Endosomal TLR signaling is required for anti-nucleic acid and rheumatoid factor autoantibodies in lupus
Using the Unc93b1 3d mutation that selectively abolishes nucleic acid-binding Toll-like receptor (TLR) (TLR3, -7, -9) signaling, we show these endosomal TLRs are required for optimal production of IgG autoAbs, IgM rheumatoid factor, and other clinical parameters of disease in 2 lupus strains, B6-Fas...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2009-07, Vol.106 (29), p.12061-12066 |
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| creator | Kono, Dwight H Haraldsson, M. Katarina Lawson, Brian R Pollard, K. Michael Koh, Yi Ting Du, Xin Arnold, Carrie N Baccala, Roberto Silverman, Gregg J Beutler, Bruce A Theofilopoulos, Argyrios N |
| description | Using the Unc93b1 3d mutation that selectively abolishes nucleic acid-binding Toll-like receptor (TLR) (TLR3, -7, -9) signaling, we show these endosomal TLRs are required for optimal production of IgG autoAbs, IgM rheumatoid factor, and other clinical parameters of disease in 2 lupus strains, B6-Faslpr and BXSB. Strikingly, treatment with lipid A, an autoAb-inducing TLR4 agonist, could not overcome this requirement. The 3d mutation slightly reduced complete Freund's adjuvant (CFA)-mediated antigen presentation, but did not affect T-independent type 1 or alum-mediated T-dependent humoral responses or TLR-independent IFN production induced by cytoplasmic nucleic acids. These findings suggest that nucleic acid-sensing TLRs might act as an Achilles' heel in susceptible individuals by providing a critical pathway by which relative tolerance for nucleic acid-containing antigens is breached and systemic autoimmunity ensues. Importantly, this helps provide an explanation for the high frequency of anti-nucleic acid Abs in lupus-like systemic autoimmunity. |
| doi_str_mv | 10.1073/pnas.0905441106 |
| format | Article |
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Katarina ; Lawson, Brian R ; Pollard, K. Michael ; Koh, Yi Ting ; Du, Xin ; Arnold, Carrie N ; Baccala, Roberto ; Silverman, Gregg J ; Beutler, Bruce A ; Theofilopoulos, Argyrios N</creator><creatorcontrib>Kono, Dwight H ; Haraldsson, M. Katarina ; Lawson, Brian R ; Pollard, K. Michael ; Koh, Yi Ting ; Du, Xin ; Arnold, Carrie N ; Baccala, Roberto ; Silverman, Gregg J ; Beutler, Bruce A ; Theofilopoulos, Argyrios N</creatorcontrib><description>Using the Unc93b1 3d mutation that selectively abolishes nucleic acid-binding Toll-like receptor (TLR) (TLR3, -7, -9) signaling, we show these endosomal TLRs are required for optimal production of IgG autoAbs, IgM rheumatoid factor, and other clinical parameters of disease in 2 lupus strains, B6-Faslpr and BXSB. Strikingly, treatment with lipid A, an autoAb-inducing TLR4 agonist, could not overcome this requirement. The 3d mutation slightly reduced complete Freund's adjuvant (CFA)-mediated antigen presentation, but did not affect T-independent type 1 or alum-mediated T-dependent humoral responses or TLR-independent IFN production induced by cytoplasmic nucleic acids. These findings suggest that nucleic acid-sensing TLRs might act as an Achilles' heel in susceptible individuals by providing a critical pathway by which relative tolerance for nucleic acid-containing antigens is breached and systemic autoimmunity ensues. Importantly, this helps provide an explanation for the high frequency of anti-nucleic acid Abs in lupus-like systemic autoimmunity.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0905441106</identifier><identifier>PMID: 19574451</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Animals ; Antibodies, Antinuclear - immunology ; B lymphocytes ; B-Lymphocytes - cytology ; B-Lymphocytes - drug effects ; B-Lymphocytes - immunology ; Biochemistry ; Biological Sciences ; Dendritic Cells - cytology ; Dendritic Cells - drug effects ; Dendritic Cells - immunology ; Endosomes - drug effects ; Endosomes - immunology ; Genetic mutation ; Immune system ; Immunoglobulin G - immunology ; Immunoglobulin M - immunology ; Lipids ; Lupus ; Lupus Erythematosus, Systemic - immunology ; Lupus Erythematosus, Systemic - pathology ; Lymphocyte Activation - drug effects ; Male ; Mice ; Mice, Inbred MRL lpr ; Mutation ; Mutation - genetics ; Nucleic acids ; Nucleic Acids - pharmacology ; Picrates - pharmacology ; Rheumatism ; Rheumatoid Factor - immunology ; RNA ; Signal Transduction - drug effects ; Signal Transduction - immunology ; Survival Analysis ; Systemic lupus erythematosus ; T lymphocytes ; T-Lymphocytes - cytology ; T-Lymphocytes - drug effects ; T-Lymphocytes - immunology ; Toll like receptors ; Toll-Like Receptor 4 - immunology ; Toll-Like Receptors - immunology</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2009-07, Vol.106 (29), p.12061-12066</ispartof><rights>Copyright National Academy of Sciences Jul 21, 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c620t-f4199a6649d13bae706780d75c0b442b1eaa4d7cd8925a48efd7ac31e518ed9b3</citedby><cites>FETCH-LOGICAL-c620t-f4199a6649d13bae706780d75c0b442b1eaa4d7cd8925a48efd7ac31e518ed9b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/106/29.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/40484082$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/40484082$$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/19574451$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kono, Dwight H</creatorcontrib><creatorcontrib>Haraldsson, M. Katarina</creatorcontrib><creatorcontrib>Lawson, Brian R</creatorcontrib><creatorcontrib>Pollard, K. Michael</creatorcontrib><creatorcontrib>Koh, Yi Ting</creatorcontrib><creatorcontrib>Du, Xin</creatorcontrib><creatorcontrib>Arnold, Carrie N</creatorcontrib><creatorcontrib>Baccala, Roberto</creatorcontrib><creatorcontrib>Silverman, Gregg J</creatorcontrib><creatorcontrib>Beutler, Bruce A</creatorcontrib><creatorcontrib>Theofilopoulos, Argyrios N</creatorcontrib><title>Endosomal TLR signaling is required for anti-nucleic acid and rheumatoid factor autoantibodies in lupus</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Using the Unc93b1 3d mutation that selectively abolishes nucleic acid-binding Toll-like receptor (TLR) (TLR3, -7, -9) signaling, we show these endosomal TLRs are required for optimal production of IgG autoAbs, IgM rheumatoid factor, and other clinical parameters of disease in 2 lupus strains, B6-Faslpr and BXSB. Strikingly, treatment with lipid A, an autoAb-inducing TLR4 agonist, could not overcome this requirement. The 3d mutation slightly reduced complete Freund's adjuvant (CFA)-mediated antigen presentation, but did not affect T-independent type 1 or alum-mediated T-dependent humoral responses or TLR-independent IFN production induced by cytoplasmic nucleic acids. These findings suggest that nucleic acid-sensing TLRs might act as an Achilles' heel in susceptible individuals by providing a critical pathway by which relative tolerance for nucleic acid-containing antigens is breached and systemic autoimmunity ensues. Importantly, this helps provide an explanation for the high frequency of anti-nucleic acid Abs in lupus-like systemic autoimmunity.</description><subject>Animals</subject><subject>Antibodies, Antinuclear - immunology</subject><subject>B lymphocytes</subject><subject>B-Lymphocytes - cytology</subject><subject>B-Lymphocytes - drug effects</subject><subject>B-Lymphocytes - immunology</subject><subject>Biochemistry</subject><subject>Biological Sciences</subject><subject>Dendritic Cells - cytology</subject><subject>Dendritic Cells - drug effects</subject><subject>Dendritic Cells - immunology</subject><subject>Endosomes - drug effects</subject><subject>Endosomes - immunology</subject><subject>Genetic mutation</subject><subject>Immune system</subject><subject>Immunoglobulin G - immunology</subject><subject>Immunoglobulin M - immunology</subject><subject>Lipids</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic - immunology</subject><subject>Lupus Erythematosus, Systemic - pathology</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred MRL lpr</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Nucleic acids</subject><subject>Nucleic Acids - pharmacology</subject><subject>Picrates - pharmacology</subject><subject>Rheumatism</subject><subject>Rheumatoid Factor - immunology</subject><subject>RNA</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - immunology</subject><subject>Survival Analysis</subject><subject>Systemic lupus erythematosus</subject><subject>T lymphocytes</subject><subject>T-Lymphocytes - cytology</subject><subject>T-Lymphocytes - drug effects</subject><subject>T-Lymphocytes - immunology</subject><subject>Toll like receptors</subject><subject>Toll-Like Receptor 4 - immunology</subject><subject>Toll-Like Receptors - immunology</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c1rFDEYBvBBFLtWz57U4EHwMO2bTD4mF0FK_YAFQdtzyCSZaZbZyTaZiP3vm2GXrnrpaci8vzwkearqNYYzDKI53006nYEERinGwJ9UKwwS15xKeFqtAIioW0roSfUipQ0ASNbC8-oESyYoZXhVDZeTDSls9Yiu1j9R8sOkRz8NyCcU3W320VnUh4j0NPt6ymZ03iBtvC1_LIo3Lm_1HMqy12ZeXJ7DYrtgvUvIT2jMu5xeVs96PSb36vA9ra6_XF5dfKvXP75-v_i8rg0nMNc9xVJqXs5vcdNpJ4CLFqxgBjpKSYed1tQKY1tJmKat663QpsGO4dZZ2TWn1ad97i53W2eNm-aoR7WLfqvjnQraq38nk79RQ_itiMCMEVoCPhwCYrjNLs1q65Nx46gnF3JSXDCQjWCPQgItiPLOBb7_D25CjuWZF4MbIjlb0s73yMSQUnT9w5ExqKVqtVStjlWXHW__vunRH7otAB3AsvMYxxWRChPgC_n4CFF9HsfZ_ZmLfbO3m1R6fsAUaEuhJWX-bj_vdVB6iD6p61_LBQFzVgg097J80dQ</recordid><startdate>20090721</startdate><enddate>20090721</enddate><creator>Kono, Dwight H</creator><creator>Haraldsson, M. Katarina</creator><creator>Lawson, Brian R</creator><creator>Pollard, K. Michael</creator><creator>Koh, Yi Ting</creator><creator>Du, Xin</creator><creator>Arnold, Carrie N</creator><creator>Baccala, Roberto</creator><creator>Silverman, Gregg J</creator><creator>Beutler, Bruce A</creator><creator>Theofilopoulos, Argyrios N</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>FBQ</scope><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>20090721</creationdate><title>Endosomal TLR signaling is required for anti-nucleic acid and rheumatoid factor autoantibodies in lupus</title><author>Kono, Dwight H ; Haraldsson, M. 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Katarina</au><au>Lawson, Brian R</au><au>Pollard, K. Michael</au><au>Koh, Yi Ting</au><au>Du, Xin</au><au>Arnold, Carrie N</au><au>Baccala, Roberto</au><au>Silverman, Gregg J</au><au>Beutler, Bruce A</au><au>Theofilopoulos, Argyrios N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endosomal TLR signaling is required for anti-nucleic acid and rheumatoid factor autoantibodies in lupus</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2009-07-21</date><risdate>2009</risdate><volume>106</volume><issue>29</issue><spage>12061</spage><epage>12066</epage><pages>12061-12066</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Using the Unc93b1 3d mutation that selectively abolishes nucleic acid-binding Toll-like receptor (TLR) (TLR3, -7, -9) signaling, we show these endosomal TLRs are required for optimal production of IgG autoAbs, IgM rheumatoid factor, and other clinical parameters of disease in 2 lupus strains, B6-Faslpr and BXSB. Strikingly, treatment with lipid A, an autoAb-inducing TLR4 agonist, could not overcome this requirement. The 3d mutation slightly reduced complete Freund's adjuvant (CFA)-mediated antigen presentation, but did not affect T-independent type 1 or alum-mediated T-dependent humoral responses or TLR-independent IFN production induced by cytoplasmic nucleic acids. These findings suggest that nucleic acid-sensing TLRs might act as an Achilles' heel in susceptible individuals by providing a critical pathway by which relative tolerance for nucleic acid-containing antigens is breached and systemic autoimmunity ensues. Importantly, this helps provide an explanation for the high frequency of anti-nucleic acid Abs in lupus-like systemic autoimmunity.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>19574451</pmid><doi>10.1073/pnas.0905441106</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies, Antinuclear - immunology B lymphocytes B-Lymphocytes - cytology B-Lymphocytes - drug effects B-Lymphocytes - immunology Biochemistry Biological Sciences Dendritic Cells - cytology Dendritic Cells - drug effects Dendritic Cells - immunology Endosomes - drug effects Endosomes - immunology Genetic mutation Immune system Immunoglobulin G - immunology Immunoglobulin M - immunology Lipids Lupus Lupus Erythematosus, Systemic - immunology Lupus Erythematosus, Systemic - pathology Lymphocyte Activation - drug effects Male Mice Mice, Inbred MRL lpr Mutation Mutation - genetics Nucleic acids Nucleic Acids - pharmacology Picrates - pharmacology Rheumatism Rheumatoid Factor - immunology RNA Signal Transduction - drug effects Signal Transduction - immunology Survival Analysis Systemic lupus erythematosus T lymphocytes T-Lymphocytes - cytology T-Lymphocytes - drug effects T-Lymphocytes - immunology Toll like receptors Toll-Like Receptor 4 - immunology Toll-Like Receptors - immunology |
| title | Endosomal TLR signaling is required for anti-nucleic acid and rheumatoid factor autoantibodies in lupus |
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