Toll-Like Receptor 2 Pathway Drives Streptococcal Cell Wall-Induced Joint Inflammation: Critical Role of Myeloid Differentiation Factor 88
The IL-1R/Toll-like receptor (TLR) superfamily of receptors has a key role in innate immunity and inflammation. In this study, we report that streptococcal cell wall (SCW)-induced joint inflammation is predominantly dependent on TLR-2 signaling, since TLR-2-deficient mice were unable to develop eith...
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| creator | Joosten, Leo A. B Koenders, Marije I Smeets, Ruben L Heuvelmans-Jacobs, Marleen Helsen, Monique M. A Takeda, Kiyoshi Akira, Shizuo Lubberts, Erik van de Loo, Fons A. J van den Berg, Wim B |
| description | The IL-1R/Toll-like receptor (TLR) superfamily of receptors has a key role in innate immunity and inflammation. In this study, we report that streptococcal cell wall (SCW)-induced joint inflammation is predominantly dependent on TLR-2 signaling, since TLR-2-deficient mice were unable to develop either joint swelling or inhibition of cartilage matrix synthesis. Myeloid differentiation factor 88 (MyD88) is a Toll/IL-1R domain containing adaptor molecule known to have a central role in both IL-1R/IL-18R and TLR signaling. Mice deficient for MyD88 did not develop SCW-induced arthritis; both joint swelling and disturbance of cartilage chondrocyte anabolic function was completely abolished. Local levels of proinflammatory cytokines and chemokines in synovial tissue washouts were strongly reduced in MyD88-deficient mice. Histology confirmed the pivotal role of MyD88 in acute joint inflammation. TLR-2-deficient mice still allow influx of inflammatory cells into the joint cavity, although the number of cells was markedly reduced. No influx of inflammatory cells was seen in joints of MyD88-deficient mice. In addition, cartilage matrix proteoglycan loss was completely absent in MyD88 knockout mice. These findings clearly demonstrated that MyD88 is a key component in SCW-induced joint inflammation. Since agonists of the Toll-like pathway are abundantly involved in both septic and rheumatoid arthritis, targeting of MyD88 may be a novel therapy in inflammatory joint diseases. |
| doi_str_mv | 10.4049/jimmunol.171.11.6145 |
| format | Article |
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B ; Koenders, Marije I ; Smeets, Ruben L ; Heuvelmans-Jacobs, Marleen ; Helsen, Monique M. A ; Takeda, Kiyoshi ; Akira, Shizuo ; Lubberts, Erik ; van de Loo, Fons A. J ; van den Berg, Wim B</creator><creatorcontrib>Joosten, Leo A. B ; Koenders, Marije I ; Smeets, Ruben L ; Heuvelmans-Jacobs, Marleen ; Helsen, Monique M. A ; Takeda, Kiyoshi ; Akira, Shizuo ; Lubberts, Erik ; van de Loo, Fons A. J ; van den Berg, Wim B</creatorcontrib><description>The IL-1R/Toll-like receptor (TLR) superfamily of receptors has a key role in innate immunity and inflammation. In this study, we report that streptococcal cell wall (SCW)-induced joint inflammation is predominantly dependent on TLR-2 signaling, since TLR-2-deficient mice were unable to develop either joint swelling or inhibition of cartilage matrix synthesis. Myeloid differentiation factor 88 (MyD88) is a Toll/IL-1R domain containing adaptor molecule known to have a central role in both IL-1R/IL-18R and TLR signaling. Mice deficient for MyD88 did not develop SCW-induced arthritis; both joint swelling and disturbance of cartilage chondrocyte anabolic function was completely abolished. Local levels of proinflammatory cytokines and chemokines in synovial tissue washouts were strongly reduced in MyD88-deficient mice. Histology confirmed the pivotal role of MyD88 in acute joint inflammation. TLR-2-deficient mice still allow influx of inflammatory cells into the joint cavity, although the number of cells was markedly reduced. No influx of inflammatory cells was seen in joints of MyD88-deficient mice. In addition, cartilage matrix proteoglycan loss was completely absent in MyD88 knockout mice. These findings clearly demonstrated that MyD88 is a key component in SCW-induced joint inflammation. Since agonists of the Toll-like pathway are abundantly involved in both septic and rheumatoid arthritis, targeting of MyD88 may be a novel therapy in inflammatory joint diseases.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.171.11.6145</identifier><identifier>PMID: 14634130</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject>Adaptor Proteins, Signal Transducing ; Animals ; Antigens, Differentiation - genetics ; Antigens, Differentiation - physiology ; Arthritis, Experimental - genetics ; Arthritis, Experimental - immunology ; Arthritis, Experimental - metabolism ; Arthritis, Experimental - pathology ; Cartilage, Articular - immunology ; Cartilage, Articular - metabolism ; Cell Wall - immunology ; Down-Regulation - genetics ; Down-Regulation - immunology ; Inflammation Mediators - antagonists & inhibitors ; Inflammation Mediators - metabolism ; Interleukin-1 - physiology ; Interleukin-18 - physiology ; Male ; Membrane Glycoproteins - biosynthesis ; Membrane Glycoproteins - deficiency ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Multigene Family - immunology ; Myeloid Differentiation Factor 88 ; Neutrophil Infiltration - genetics ; Neutrophil Infiltration - immunology ; Proteoglycans - immunology ; Proteoglycans - metabolism ; Receptors, Cell Surface - biosynthesis ; Receptors, Cell Surface - deficiency ; Receptors, Cell Surface - genetics ; Receptors, Cell Surface - physiology ; Receptors, Immunologic - deficiency ; Receptors, Immunologic - genetics ; Receptors, Immunologic - physiology ; Receptors, Interleukin-1 - antagonists & inhibitors ; Receptors, Interleukin-1 - biosynthesis ; Receptors, Interleukin-1 - physiology ; Signal Transduction - genetics ; Signal Transduction - immunology ; Streptococcus pyogenes - immunology ; Toll-Like Receptor 2 ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha - physiology</subject><ispartof>The Journal of immunology (1950), 2003-12, Vol.171 (11), p.6145-6153</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c481t-f04464866e287462bd103d951cc77f3624bb31e89edd528b789e54cac3a8ece83</citedby><cites>FETCH-LOGICAL-c481t-f04464866e287462bd103d951cc77f3624bb31e89edd528b789e54cac3a8ece83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14634130$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Joosten, Leo A. B</creatorcontrib><creatorcontrib>Koenders, Marije I</creatorcontrib><creatorcontrib>Smeets, Ruben L</creatorcontrib><creatorcontrib>Heuvelmans-Jacobs, Marleen</creatorcontrib><creatorcontrib>Helsen, Monique M. A</creatorcontrib><creatorcontrib>Takeda, Kiyoshi</creatorcontrib><creatorcontrib>Akira, Shizuo</creatorcontrib><creatorcontrib>Lubberts, Erik</creatorcontrib><creatorcontrib>van de Loo, Fons A. J</creatorcontrib><creatorcontrib>van den Berg, Wim B</creatorcontrib><title>Toll-Like Receptor 2 Pathway Drives Streptococcal Cell Wall-Induced Joint Inflammation: Critical Role of Myeloid Differentiation Factor 88</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>The IL-1R/Toll-like receptor (TLR) superfamily of receptors has a key role in innate immunity and inflammation. In this study, we report that streptococcal cell wall (SCW)-induced joint inflammation is predominantly dependent on TLR-2 signaling, since TLR-2-deficient mice were unable to develop either joint swelling or inhibition of cartilage matrix synthesis. Myeloid differentiation factor 88 (MyD88) is a Toll/IL-1R domain containing adaptor molecule known to have a central role in both IL-1R/IL-18R and TLR signaling. Mice deficient for MyD88 did not develop SCW-induced arthritis; both joint swelling and disturbance of cartilage chondrocyte anabolic function was completely abolished. Local levels of proinflammatory cytokines and chemokines in synovial tissue washouts were strongly reduced in MyD88-deficient mice. Histology confirmed the pivotal role of MyD88 in acute joint inflammation. TLR-2-deficient mice still allow influx of inflammatory cells into the joint cavity, although the number of cells was markedly reduced. No influx of inflammatory cells was seen in joints of MyD88-deficient mice. In addition, cartilage matrix proteoglycan loss was completely absent in MyD88 knockout mice. These findings clearly demonstrated that MyD88 is a key component in SCW-induced joint inflammation. Since agonists of the Toll-like pathway are abundantly involved in both septic and rheumatoid arthritis, targeting of MyD88 may be a novel therapy in inflammatory joint diseases.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Animals</subject><subject>Antigens, Differentiation - genetics</subject><subject>Antigens, Differentiation - physiology</subject><subject>Arthritis, Experimental - genetics</subject><subject>Arthritis, Experimental - immunology</subject><subject>Arthritis, Experimental - metabolism</subject><subject>Arthritis, Experimental - pathology</subject><subject>Cartilage, Articular - immunology</subject><subject>Cartilage, Articular - metabolism</subject><subject>Cell Wall - immunology</subject><subject>Down-Regulation - genetics</subject><subject>Down-Regulation - immunology</subject><subject>Inflammation Mediators - antagonists & inhibitors</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin-1 - physiology</subject><subject>Interleukin-18 - physiology</subject><subject>Male</subject><subject>Membrane Glycoproteins - biosynthesis</subject><subject>Membrane Glycoproteins - deficiency</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Membrane Glycoproteins - physiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Multigene Family - immunology</subject><subject>Myeloid Differentiation Factor 88</subject><subject>Neutrophil Infiltration - genetics</subject><subject>Neutrophil Infiltration - immunology</subject><subject>Proteoglycans - immunology</subject><subject>Proteoglycans - metabolism</subject><subject>Receptors, Cell Surface - biosynthesis</subject><subject>Receptors, Cell Surface - deficiency</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Cell Surface - physiology</subject><subject>Receptors, Immunologic - deficiency</subject><subject>Receptors, Immunologic - genetics</subject><subject>Receptors, Immunologic - physiology</subject><subject>Receptors, Interleukin-1 - antagonists & inhibitors</subject><subject>Receptors, Interleukin-1 - biosynthesis</subject><subject>Receptors, Interleukin-1 - physiology</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - immunology</subject><subject>Streptococcus pyogenes - immunology</subject><subject>Toll-Like Receptor 2</subject><subject>Toll-Like Receptors</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcGO0zAURS0EYsrAHyDkFWKT4pc4jssOdZihqAg0DGJpOc4L9eDEHTsh6i_w1ePQItixsiWfe633DiHPgS0546vXt7brxt67JVSwBFgK4OUDsoCyZJkQTDwkC8byPINKVGfkSYy3jDHBcv6YnAEXBYeCLcivG-9ctrU_kF6jwf3gA83pZz3sJn2gF8H-xEi_DGF-Md4Y7eganaPfdIpt-mY02NAP3vYD3fSt012nB-v7N3Qd7GBn_No7pL6lHw_ovG3ohW1bDNgP9jdJL7WZP5XyKXnUahfx2ek8J18v392s32fbT1eb9dttZriEIWsZ54JLITCXFRd53QArmlUJxlRVW4ic13UBKFfYNGUu6yrdSm60KbRME8rinLw89u6DvxsxDqqz0aShdI9-jKqCYgVpjf8FQUoOwKoE8iNogo8xYKv2wXY6HBQwNctSf2SpJEsBqFlWir049Y91h83f0MlOAl4dgZ39vptsQBW7tPeEg5qm6d-ue1raoNk</recordid><startdate>20031201</startdate><enddate>20031201</enddate><creator>Joosten, Leo A. B</creator><creator>Koenders, Marije I</creator><creator>Smeets, Ruben L</creator><creator>Heuvelmans-Jacobs, Marleen</creator><creator>Helsen, Monique M. A</creator><creator>Takeda, Kiyoshi</creator><creator>Akira, Shizuo</creator><creator>Lubberts, Erik</creator><creator>van de Loo, Fons A. J</creator><creator>van den Berg, Wim B</creator><general>Am Assoc Immnol</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>20031201</creationdate><title>Toll-Like Receptor 2 Pathway Drives Streptococcal Cell Wall-Induced Joint Inflammation: Critical Role of Myeloid Differentiation Factor 88</title><author>Joosten, Leo A. B ; Koenders, Marije I ; Smeets, Ruben L ; Heuvelmans-Jacobs, Marleen ; Helsen, Monique M. A ; Takeda, Kiyoshi ; Akira, Shizuo ; Lubberts, Erik ; van de Loo, Fons A. J ; van den Berg, Wim B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-f04464866e287462bd103d951cc77f3624bb31e89edd528b789e54cac3a8ece83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>Animals</topic><topic>Antigens, Differentiation - genetics</topic><topic>Antigens, Differentiation - physiology</topic><topic>Arthritis, Experimental - genetics</topic><topic>Arthritis, Experimental - immunology</topic><topic>Arthritis, Experimental - metabolism</topic><topic>Arthritis, Experimental - pathology</topic><topic>Cartilage, Articular - immunology</topic><topic>Cartilage, Articular - metabolism</topic><topic>Cell Wall - immunology</topic><topic>Down-Regulation - genetics</topic><topic>Down-Regulation - immunology</topic><topic>Inflammation Mediators - antagonists & inhibitors</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukin-1 - physiology</topic><topic>Interleukin-18 - physiology</topic><topic>Male</topic><topic>Membrane Glycoproteins - biosynthesis</topic><topic>Membrane Glycoproteins - deficiency</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Membrane Glycoproteins - physiology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Multigene Family - immunology</topic><topic>Myeloid Differentiation Factor 88</topic><topic>Neutrophil Infiltration - genetics</topic><topic>Neutrophil Infiltration - immunology</topic><topic>Proteoglycans - immunology</topic><topic>Proteoglycans - metabolism</topic><topic>Receptors, Cell Surface - biosynthesis</topic><topic>Receptors, Cell Surface - deficiency</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Cell Surface - physiology</topic><topic>Receptors, Immunologic - deficiency</topic><topic>Receptors, Immunologic - genetics</topic><topic>Receptors, Immunologic - physiology</topic><topic>Receptors, Interleukin-1 - antagonists & inhibitors</topic><topic>Receptors, Interleukin-1 - biosynthesis</topic><topic>Receptors, Interleukin-1 - physiology</topic><topic>Signal Transduction - genetics</topic><topic>Signal Transduction - immunology</topic><topic>Streptococcus pyogenes - immunology</topic><topic>Toll-Like Receptor 2</topic><topic>Toll-Like Receptors</topic><topic>Tumor Necrosis Factor-alpha - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Joosten, Leo A. B</creatorcontrib><creatorcontrib>Koenders, Marije I</creatorcontrib><creatorcontrib>Smeets, Ruben L</creatorcontrib><creatorcontrib>Heuvelmans-Jacobs, Marleen</creatorcontrib><creatorcontrib>Helsen, Monique M. A</creatorcontrib><creatorcontrib>Takeda, Kiyoshi</creatorcontrib><creatorcontrib>Akira, Shizuo</creatorcontrib><creatorcontrib>Lubberts, Erik</creatorcontrib><creatorcontrib>van de Loo, Fons A. J</creatorcontrib><creatorcontrib>van den Berg, Wim B</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>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Joosten, Leo A. B</au><au>Koenders, Marije I</au><au>Smeets, Ruben L</au><au>Heuvelmans-Jacobs, Marleen</au><au>Helsen, Monique M. A</au><au>Takeda, Kiyoshi</au><au>Akira, Shizuo</au><au>Lubberts, Erik</au><au>van de Loo, Fons A. J</au><au>van den Berg, Wim B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Toll-Like Receptor 2 Pathway Drives Streptococcal Cell Wall-Induced Joint Inflammation: Critical Role of Myeloid Differentiation Factor 88</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2003-12-01</date><risdate>2003</risdate><volume>171</volume><issue>11</issue><spage>6145</spage><epage>6153</epage><pages>6145-6153</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>The IL-1R/Toll-like receptor (TLR) superfamily of receptors has a key role in innate immunity and inflammation. In this study, we report that streptococcal cell wall (SCW)-induced joint inflammation is predominantly dependent on TLR-2 signaling, since TLR-2-deficient mice were unable to develop either joint swelling or inhibition of cartilage matrix synthesis. Myeloid differentiation factor 88 (MyD88) is a Toll/IL-1R domain containing adaptor molecule known to have a central role in both IL-1R/IL-18R and TLR signaling. Mice deficient for MyD88 did not develop SCW-induced arthritis; both joint swelling and disturbance of cartilage chondrocyte anabolic function was completely abolished. Local levels of proinflammatory cytokines and chemokines in synovial tissue washouts were strongly reduced in MyD88-deficient mice. Histology confirmed the pivotal role of MyD88 in acute joint inflammation. TLR-2-deficient mice still allow influx of inflammatory cells into the joint cavity, although the number of cells was markedly reduced. No influx of inflammatory cells was seen in joints of MyD88-deficient mice. In addition, cartilage matrix proteoglycan loss was completely absent in MyD88 knockout mice. These findings clearly demonstrated that MyD88 is a key component in SCW-induced joint inflammation. Since agonists of the Toll-like pathway are abundantly involved in both septic and rheumatoid arthritis, targeting of MyD88 may be a novel therapy in inflammatory joint diseases.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>14634130</pmid><doi>10.4049/jimmunol.171.11.6145</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of immunology (1950), 2003-12, Vol.171 (11), p.6145-6153 |
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| subjects | Adaptor Proteins, Signal Transducing Animals Antigens, Differentiation - genetics Antigens, Differentiation - physiology Arthritis, Experimental - genetics Arthritis, Experimental - immunology Arthritis, Experimental - metabolism Arthritis, Experimental - pathology Cartilage, Articular - immunology Cartilage, Articular - metabolism Cell Wall - immunology Down-Regulation - genetics Down-Regulation - immunology Inflammation Mediators - antagonists & inhibitors Inflammation Mediators - metabolism Interleukin-1 - physiology Interleukin-18 - physiology Male Membrane Glycoproteins - biosynthesis Membrane Glycoproteins - deficiency Membrane Glycoproteins - genetics Membrane Glycoproteins - physiology Mice Mice, Inbred C57BL Mice, Knockout Multigene Family - immunology Myeloid Differentiation Factor 88 Neutrophil Infiltration - genetics Neutrophil Infiltration - immunology Proteoglycans - immunology Proteoglycans - metabolism Receptors, Cell Surface - biosynthesis Receptors, Cell Surface - deficiency Receptors, Cell Surface - genetics Receptors, Cell Surface - physiology Receptors, Immunologic - deficiency Receptors, Immunologic - genetics Receptors, Immunologic - physiology Receptors, Interleukin-1 - antagonists & inhibitors Receptors, Interleukin-1 - biosynthesis Receptors, Interleukin-1 - physiology Signal Transduction - genetics Signal Transduction - immunology Streptococcus pyogenes - immunology Toll-Like Receptor 2 Toll-Like Receptors Tumor Necrosis Factor-alpha - physiology |
| title | Toll-Like Receptor 2 Pathway Drives Streptococcal Cell Wall-Induced Joint Inflammation: Critical Role of Myeloid Differentiation Factor 88 |
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