Tracking the response of Xid B cells in vivo: TI‐2 antigen induces migration and proliferation but Btk is essential for terminal differentiation
X‐linked immunodeficient (Xid) mice carry a Bruton′s tyrosine kinase (Btk) mutation and exhibit a selective failure to produce antibodies against bacterial capsular polysaccharides. Studies in vitro point to a fundamental survival defect of Xid B cells after receptor cross‐linking by thymus‐independ...
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| Veröffentlicht in: | European journal of immunology 2001-05, Vol.31 (5), p.1340-1350 |
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| container_title | European journal of immunology |
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| creator | Vinuesa, Carola G. Sunners, Yvonne Pongracz, Judit Ball, Jennifer Toellner, Kai‐Michael Taylor, Dale MacLennan, Ian C.M. Cook, Matthew C. |
| description | X‐linked immunodeficient (Xid) mice carry a Bruton′s tyrosine kinase (Btk) mutation and exhibit a selective failure to produce antibodies against bacterial capsular polysaccharides. Studies in vitro point to a fundamental survival defect of Xid B cells after receptor cross‐linking by thymus‐independent type‐2 (TI‐2) antigen because B cells undergo apoptosis without proliferating. We describe results from a novel model, which we have used to investigate the impact of the Xid mutation on migration, proliferation and differentiation of B cells after polysaccharide immunization in vivo. Immunoglobulin knock‐in mice, in which a large proportion of B cells express transgene‐encoded receptors specific for (4‐hydroxy‐3‐nitrophenyl)‐acetyl (NP), were crossed with CBA/N mice. The male progeny contain NP‐specific Xid B cells, while the female progeny contain NP‐specific B cells with normal Btk. After immunization with the TI‐2 antigen NP‐Ficoll, NP‐specific Xid B cells migrate to the T zones and proliferate. Despite transient up‐regulation of blimp‐1 and survival beyond the time when terminal differentiation is normally underway, Btk‐defective B cells fail to differentiate to plasmablasts or germinal center cells. CD40 ligation partially restores their ability to form plasma cells in response to TI‐2 antigen. |
| doi_str_mv | 10.1002/1521-4141(200105)31:5<1340::AID-IMMU1340>3.0.CO;2-H |
| format | Article |
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Studies in vitro point to a fundamental survival defect of Xid B cells after receptor cross‐linking by thymus‐independent type‐2 (TI‐2) antigen because B cells undergo apoptosis without proliferating. We describe results from a novel model, which we have used to investigate the impact of the Xid mutation on migration, proliferation and differentiation of B cells after polysaccharide immunization in vivo. Immunoglobulin knock‐in mice, in which a large proportion of B cells express transgene‐encoded receptors specific for (4‐hydroxy‐3‐nitrophenyl)‐acetyl (NP), were crossed with CBA/N mice. The male progeny contain NP‐specific Xid B cells, while the female progeny contain NP‐specific B cells with normal Btk. After immunization with the TI‐2 antigen NP‐Ficoll, NP‐specific Xid B cells migrate to the T zones and proliferate. Despite transient up‐regulation of blimp‐1 and survival beyond the time when terminal differentiation is normally underway, Btk‐defective B cells fail to differentiate to plasmablasts or germinal center cells. CD40 ligation partially restores their ability to form plasma cells in response to TI‐2 antigen.</description><identifier>ISSN: 0014-2980</identifier><identifier>EISSN: 1521-4141</identifier><identifier>DOI: 10.1002/1521-4141(200105)31:5<1340::AID-IMMU1340>3.0.CO;2-H</identifier><identifier>PMID: 11465091</identifier><language>eng</language><publisher>Weinheim: WILEY‐VCH Verlag GmbH</publisher><subject>(4-hydroxy-3-nitrophenyl)acetyl ; Animals ; Antibodies - immunology ; Antibody formation ; Antigens, T-Independent - immunology ; Apoptosis ; B-Lymphocytes - cytology ; B-Lymphocytes - enzymology ; B-Lymphocytes - immunology ; B-Lymphocytes - metabolism ; Bruton′s tyrosine kinase ; Btk protein ; CD40 Antigen ; CD40 Antigens - immunology ; CD40 Antigens - metabolism ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Chemotaxis, Leukocyte ; Female ; Ficoll ; Gene Deletion ; Genetic Linkage - genetics ; Immunologic Deficiency Syndromes - enzymology ; Immunologic Deficiency Syndromes - genetics ; Immunologic Deficiency Syndromes - immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Transgenic ; Nitrophenols - immunology ; Phenotype ; Positive Regulatory Domain I-Binding Factor 1 ; Protein-Tyrosine Kinases - genetics ; Protein-Tyrosine Kinases - metabolism ; Repressor Proteins ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Thymus‐independent antigen ; TI-2 antigen ; Transcription Factors - metabolism ; Up-Regulation ; X Chromosome - genetics</subject><ispartof>European journal of immunology, 2001-05, Vol.31 (5), p.1340-1350</ispartof><rights>WILEY‐VCH Verlag GmbH, Weinheim, Fed. 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Studies in vitro point to a fundamental survival defect of Xid B cells after receptor cross‐linking by thymus‐independent type‐2 (TI‐2) antigen because B cells undergo apoptosis without proliferating. We describe results from a novel model, which we have used to investigate the impact of the Xid mutation on migration, proliferation and differentiation of B cells after polysaccharide immunization in vivo. Immunoglobulin knock‐in mice, in which a large proportion of B cells express transgene‐encoded receptors specific for (4‐hydroxy‐3‐nitrophenyl)‐acetyl (NP), were crossed with CBA/N mice. The male progeny contain NP‐specific Xid B cells, while the female progeny contain NP‐specific B cells with normal Btk. After immunization with the TI‐2 antigen NP‐Ficoll, NP‐specific Xid B cells migrate to the T zones and proliferate. Despite transient up‐regulation of blimp‐1 and survival beyond the time when terminal differentiation is normally underway, Btk‐defective B cells fail to differentiate to plasmablasts or germinal center cells. CD40 ligation partially restores their ability to form plasma cells in response to TI‐2 antigen.</description><subject>(4-hydroxy-3-nitrophenyl)acetyl</subject><subject>Animals</subject><subject>Antibodies - immunology</subject><subject>Antibody formation</subject><subject>Antigens, T-Independent - immunology</subject><subject>Apoptosis</subject><subject>B-Lymphocytes - cytology</subject><subject>B-Lymphocytes - enzymology</subject><subject>B-Lymphocytes - immunology</subject><subject>B-Lymphocytes - metabolism</subject><subject>Bruton′s tyrosine kinase</subject><subject>Btk protein</subject><subject>CD40 Antigen</subject><subject>CD40 Antigens - immunology</subject><subject>CD40 Antigens - metabolism</subject><subject>Cell Differentiation</subject><subject>Cell Division</subject><subject>Cells, Cultured</subject><subject>Chemotaxis, Leukocyte</subject><subject>Female</subject><subject>Ficoll</subject><subject>Gene Deletion</subject><subject>Genetic Linkage - genetics</subject><subject>Immunologic Deficiency Syndromes - enzymology</subject><subject>Immunologic Deficiency Syndromes - genetics</subject><subject>Immunologic Deficiency Syndromes - immunology</subject><subject>Lymphocyte Activation</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Nitrophenols - immunology</subject><subject>Phenotype</subject><subject>Positive Regulatory Domain I-Binding Factor 1</subject><subject>Protein-Tyrosine Kinases - genetics</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Repressor Proteins</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Thymus‐independent antigen</subject><subject>TI-2 antigen</subject><subject>Transcription Factors - metabolism</subject><subject>Up-Regulation</subject><subject>X Chromosome - genetics</subject><issn>0014-2980</issn><issn>1521-4141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkc9uEzEQxi0EoqHwCsgnBIcNY3u9f1KE1IY_idQqB1KpN8vrHQfTzW6wd4t64xEQj8iT4CWhnBDiZM3M983n0Y-QEwZTBsBfMslZkrKUPecADOQLwWbyFRMpzGanyzfJ8uLicqxeiylM56sTnizukcmd6z6ZRFua8LKAI_IohE8AUGayfEiOGEszCSWbkO9rr821aze0_4jUY9h1bUDaWXrlanpGDTZNoK6lN-6mm9H18sfXb5zqtncbbGO_HgwGunUbr3vXtXFS053vGmfx0KmGnp7119QFiiFgdOqG2s7THv3WtbGonY3qX5PR8Zg8sLoJ-OTwHpPLd2_X80Vyvnq_nJ-eJ0bkGSRpakVVAzPSyDIvc13WtbTxrNQYmQsOurBYIBjQJdRCFFlVMIG5zWUFJRbimDzb743__Txg6NXWhfFe3WI3BJUz4Dxj8E8hKyDPoRBR-GEvNL4LwaNVO--22t8qBmpkqkY6aqSj9kyVYEqqkaJSkan6zVQJBWq-Ulwt4tanh_ih2mL9Z-cBYhRc7QVfXIO3_5P5l8i7nvgJp2m9OA</recordid><startdate>200105</startdate><enddate>200105</enddate><creator>Vinuesa, Carola G.</creator><creator>Sunners, Yvonne</creator><creator>Pongracz, Judit</creator><creator>Ball, Jennifer</creator><creator>Toellner, Kai‐Michael</creator><creator>Taylor, Dale</creator><creator>MacLennan, Ian C.M.</creator><creator>Cook, Matthew C.</creator><general>WILEY‐VCH Verlag GmbH</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>200105</creationdate><title>Tracking the response of Xid B cells in vivo: TI‐2 antigen induces migration and proliferation but Btk is essential for terminal differentiation</title><author>Vinuesa, Carola G. ; Sunners, Yvonne ; Pongracz, Judit ; Ball, Jennifer ; Toellner, Kai‐Michael ; Taylor, Dale ; MacLennan, Ian C.M. ; Cook, Matthew C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3760-44f3bd01c5c59797a9dd5f6504cc57320a8fe8e0c0a90d3386b813e7f75b09e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>(4-hydroxy-3-nitrophenyl)acetyl</topic><topic>Animals</topic><topic>Antibodies - immunology</topic><topic>Antibody formation</topic><topic>Antigens, T-Independent - immunology</topic><topic>Apoptosis</topic><topic>B-Lymphocytes - cytology</topic><topic>B-Lymphocytes - enzymology</topic><topic>B-Lymphocytes - immunology</topic><topic>B-Lymphocytes - metabolism</topic><topic>Bruton′s tyrosine kinase</topic><topic>Btk protein</topic><topic>CD40 Antigen</topic><topic>CD40 Antigens - immunology</topic><topic>CD40 Antigens - metabolism</topic><topic>Cell Differentiation</topic><topic>Cell Division</topic><topic>Cells, Cultured</topic><topic>Chemotaxis, Leukocyte</topic><topic>Female</topic><topic>Ficoll</topic><topic>Gene Deletion</topic><topic>Genetic Linkage - genetics</topic><topic>Immunologic Deficiency Syndromes - enzymology</topic><topic>Immunologic Deficiency Syndromes - genetics</topic><topic>Immunologic Deficiency Syndromes - immunology</topic><topic>Lymphocyte Activation</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Nitrophenols - immunology</topic><topic>Phenotype</topic><topic>Positive Regulatory Domain I-Binding Factor 1</topic><topic>Protein-Tyrosine Kinases - genetics</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Repressor Proteins</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Thymus‐independent antigen</topic><topic>TI-2 antigen</topic><topic>Transcription Factors - metabolism</topic><topic>Up-Regulation</topic><topic>X Chromosome - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vinuesa, Carola G.</creatorcontrib><creatorcontrib>Sunners, Yvonne</creatorcontrib><creatorcontrib>Pongracz, Judit</creatorcontrib><creatorcontrib>Ball, Jennifer</creatorcontrib><creatorcontrib>Toellner, Kai‐Michael</creatorcontrib><creatorcontrib>Taylor, Dale</creatorcontrib><creatorcontrib>MacLennan, Ian C.M.</creatorcontrib><creatorcontrib>Cook, Matthew 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>European journal of immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vinuesa, Carola G.</au><au>Sunners, Yvonne</au><au>Pongracz, Judit</au><au>Ball, Jennifer</au><au>Toellner, Kai‐Michael</au><au>Taylor, Dale</au><au>MacLennan, Ian C.M.</au><au>Cook, Matthew C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tracking the response of Xid B cells in vivo: TI‐2 antigen induces migration and proliferation but Btk is essential for terminal differentiation</atitle><jtitle>European journal of immunology</jtitle><addtitle>Eur J Immunol</addtitle><date>2001-05</date><risdate>2001</risdate><volume>31</volume><issue>5</issue><spage>1340</spage><epage>1350</epage><pages>1340-1350</pages><issn>0014-2980</issn><eissn>1521-4141</eissn><abstract>X‐linked immunodeficient (Xid) mice carry a Bruton′s tyrosine kinase (Btk) mutation and exhibit a selective failure to produce antibodies against bacterial capsular polysaccharides. Studies in vitro point to a fundamental survival defect of Xid B cells after receptor cross‐linking by thymus‐independent type‐2 (TI‐2) antigen because B cells undergo apoptosis without proliferating. We describe results from a novel model, which we have used to investigate the impact of the Xid mutation on migration, proliferation and differentiation of B cells after polysaccharide immunization in vivo. Immunoglobulin knock‐in mice, in which a large proportion of B cells express transgene‐encoded receptors specific for (4‐hydroxy‐3‐nitrophenyl)‐acetyl (NP), were crossed with CBA/N mice. The male progeny contain NP‐specific Xid B cells, while the female progeny contain NP‐specific B cells with normal Btk. After immunization with the TI‐2 antigen NP‐Ficoll, NP‐specific Xid B cells migrate to the T zones and proliferate. Despite transient up‐regulation of blimp‐1 and survival beyond the time when terminal differentiation is normally underway, Btk‐defective B cells fail to differentiate to plasmablasts or germinal center cells. CD40 ligation partially restores their ability to form plasma cells in response to TI‐2 antigen.</abstract><cop>Weinheim</cop><pub>WILEY‐VCH Verlag GmbH</pub><pmid>11465091</pmid><doi>10.1002/1521-4141(200105)31:5<1340::AID-IMMU1340>3.0.CO;2-H</doi><tpages>11</tpages></addata></record> |
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| ispartof | European journal of immunology, 2001-05, Vol.31 (5), p.1340-1350 |
| issn | 0014-2980 1521-4141 |
| language | eng |
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| source | Wiley Free Content; MEDLINE; Wiley Online Library Journals Frontfile Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | (4-hydroxy-3-nitrophenyl)acetyl Animals Antibodies - immunology Antibody formation Antigens, T-Independent - immunology Apoptosis B-Lymphocytes - cytology B-Lymphocytes - enzymology B-Lymphocytes - immunology B-Lymphocytes - metabolism Bruton′s tyrosine kinase Btk protein CD40 Antigen CD40 Antigens - immunology CD40 Antigens - metabolism Cell Differentiation Cell Division Cells, Cultured Chemotaxis, Leukocyte Female Ficoll Gene Deletion Genetic Linkage - genetics Immunologic Deficiency Syndromes - enzymology Immunologic Deficiency Syndromes - genetics Immunologic Deficiency Syndromes - immunology Lymphocyte Activation Male Mice Mice, Transgenic Nitrophenols - immunology Phenotype Positive Regulatory Domain I-Binding Factor 1 Protein-Tyrosine Kinases - genetics Protein-Tyrosine Kinases - metabolism Repressor Proteins RNA, Messenger - genetics RNA, Messenger - metabolism Thymus‐independent antigen TI-2 antigen Transcription Factors - metabolism Up-Regulation X Chromosome - genetics |
| title | Tracking the response of Xid B cells in vivo: TI‐2 antigen induces migration and proliferation but Btk is essential for terminal differentiation |
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