A Tlr7 Translocation Accelerates Systemic Autoimmunity in Murine Lupus
The y-linked autoimmune accelerating (yaa) locus is a potent autoimmune disease allele. Transcription profiling of yaa-bearing B cells revealed the overexpression of a cluster of X-linked genes that included T/r7. FISH analysis demonstrated the translocation of this segment onto the yaa chromosome....
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2006-06, Vol.103 (26), p.9970-9975 |
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| creator | Subramanian, Srividya Tus, Katalin Li, Quan-Zhen Wang, Andrew Tian, Xiang-Hong Zhou, Jinchun Liang, Chaoying Bartov, Guy McDaniel, Lisa D. Zhou, Xin J. Schultz, Roger A. Wakeland, Edward K. |
| description | The y-linked autoimmune accelerating (yaa) locus is a potent autoimmune disease allele. Transcription profiling of yaa-bearing B cells revealed the overexpression of a cluster of X-linked genes that included T/r7. FISH analysis demonstrated the translocation of this segment onto the yaa chromosome. The resulting overexpression of T/r7 increased in vitro responses to Toll-like receptor (TLR) 7 signaling in all yaa-bearing males. B6.yaa mice are not overtly autoimmune, but the addition of Slel, which contains the autoimmune-predisposing Slam/Cd2 haplotype, causes the development of fatal lupus with numerous immunological aberrations. B6.Slelyaa CD4 T cells develop the molecular signature for TFH cells and also show expression changes in numerous cytokines and chemokines. Disease development and all component autoimmune phenotypes were inhibited by Sles1, a potent suppressor locus. Slesl had no effect on yaa-enhanced TLR7 signaling in vitro, and these data place Sles1 downstream from the lesion in innate immune responses mediated by TLR7, suggesting that Sles1 modulates the activation of adaptive immunity in response to innate immune signaling. |
| doi_str_mv | 10.1073/pnas.0603912103 |
| format | Article |
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Transcription profiling of yaa-bearing B cells revealed the overexpression of a cluster of X-linked genes that included T/r7. FISH analysis demonstrated the translocation of this segment onto the yaa chromosome. The resulting overexpression of T/r7 increased in vitro responses to Toll-like receptor (TLR) 7 signaling in all yaa-bearing males. B6.yaa mice are not overtly autoimmune, but the addition of Slel, which contains the autoimmune-predisposing Slam/Cd2 haplotype, causes the development of fatal lupus with numerous immunological aberrations. B6.Slelyaa CD4 T cells develop the molecular signature for TFH cells and also show expression changes in numerous cytokines and chemokines. Disease development and all component autoimmune phenotypes were inhibited by Sles1, a potent suppressor locus. Slesl had no effect on yaa-enhanced TLR7 signaling in vitro, and these data place Sles1 downstream from the lesion in innate immune responses mediated by TLR7, suggesting that Sles1 modulates the activation of adaptive immunity in response to innate immune signaling.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0603912103</identifier><identifier>PMID: 16777955</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Animals ; Autoimmune diseases ; Autoimmunity ; Autoimmunity - genetics ; B lymphocytes ; B-Lymphocytes - immunology ; Biological Sciences ; CD4-Positive T-Lymphocytes - immunology ; Chromosomes ; Gene Expression Profiling ; Gene loci ; Genes ; Genetic loci ; Genetics ; Immune system ; Immunity, Innate - genetics ; Lupus ; Lupus Erythematosus, Systemic - genetics ; Male ; Medical genetics ; Mice ; Mice, Mutant Strains ; Phenotypes ; T lymphocytes ; Toll-Like Receptor 7 - genetics ; Transcriptional Activation ; Translocation, Genetic</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2006-06, Vol.103 (26), p.9970-9975</ispartof><rights>Copyright 2006 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Jun 27, 2006</rights><rights>2006 by The National Academy of Sciences of the USA 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-75dc07c06525d4d0af866671b5e6cc60a7b9ebd02277f7b8c3be480bbf1336003</citedby><cites>FETCH-LOGICAL-c487t-75dc07c06525d4d0af866671b5e6cc60a7b9ebd02277f7b8c3be480bbf1336003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/103/26.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/30051025$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/30051025$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16777955$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Subramanian, Srividya</creatorcontrib><creatorcontrib>Tus, Katalin</creatorcontrib><creatorcontrib>Li, Quan-Zhen</creatorcontrib><creatorcontrib>Wang, Andrew</creatorcontrib><creatorcontrib>Tian, Xiang-Hong</creatorcontrib><creatorcontrib>Zhou, Jinchun</creatorcontrib><creatorcontrib>Liang, Chaoying</creatorcontrib><creatorcontrib>Bartov, Guy</creatorcontrib><creatorcontrib>McDaniel, Lisa D.</creatorcontrib><creatorcontrib>Zhou, Xin J.</creatorcontrib><creatorcontrib>Schultz, Roger A.</creatorcontrib><creatorcontrib>Wakeland, Edward K.</creatorcontrib><title>A Tlr7 Translocation Accelerates Systemic Autoimmunity in Murine Lupus</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>The y-linked autoimmune accelerating (yaa) locus is a potent autoimmune disease allele. Transcription profiling of yaa-bearing B cells revealed the overexpression of a cluster of X-linked genes that included T/r7. FISH analysis demonstrated the translocation of this segment onto the yaa chromosome. The resulting overexpression of T/r7 increased in vitro responses to Toll-like receptor (TLR) 7 signaling in all yaa-bearing males. B6.yaa mice are not overtly autoimmune, but the addition of Slel, which contains the autoimmune-predisposing Slam/Cd2 haplotype, causes the development of fatal lupus with numerous immunological aberrations. B6.Slelyaa CD4 T cells develop the molecular signature for TFH cells and also show expression changes in numerous cytokines and chemokines. Disease development and all component autoimmune phenotypes were inhibited by Sles1, a potent suppressor locus. Slesl had no effect on yaa-enhanced TLR7 signaling in vitro, and these data place Sles1 downstream from the lesion in innate immune responses mediated by TLR7, suggesting that Sles1 modulates the activation of adaptive immunity in response to innate immune signaling.</description><subject>Animals</subject><subject>Autoimmune diseases</subject><subject>Autoimmunity</subject><subject>Autoimmunity - genetics</subject><subject>B lymphocytes</subject><subject>B-Lymphocytes - immunology</subject><subject>Biological Sciences</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>Chromosomes</subject><subject>Gene Expression Profiling</subject><subject>Gene loci</subject><subject>Genes</subject><subject>Genetic loci</subject><subject>Genetics</subject><subject>Immune system</subject><subject>Immunity, Innate - genetics</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic - genetics</subject><subject>Male</subject><subject>Medical genetics</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Phenotypes</subject><subject>T lymphocytes</subject><subject>Toll-Like Receptor 7 - genetics</subject><subject>Transcriptional Activation</subject><subject>Translocation, Genetic</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkb2P1DAQxS0E4paDmgqIKBBN7sZ2bCcN0urEAdIiCpbachwHvErsxR-I_e9xtKtboIBqivnN07z3EHqK4QqDoNd7p-IVcKAdJhjoPbTC0OGaNx3cRysAIuq2Ic0FehTjDgA61sJDdIG5EKJjbIVu19V2CqLaBuXi5LVK1rtqrbWZTFDJxOrzISYzW12tc_J2nrOz6VBZV33MwTpTbfI-x8fowaimaJ6c5iX6cvt2e_O-3nx69-Fmval104pUCzZoEBo4I2xoBlBjyzkXuGeGa81Bib4z_QCECDGKvtW0N00LfT9iSjkAvURvjrr73M9m0MaloCa5D3ZW4SC9svLPjbPf5Ff_Q2IGhHFaBF6dBIL_nk1McraxmJ2UMz5HyVsmaIvxf0EsiCixdwV8-Re48zm4koIkgGmxSha16yOkg48xmPHuZQxyaVIuTcpzk-Xi-e9Oz_ypugK8OAHL5VmOSsJl14klrNf_JuSYpymZn6mgz47oLiYf7lgKwHAJjv4C0Ju7gA</recordid><startdate>20060627</startdate><enddate>20060627</enddate><creator>Subramanian, Srividya</creator><creator>Tus, Katalin</creator><creator>Li, Quan-Zhen</creator><creator>Wang, Andrew</creator><creator>Tian, Xiang-Hong</creator><creator>Zhou, Jinchun</creator><creator>Liang, Chaoying</creator><creator>Bartov, Guy</creator><creator>McDaniel, Lisa D.</creator><creator>Zhou, Xin J.</creator><creator>Schultz, Roger A.</creator><creator>Wakeland, Edward K.</creator><general>National Academy of Sciences</general><general>National Acad 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>20060627</creationdate><title>A Tlr7 Translocation Accelerates Systemic Autoimmunity in Murine Lupus</title><author>Subramanian, Srividya ; 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Transcription profiling of yaa-bearing B cells revealed the overexpression of a cluster of X-linked genes that included T/r7. FISH analysis demonstrated the translocation of this segment onto the yaa chromosome. The resulting overexpression of T/r7 increased in vitro responses to Toll-like receptor (TLR) 7 signaling in all yaa-bearing males. B6.yaa mice are not overtly autoimmune, but the addition of Slel, which contains the autoimmune-predisposing Slam/Cd2 haplotype, causes the development of fatal lupus with numerous immunological aberrations. B6.Slelyaa CD4 T cells develop the molecular signature for TFH cells and also show expression changes in numerous cytokines and chemokines. Disease development and all component autoimmune phenotypes were inhibited by Sles1, a potent suppressor locus. Slesl had no effect on yaa-enhanced TLR7 signaling in vitro, and these data place Sles1 downstream from the lesion in innate immune responses mediated by TLR7, suggesting that Sles1 modulates the activation of adaptive immunity in response to innate immune signaling.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>16777955</pmid><doi>10.1073/pnas.0603912103</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Autoimmune diseases Autoimmunity Autoimmunity - genetics B lymphocytes B-Lymphocytes - immunology Biological Sciences CD4-Positive T-Lymphocytes - immunology Chromosomes Gene Expression Profiling Gene loci Genes Genetic loci Genetics Immune system Immunity, Innate - genetics Lupus Lupus Erythematosus, Systemic - genetics Male Medical genetics Mice Mice, Mutant Strains Phenotypes T lymphocytes Toll-Like Receptor 7 - genetics Transcriptional Activation Translocation, Genetic |
| title | A Tlr7 Translocation Accelerates Systemic Autoimmunity in Murine Lupus |
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