development. Because B1 cells are less dependent on the bone marrow, a separate mechanism for their loss is suggested.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>11683951</pmid><doi>10.1046/j.1365-2567.2001.01308.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | AB-1 cells Animals Ascitic Fluid - immunology B-Lymphocytes - immunology B-Lymphocytes - pathology Bone Marrow Cells - immunology Cell Differentiation - immunology Cell Survival - immunology Flow Cytometry Hematopoietic Stem Cells - immunology Immunoglobulin G - biosynthesis Immunoglobulin G - blood Interleukin-2 - deficiency Interleukin-2 - immunology Mice Mice, Inbred C57BL Spleen - immunology T-Lymphocyte Subsets - immunology |
| title | Disrupted B‐lymphocyte development and survival in interleukin‐2‐deficient mice |
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