Pathogenesis of Joint Destruction in Rheumatoid Arthritis
Abstract Synovial mesenchymal cells, matrix metalloproteinases (MMPs), and osteoclasts are the three major players directly responsible for the pathogenesis of rheumatoid joint destruction. First, synovial mesenchymal cells, internally driven by a transcription factor c-Fos/AP-1, not only directly i...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Shiozawa, Shunichi [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2011 |
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| Schlagwörter: |
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| Anmerkung: |
© L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2011 |
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| Übergeordnetes Werk: |
Enthalten in: Archivum immunologiae et therapiae experimentalis - [Cham (ZG)] : [Springer International Publishing AG], 1994, 59(2011), 2 vom: 16. Feb., Seite 89-95 |
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| Übergeordnetes Werk: |
volume:59 ; year:2011 ; number:2 ; day:16 ; month:02 ; pages:89-95 |
| Links: |
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| DOI / URN: |
10.1007/s00005-011-0116-3 |
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| Katalog-ID: |
SPR000040770 |
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| 100 | 1 | |a Shiozawa, Shunichi |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Pathogenesis of Joint Destruction in Rheumatoid Arthritis |
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| 520 | |a Abstract Synovial mesenchymal cells, matrix metalloproteinases (MMPs), and osteoclasts are the three major players directly responsible for the pathogenesis of rheumatoid joint destruction. First, synovial mesenchymal cells, internally driven by a transcription factor c-Fos/AP-1, not only directly invade cartilage and bone as a granulation tissue called “pannus” but also release inflammatory cytokine interleukin (IL)-1β. IL-1β induces MMPs and activates osteoclasts. Synovial cells can also present antigen to T cells to drive antigen-specific immune responses. Second, cartilaginous joint matrix can only be degraded after the first attack of collagen fibrils by MMPs, and importantly, most of the MMPs are under the control of c-Fos/AP-1 and IL-1β as well. Third, differentiation of osteoclast is driven internally by NFATc1, where NFATc1 is under the control of TRAF6, c-Fos/AP-1 and osteoclastogenic signaling complex. IL-1β has been shown to induce osteoclastogenesis directly and also indirectly via signaling through RANKL. Therefore, IL-1β and c-Fos/AP-1 influence each other’s gene expression and activity, resulting in an orchestrated cross-talk that is crucial to arthritic joint destruction, and thus, blockade of IL-1β and/or c-Fos/AP-1 can be most promising as a therapeutic target, and in fact, a selective inhibition of c-Fos/AP-1 does resolve arthritic joint destruction. | ||
| 650 | 4 | |a Rheumatoid arthritis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Joint destruction |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a c-Fos |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a c-Fos/AP-1 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a IL-1beta |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Tsumiyama, Ken |4 aut | |
| 700 | 1 | |a Yoshida, Kohsuke |4 aut | |
| 700 | 1 | |a Hashiramoto, Akira |4 aut | |
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10.1007/s00005-011-0116-3 doi (DE-627)SPR000040770 (SPR)s00005-011-0116-3-e DE-627 ger DE-627 rakwb eng Shiozawa, Shunichi verfasserin aut Pathogenesis of Joint Destruction in Rheumatoid Arthritis 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2011 Abstract Synovial mesenchymal cells, matrix metalloproteinases (MMPs), and osteoclasts are the three major players directly responsible for the pathogenesis of rheumatoid joint destruction. First, synovial mesenchymal cells, internally driven by a transcription factor c-Fos/AP-1, not only directly invade cartilage and bone as a granulation tissue called “pannus” but also release inflammatory cytokine interleukin (IL)-1β. IL-1β induces MMPs and activates osteoclasts. Synovial cells can also present antigen to T cells to drive antigen-specific immune responses. Second, cartilaginous joint matrix can only be degraded after the first attack of collagen fibrils by MMPs, and importantly, most of the MMPs are under the control of c-Fos/AP-1 and IL-1β as well. Third, differentiation of osteoclast is driven internally by NFATc1, where NFATc1 is under the control of TRAF6, c-Fos/AP-1 and osteoclastogenic signaling complex. IL-1β has been shown to induce osteoclastogenesis directly and also indirectly via signaling through RANKL. Therefore, IL-1β and c-Fos/AP-1 influence each other’s gene expression and activity, resulting in an orchestrated cross-talk that is crucial to arthritic joint destruction, and thus, blockade of IL-1β and/or c-Fos/AP-1 can be most promising as a therapeutic target, and in fact, a selective inhibition of c-Fos/AP-1 does resolve arthritic joint destruction. Rheumatoid arthritis (dpeaa)DE-He213 Joint destruction (dpeaa)DE-He213 c-Fos (dpeaa)DE-He213 c-Fos/AP-1 (dpeaa)DE-He213 IL-1beta (dpeaa)DE-He213 Tsumiyama, Ken aut Yoshida, Kohsuke aut Hashiramoto, Akira aut Enthalten in Archivum immunologiae et therapiae experimentalis [Cham (ZG)] : [Springer International Publishing AG], 1994 59(2011), 2 vom: 16. Feb., Seite 89-95 (DE-627)389872318 (DE-600)2149971-8 1661-4917 nnns volume:59 year:2011 number:2 day:16 month:02 pages:89-95 https://dx.doi.org/10.1007/s00005-011-0116-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 59 2011 2 16 02 89-95 |
| spelling |
10.1007/s00005-011-0116-3 doi (DE-627)SPR000040770 (SPR)s00005-011-0116-3-e DE-627 ger DE-627 rakwb eng Shiozawa, Shunichi verfasserin aut Pathogenesis of Joint Destruction in Rheumatoid Arthritis 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2011 Abstract Synovial mesenchymal cells, matrix metalloproteinases (MMPs), and osteoclasts are the three major players directly responsible for the pathogenesis of rheumatoid joint destruction. First, synovial mesenchymal cells, internally driven by a transcription factor c-Fos/AP-1, not only directly invade cartilage and bone as a granulation tissue called “pannus” but also release inflammatory cytokine interleukin (IL)-1β. IL-1β induces MMPs and activates osteoclasts. Synovial cells can also present antigen to T cells to drive antigen-specific immune responses. Second, cartilaginous joint matrix can only be degraded after the first attack of collagen fibrils by MMPs, and importantly, most of the MMPs are under the control of c-Fos/AP-1 and IL-1β as well. Third, differentiation of osteoclast is driven internally by NFATc1, where NFATc1 is under the control of TRAF6, c-Fos/AP-1 and osteoclastogenic signaling complex. IL-1β has been shown to induce osteoclastogenesis directly and also indirectly via signaling through RANKL. Therefore, IL-1β and c-Fos/AP-1 influence each other’s gene expression and activity, resulting in an orchestrated cross-talk that is crucial to arthritic joint destruction, and thus, blockade of IL-1β and/or c-Fos/AP-1 can be most promising as a therapeutic target, and in fact, a selective inhibition of c-Fos/AP-1 does resolve arthritic joint destruction. Rheumatoid arthritis (dpeaa)DE-He213 Joint destruction (dpeaa)DE-He213 c-Fos (dpeaa)DE-He213 c-Fos/AP-1 (dpeaa)DE-He213 IL-1beta (dpeaa)DE-He213 Tsumiyama, Ken aut Yoshida, Kohsuke aut Hashiramoto, Akira aut Enthalten in Archivum immunologiae et therapiae experimentalis [Cham (ZG)] : [Springer International Publishing AG], 1994 59(2011), 2 vom: 16. Feb., Seite 89-95 (DE-627)389872318 (DE-600)2149971-8 1661-4917 nnns volume:59 year:2011 number:2 day:16 month:02 pages:89-95 https://dx.doi.org/10.1007/s00005-011-0116-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 59 2011 2 16 02 89-95 |
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10.1007/s00005-011-0116-3 doi (DE-627)SPR000040770 (SPR)s00005-011-0116-3-e DE-627 ger DE-627 rakwb eng Shiozawa, Shunichi verfasserin aut Pathogenesis of Joint Destruction in Rheumatoid Arthritis 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2011 Abstract Synovial mesenchymal cells, matrix metalloproteinases (MMPs), and osteoclasts are the three major players directly responsible for the pathogenesis of rheumatoid joint destruction. First, synovial mesenchymal cells, internally driven by a transcription factor c-Fos/AP-1, not only directly invade cartilage and bone as a granulation tissue called “pannus” but also release inflammatory cytokine interleukin (IL)-1β. IL-1β induces MMPs and activates osteoclasts. Synovial cells can also present antigen to T cells to drive antigen-specific immune responses. Second, cartilaginous joint matrix can only be degraded after the first attack of collagen fibrils by MMPs, and importantly, most of the MMPs are under the control of c-Fos/AP-1 and IL-1β as well. Third, differentiation of osteoclast is driven internally by NFATc1, where NFATc1 is under the control of TRAF6, c-Fos/AP-1 and osteoclastogenic signaling complex. IL-1β has been shown to induce osteoclastogenesis directly and also indirectly via signaling through RANKL. Therefore, IL-1β and c-Fos/AP-1 influence each other’s gene expression and activity, resulting in an orchestrated cross-talk that is crucial to arthritic joint destruction, and thus, blockade of IL-1β and/or c-Fos/AP-1 can be most promising as a therapeutic target, and in fact, a selective inhibition of c-Fos/AP-1 does resolve arthritic joint destruction. Rheumatoid arthritis (dpeaa)DE-He213 Joint destruction (dpeaa)DE-He213 c-Fos (dpeaa)DE-He213 c-Fos/AP-1 (dpeaa)DE-He213 IL-1beta (dpeaa)DE-He213 Tsumiyama, Ken aut Yoshida, Kohsuke aut Hashiramoto, Akira aut Enthalten in Archivum immunologiae et therapiae experimentalis [Cham (ZG)] : [Springer International Publishing AG], 1994 59(2011), 2 vom: 16. Feb., Seite 89-95 (DE-627)389872318 (DE-600)2149971-8 1661-4917 nnns volume:59 year:2011 number:2 day:16 month:02 pages:89-95 https://dx.doi.org/10.1007/s00005-011-0116-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 59 2011 2 16 02 89-95 |
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Shiozawa, Shunichi @@aut@@ Tsumiyama, Ken @@aut@@ Yoshida, Kohsuke @@aut@@ Hashiramoto, Akira @@aut@@ |
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Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2011</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Synovial mesenchymal cells, matrix metalloproteinases (MMPs), and osteoclasts are the three major players directly responsible for the pathogenesis of rheumatoid joint destruction. First, synovial mesenchymal cells, internally driven by a transcription factor c-Fos/AP-1, not only directly invade cartilage and bone as a granulation tissue called “pannus” but also release inflammatory cytokine interleukin (IL)-1β. IL-1β induces MMPs and activates osteoclasts. Synovial cells can also present antigen to T cells to drive antigen-specific immune responses. Second, cartilaginous joint matrix can only be degraded after the first attack of collagen fibrils by MMPs, and importantly, most of the MMPs are under the control of c-Fos/AP-1 and IL-1β as well. Third, differentiation of osteoclast is driven internally by NFATc1, where NFATc1 is under the control of TRAF6, c-Fos/AP-1 and osteoclastogenic signaling complex. IL-1β has been shown to induce osteoclastogenesis directly and also indirectly via signaling through RANKL. Therefore, IL-1β and c-Fos/AP-1 influence each other’s gene expression and activity, resulting in an orchestrated cross-talk that is crucial to arthritic joint destruction, and thus, blockade of IL-1β and/or c-Fos/AP-1 can be most promising as a therapeutic target, and in fact, a selective inhibition of c-Fos/AP-1 does resolve arthritic joint destruction.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Rheumatoid arthritis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Joint destruction</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">c-Fos</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">c-Fos/AP-1</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">IL-1beta</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tsumiyama, Ken</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yoshida, Kohsuke</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hashiramoto, Akira</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Archivum immunologiae et therapiae experimentalis</subfield><subfield code="d">[Cham (ZG)] : [Springer International Publishing AG], 1994</subfield><subfield code="g">59(2011), 2 vom: 16. 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Shiozawa, Shunichi |
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Shiozawa, Shunichi misc Rheumatoid arthritis misc Joint destruction misc c-Fos misc c-Fos/AP-1 misc IL-1beta Pathogenesis of Joint Destruction in Rheumatoid Arthritis |
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Pathogenesis of Joint Destruction in Rheumatoid Arthritis Rheumatoid arthritis (dpeaa)DE-He213 Joint destruction (dpeaa)DE-He213 c-Fos (dpeaa)DE-He213 c-Fos/AP-1 (dpeaa)DE-He213 IL-1beta (dpeaa)DE-He213 |
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Pathogenesis of Joint Destruction in Rheumatoid Arthritis |
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Shiozawa, Shunichi |
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Shiozawa, Shunichi Tsumiyama, Ken Yoshida, Kohsuke Hashiramoto, Akira |
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Shiozawa, Shunichi |
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pathogenesis of joint destruction in rheumatoid arthritis |
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Pathogenesis of Joint Destruction in Rheumatoid Arthritis |
| abstract |
Abstract Synovial mesenchymal cells, matrix metalloproteinases (MMPs), and osteoclasts are the three major players directly responsible for the pathogenesis of rheumatoid joint destruction. First, synovial mesenchymal cells, internally driven by a transcription factor c-Fos/AP-1, not only directly invade cartilage and bone as a granulation tissue called “pannus” but also release inflammatory cytokine interleukin (IL)-1β. IL-1β induces MMPs and activates osteoclasts. Synovial cells can also present antigen to T cells to drive antigen-specific immune responses. Second, cartilaginous joint matrix can only be degraded after the first attack of collagen fibrils by MMPs, and importantly, most of the MMPs are under the control of c-Fos/AP-1 and IL-1β as well. Third, differentiation of osteoclast is driven internally by NFATc1, where NFATc1 is under the control of TRAF6, c-Fos/AP-1 and osteoclastogenic signaling complex. IL-1β has been shown to induce osteoclastogenesis directly and also indirectly via signaling through RANKL. Therefore, IL-1β and c-Fos/AP-1 influence each other’s gene expression and activity, resulting in an orchestrated cross-talk that is crucial to arthritic joint destruction, and thus, blockade of IL-1β and/or c-Fos/AP-1 can be most promising as a therapeutic target, and in fact, a selective inhibition of c-Fos/AP-1 does resolve arthritic joint destruction. © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2011 |
| abstractGer |
Abstract Synovial mesenchymal cells, matrix metalloproteinases (MMPs), and osteoclasts are the three major players directly responsible for the pathogenesis of rheumatoid joint destruction. First, synovial mesenchymal cells, internally driven by a transcription factor c-Fos/AP-1, not only directly invade cartilage and bone as a granulation tissue called “pannus” but also release inflammatory cytokine interleukin (IL)-1β. IL-1β induces MMPs and activates osteoclasts. Synovial cells can also present antigen to T cells to drive antigen-specific immune responses. Second, cartilaginous joint matrix can only be degraded after the first attack of collagen fibrils by MMPs, and importantly, most of the MMPs are under the control of c-Fos/AP-1 and IL-1β as well. Third, differentiation of osteoclast is driven internally by NFATc1, where NFATc1 is under the control of TRAF6, c-Fos/AP-1 and osteoclastogenic signaling complex. IL-1β has been shown to induce osteoclastogenesis directly and also indirectly via signaling through RANKL. Therefore, IL-1β and c-Fos/AP-1 influence each other’s gene expression and activity, resulting in an orchestrated cross-talk that is crucial to arthritic joint destruction, and thus, blockade of IL-1β and/or c-Fos/AP-1 can be most promising as a therapeutic target, and in fact, a selective inhibition of c-Fos/AP-1 does resolve arthritic joint destruction. © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2011 |
| abstract_unstemmed |
Abstract Synovial mesenchymal cells, matrix metalloproteinases (MMPs), and osteoclasts are the three major players directly responsible for the pathogenesis of rheumatoid joint destruction. First, synovial mesenchymal cells, internally driven by a transcription factor c-Fos/AP-1, not only directly invade cartilage and bone as a granulation tissue called “pannus” but also release inflammatory cytokine interleukin (IL)-1β. IL-1β induces MMPs and activates osteoclasts. Synovial cells can also present antigen to T cells to drive antigen-specific immune responses. Second, cartilaginous joint matrix can only be degraded after the first attack of collagen fibrils by MMPs, and importantly, most of the MMPs are under the control of c-Fos/AP-1 and IL-1β as well. Third, differentiation of osteoclast is driven internally by NFATc1, where NFATc1 is under the control of TRAF6, c-Fos/AP-1 and osteoclastogenic signaling complex. IL-1β has been shown to induce osteoclastogenesis directly and also indirectly via signaling through RANKL. Therefore, IL-1β and c-Fos/AP-1 influence each other’s gene expression and activity, resulting in an orchestrated cross-talk that is crucial to arthritic joint destruction, and thus, blockade of IL-1β and/or c-Fos/AP-1 can be most promising as a therapeutic target, and in fact, a selective inhibition of c-Fos/AP-1 does resolve arthritic joint destruction. © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2011 |
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Pathogenesis of Joint Destruction in Rheumatoid Arthritis |
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Tsumiyama, Ken Yoshida, Kohsuke Hashiramoto, Akira |
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| score |
7.400773 |