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Severe B Cell Hyperplasia and Autoimmune Disease in TALL-1 Transgenic Mice
TALL-1/Blys/BAFF is a member of the tumor necrosis factor (TNF) ligand superfamily that is functionally involved in B cell proliferation. Here, we describe B cell hyperplasia and autoimmune lupus-like changes in transgenic mice expressing TALL-1 under the control of a β -actin promoter. The TALL-1 t...
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| Published in: | Proceedings of the National Academy of Sciences - PNAS 2000-03, Vol.97 (7), p.3370-3375 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Khare, Sanjay D. Sarosi, Ildiko Xia, Xing-Zhong McCabe, Susan Miner, Kent Solovyev, Irina Hawkins, Nessa Kelley, Michael Chang, David Van, Gwyneth Ross, Larry Delaney, John Wang, Ling Lacey, David Boyle, William J. Hsu, Hailing |
| description | TALL-1/Blys/BAFF is a member of the tumor necrosis factor (TNF) ligand superfamily that is functionally involved in B cell proliferation. Here, we describe B cell hyperplasia and autoimmune lupus-like changes in transgenic mice expressing TALL-1 under the control of a β -actin promoter. The TALL-1 transgenic mice showed severe enlargement of spleen, lymph nodes, and Peyer's patches because of an increased number of B220+ cells. The transgenic mice also had hypergammaglobulinemia contributed by elevations of serum IgM, IgG, IgA, and IgE. In addition, a phenotype similar to autoimmune lupus-like disease was also seen in TALL-1 transgenic mice, characterized by the presence of autoantibodies to nuclear antigens and immune complex deposits in the kidney. Prolonged survival and hyperactivity of transgenic B cells may contribute to the autoimmune lupus-like phenotype in these animals. Our studies further confirm TALL-1 as a stimulator of B cells that affect Ig production. Thus, TALL-1 may be a primary mediator in B cell-associated autoimmune diseases. |
| doi_str_mv | 10.1073/pnas.97.7.3370 |
| format | article |
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Here, we describe B cell hyperplasia and autoimmune lupus-like changes in transgenic mice expressing TALL-1 under the control of a β -actin promoter. The TALL-1 transgenic mice showed severe enlargement of spleen, lymph nodes, and Peyer's patches because of an increased number of B220+ cells. The transgenic mice also had hypergammaglobulinemia contributed by elevations of serum IgM, IgG, IgA, and IgE. In addition, a phenotype similar to autoimmune lupus-like disease was also seen in TALL-1 transgenic mice, characterized by the presence of autoantibodies to nuclear antigens and immune complex deposits in the kidney. Prolonged survival and hyperactivity of transgenic B cells may contribute to the autoimmune lupus-like phenotype in these animals. Our studies further confirm TALL-1 as a stimulator of B cells that affect Ig production. Thus, TALL-1 may be a primary mediator in B cell-associated autoimmune diseases.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.97.7.3370</identifier><identifier>PMID: 10716715</identifier><language>eng</language><publisher>United States: National Academy of Sciences of the United States of America</publisher><subject>Animals ; Antibodies ; Antigen-Antibody Complex - analysis ; Autoantibodies ; Autoantibodies - immunology ; Autoimmune diseases ; Autoimmune Diseases - immunology ; Autoimmune Diseases - pathology ; B lymphocytes ; B-Cell Activating Factor ; B-Lymphocytes - immunology ; B-Lymphocytes - pathology ; Base Sequence ; Biological Sciences ; Cytokines ; Disease ; DNA Primers ; Genetics ; Hypergammaglobulinemia - immunology ; Immunology ; Kidney - immunology ; Lupus ; Membrane Proteins - genetics ; Mice ; Mice, Transgenic ; Receptors ; Rodents ; Spleen ; T lymphocytes ; Transgenic animals ; Tumor Necrosis Factor-alpha - genetics</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2000-03, Vol.97 (7), p.3370-3375</ispartof><rights>Copyright 1993-2000 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Mar 28, 2000</rights><rights>Copyright © The National Academy of Sciences 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4670-44b39f24186b085cfdb1b99e1a3e4d06e47cffc2685b62040e0ea6befa2c7ba03</citedby><cites>FETCH-LOGICAL-c4670-44b39f24186b085cfdb1b99e1a3e4d06e47cffc2685b62040e0ea6befa2c7ba03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/97/7.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/121899$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/121899$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793,58238,58471</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10716715$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Khare, Sanjay D.</creatorcontrib><creatorcontrib>Sarosi, Ildiko</creatorcontrib><creatorcontrib>Xia, Xing-Zhong</creatorcontrib><creatorcontrib>McCabe, Susan</creatorcontrib><creatorcontrib>Miner, Kent</creatorcontrib><creatorcontrib>Solovyev, Irina</creatorcontrib><creatorcontrib>Hawkins, Nessa</creatorcontrib><creatorcontrib>Kelley, Michael</creatorcontrib><creatorcontrib>Chang, David</creatorcontrib><creatorcontrib>Van, Gwyneth</creatorcontrib><creatorcontrib>Ross, Larry</creatorcontrib><creatorcontrib>Delaney, John</creatorcontrib><creatorcontrib>Wang, Ling</creatorcontrib><creatorcontrib>Lacey, David</creatorcontrib><creatorcontrib>Boyle, William J.</creatorcontrib><creatorcontrib>Hsu, Hailing</creatorcontrib><title>Severe B Cell Hyperplasia and Autoimmune Disease in TALL-1 Transgenic Mice</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>TALL-1/Blys/BAFF is a member of the tumor necrosis factor (TNF) ligand superfamily that is functionally involved in B cell proliferation. Here, we describe B cell hyperplasia and autoimmune lupus-like changes in transgenic mice expressing TALL-1 under the control of a β -actin promoter. The TALL-1 transgenic mice showed severe enlargement of spleen, lymph nodes, and Peyer's patches because of an increased number of B220+ cells. The transgenic mice also had hypergammaglobulinemia contributed by elevations of serum IgM, IgG, IgA, and IgE. In addition, a phenotype similar to autoimmune lupus-like disease was also seen in TALL-1 transgenic mice, characterized by the presence of autoantibodies to nuclear antigens and immune complex deposits in the kidney. Prolonged survival and hyperactivity of transgenic B cells may contribute to the autoimmune lupus-like phenotype in these animals. Our studies further confirm TALL-1 as a stimulator of B cells that affect Ig production. Thus, TALL-1 may be a primary mediator in B cell-associated autoimmune diseases.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Antigen-Antibody Complex - analysis</subject><subject>Autoantibodies</subject><subject>Autoantibodies - immunology</subject><subject>Autoimmune diseases</subject><subject>Autoimmune Diseases - immunology</subject><subject>Autoimmune Diseases - pathology</subject><subject>B lymphocytes</subject><subject>B-Cell Activating Factor</subject><subject>B-Lymphocytes - immunology</subject><subject>B-Lymphocytes - pathology</subject><subject>Base Sequence</subject><subject>Biological Sciences</subject><subject>Cytokines</subject><subject>Disease</subject><subject>DNA Primers</subject><subject>Genetics</subject><subject>Hypergammaglobulinemia - immunology</subject><subject>Immunology</subject><subject>Kidney - immunology</subject><subject>Lupus</subject><subject>Membrane Proteins - genetics</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Receptors</subject><subject>Rodents</subject><subject>Spleen</subject><subject>T lymphocytes</subject><subject>Transgenic animals</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNp9kUGP0zAQhS0EYrsLVy4IZHHYW8I4ce1Y4lK6wIKKOFDOluNOFleJk7WTFfvvcdQChQMnH973nmfmEfKMQc5Alq8Hb2KuZC7zspTwgCwYKJYJruAhWQAUMqt4wc_IeYx7AFDLCh6Ts2RlQrLlgnz6incYkL6la2xben0_YBhaE52hxu_oahp713WTR3rlIpqI1Hm6XW02GaPbYHy8Qe8s_ewsPiGPGtNGfHp8L8i39--26-ts8-XDx_Vqk1kuJGSc16VqCs4qUUO1tM2uZrVSyEyJfAcCubRNYwtRLWtRAAcENKLGxhRW1gbKC_LmkDtMdYc7i34MptVDcJ0J97o3Tv-tePdd3_R3momCi2S_PNpDfzthHHXnok3LG4_9FLVk6WwlZwl89Q-476fg02q6AFamMDkPkx8gG_oYAza_52Cg54b03JBWUks9N5QML0-nP8EPlSTgxRGYjb_k04DL_-m6mdp2xB9jAp8fwH0c-_Dno4JVSpU_AadyrL4</recordid><startdate>20000328</startdate><enddate>20000328</enddate><creator>Khare, Sanjay D.</creator><creator>Sarosi, Ildiko</creator><creator>Xia, Xing-Zhong</creator><creator>McCabe, Susan</creator><creator>Miner, Kent</creator><creator>Solovyev, Irina</creator><creator>Hawkins, Nessa</creator><creator>Kelley, Michael</creator><creator>Chang, David</creator><creator>Van, Gwyneth</creator><creator>Ross, Larry</creator><creator>Delaney, John</creator><creator>Wang, Ling</creator><creator>Lacey, David</creator><creator>Boyle, William J.</creator><creator>Hsu, Hailing</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</general><general>National Academy of Sciences</general><general>The National Academy of Sciences</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20000328</creationdate><title>Severe B Cell Hyperplasia and Autoimmune Disease in TALL-1 Transgenic Mice</title><author>Khare, Sanjay D. ; 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Here, we describe B cell hyperplasia and autoimmune lupus-like changes in transgenic mice expressing TALL-1 under the control of a β -actin promoter. The TALL-1 transgenic mice showed severe enlargement of spleen, lymph nodes, and Peyer's patches because of an increased number of B220+ cells. The transgenic mice also had hypergammaglobulinemia contributed by elevations of serum IgM, IgG, IgA, and IgE. In addition, a phenotype similar to autoimmune lupus-like disease was also seen in TALL-1 transgenic mice, characterized by the presence of autoantibodies to nuclear antigens and immune complex deposits in the kidney. Prolonged survival and hyperactivity of transgenic B cells may contribute to the autoimmune lupus-like phenotype in these animals. Our studies further confirm TALL-1 as a stimulator of B cells that affect Ig production. Thus, TALL-1 may be a primary mediator in B cell-associated autoimmune diseases.</abstract><cop>United States</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>10716715</pmid><doi>10.1073/pnas.97.7.3370</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Proceedings of the National Academy of Sciences - PNAS, 2000-03, Vol.97 (7), p.3370-3375 |
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| source | Open Access: PubMed Central; JSTOR Archival Journals and Primary Sources Collection |
| subjects | Animals Antibodies Antigen-Antibody Complex - analysis Autoantibodies Autoantibodies - immunology Autoimmune diseases Autoimmune Diseases - immunology Autoimmune Diseases - pathology B lymphocytes B-Cell Activating Factor B-Lymphocytes - immunology B-Lymphocytes - pathology Base Sequence Biological Sciences Cytokines Disease DNA Primers Genetics Hypergammaglobulinemia - immunology Immunology Kidney - immunology Lupus Membrane Proteins - genetics Mice Mice, Transgenic Receptors Rodents Spleen T lymphocytes Transgenic animals Tumor Necrosis Factor-alpha - genetics |
| title | Severe B Cell Hyperplasia and Autoimmune Disease in TALL-1 Transgenic Mice |
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