Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice

Background Peptidylarginine deiminase type 4 (PADI4) has been identified as a susceptibility gene for rheumatoid arthritis (RA) by genome-wide association studies. PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in...
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Autor*in:	Suzuki, Akari [verfasserIn] Kochi, Yuta Shoda, Hirofumi Seri, Yu Fujio, Keishi Sawada, Tetsuji Yamada, Ryo Yamamoto, Kazuhiko

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Peptidylarginine deiminase type 4 Rheumatoid arthritis Collagen-induced arthritis mice TNF-α Citrullination

Anmerkung:	© Suzuki et al. 2016

Übergeordnetes Werk:	Enthalten in: BMC musculoskeletal disorders - London : BioMed Central, 2000, 17(2016), 1 vom: 05. Mai
Übergeordnetes Werk:	volume:17 ; year:2016 ; number:1 ; day:05 ; month:05

Links:	Volltext

DOI / URN:	10.1186/s12891-016-1055-2

Katalog-ID:	SPR028036425

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245	1	0	\|a Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice
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520			\|a Background Peptidylarginine deiminase type 4 (PADI4) has been identified as a susceptibility gene for rheumatoid arthritis (RA) by genome-wide association studies. PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in RA because it is a target antigen for anti-citrullinated peptide antibodies, and only PADs (translated proteins from PADI genes) can provide peptidyl citrulline via the modification of protein substrates. The aim of this study was to evaluate the importance of the PADI4 gene in the progression of RA. Methods We generated Padi4 knockout ($ Padi4^{−/−} $) DBA1J mice. The $ Padi4^{−/−} $ DBA1J and wild-type mice were immunized with bovine type II collagen (CII) to develop collagen-induced arthritis (CIA). The expression of various inflammatory cytokines and Padi genes in immune cells was detected by the real-time TaqMan assay. Cytokine concentrations in sera were measured by enzyme-linked immunosorbent assays. Localization of the PAD4 and PAD2 proteins was indicated by immunohistochemistry. Results We demonstrated that the clinical disease score was significantly decreased in the $ Padi4^{−/−} $ mice and Padi4 expression was induced by CII immunization. In the $ Padi4^{−/−} $ mice, serum anti-type II collagen (CII) immunoglobulin M (IgM), IgG, and inflammatory cytokine levels were significantly decreased compared with those in the wild-type mice. Padi2 expression was induced in the immune cells of the $ Padi4^{−/−} $ mice as a compensation for the defect in Padi4. Conclusions Padi4 affected disease severity in the CIA mice and was involved in the enhancement of the collagen-initiated inflammatory responses.
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700	1		\|a Yamamoto, Kazuhiko \|4 aut
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publishDate	2016
allfields	10.1186/s12891-016-1055-2 doi (DE-627)SPR028036425 (SPR)s12891-016-1055-2-e DE-627 ger DE-627 rakwb eng Suzuki, Akari verfasserin aut Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Suzuki et al. 2016 Background Peptidylarginine deiminase type 4 (PADI4) has been identified as a susceptibility gene for rheumatoid arthritis (RA) by genome-wide association studies. PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in RA because it is a target antigen for anti-citrullinated peptide antibodies, and only PADs (translated proteins from PADI genes) can provide peptidyl citrulline via the modification of protein substrates. The aim of this study was to evaluate the importance of the PADI4 gene in the progression of RA. Methods We generated Padi4 knockout ($ Padi4^{−/−} $) DBA1J mice. The $ Padi4^{−/−} $ DBA1J and wild-type mice were immunized with bovine type II collagen (CII) to develop collagen-induced arthritis (CIA). The expression of various inflammatory cytokines and Padi genes in immune cells was detected by the real-time TaqMan assay. Cytokine concentrations in sera were measured by enzyme-linked immunosorbent assays. Localization of the PAD4 and PAD2 proteins was indicated by immunohistochemistry. Results We demonstrated that the clinical disease score was significantly decreased in the $ Padi4^{−/−} $ mice and Padi4 expression was induced by CII immunization. In the $ Padi4^{−/−} $ mice, serum anti-type II collagen (CII) immunoglobulin M (IgM), IgG, and inflammatory cytokine levels were significantly decreased compared with those in the wild-type mice. Padi2 expression was induced in the immune cells of the $ Padi4^{−/−} $ mice as a compensation for the defect in Padi4. Conclusions Padi4 affected disease severity in the CIA mice and was involved in the enhancement of the collagen-initiated inflammatory responses. Peptidylarginine deiminase type 4 (dpeaa)DE-He213 Rheumatoid arthritis (dpeaa)DE-He213 Collagen-induced arthritis mice (dpeaa)DE-He213 TNF-α (dpeaa)DE-He213 Citrullination (dpeaa)DE-He213 Kochi, Yuta aut Shoda, Hirofumi aut Seri, Yu aut Fujio, Keishi aut Sawada, Tetsuji aut Yamada, Ryo aut Yamamoto, Kazuhiko aut Enthalten in BMC musculoskeletal disorders London : BioMed Central, 2000 17(2016), 1 vom: 05. Mai (DE-627)326643745 (DE-600)2041355-5 1471-2474 nnns volume:17 year:2016 number:1 day:05 month:05 https://dx.doi.org/10.1186/s12891-016-1055-2 kostenfrei 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2016 1 05 05
spelling	10.1186/s12891-016-1055-2 doi (DE-627)SPR028036425 (SPR)s12891-016-1055-2-e DE-627 ger DE-627 rakwb eng Suzuki, Akari verfasserin aut Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Suzuki et al. 2016 Background Peptidylarginine deiminase type 4 (PADI4) has been identified as a susceptibility gene for rheumatoid arthritis (RA) by genome-wide association studies. PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in RA because it is a target antigen for anti-citrullinated peptide antibodies, and only PADs (translated proteins from PADI genes) can provide peptidyl citrulline via the modification of protein substrates. The aim of this study was to evaluate the importance of the PADI4 gene in the progression of RA. Methods We generated Padi4 knockout ($ Padi4^{−/−} $) DBA1J mice. The $ Padi4^{−/−} $ DBA1J and wild-type mice were immunized with bovine type II collagen (CII) to develop collagen-induced arthritis (CIA). The expression of various inflammatory cytokines and Padi genes in immune cells was detected by the real-time TaqMan assay. Cytokine concentrations in sera were measured by enzyme-linked immunosorbent assays. Localization of the PAD4 and PAD2 proteins was indicated by immunohistochemistry. Results We demonstrated that the clinical disease score was significantly decreased in the $ Padi4^{−/−} $ mice and Padi4 expression was induced by CII immunization. In the $ Padi4^{−/−} $ mice, serum anti-type II collagen (CII) immunoglobulin M (IgM), IgG, and inflammatory cytokine levels were significantly decreased compared with those in the wild-type mice. Padi2 expression was induced in the immune cells of the $ Padi4^{−/−} $ mice as a compensation for the defect in Padi4. Conclusions Padi4 affected disease severity in the CIA mice and was involved in the enhancement of the collagen-initiated inflammatory responses. Peptidylarginine deiminase type 4 (dpeaa)DE-He213 Rheumatoid arthritis (dpeaa)DE-He213 Collagen-induced arthritis mice (dpeaa)DE-He213 TNF-α (dpeaa)DE-He213 Citrullination (dpeaa)DE-He213 Kochi, Yuta aut Shoda, Hirofumi aut Seri, Yu aut Fujio, Keishi aut Sawada, Tetsuji aut Yamada, Ryo aut Yamamoto, Kazuhiko aut Enthalten in BMC musculoskeletal disorders London : BioMed Central, 2000 17(2016), 1 vom: 05. Mai (DE-627)326643745 (DE-600)2041355-5 1471-2474 nnns volume:17 year:2016 number:1 day:05 month:05 https://dx.doi.org/10.1186/s12891-016-1055-2 kostenfrei 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2016 1 05 05
allfields_unstemmed	10.1186/s12891-016-1055-2 doi (DE-627)SPR028036425 (SPR)s12891-016-1055-2-e DE-627 ger DE-627 rakwb eng Suzuki, Akari verfasserin aut Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Suzuki et al. 2016 Background Peptidylarginine deiminase type 4 (PADI4) has been identified as a susceptibility gene for rheumatoid arthritis (RA) by genome-wide association studies. PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in RA because it is a target antigen for anti-citrullinated peptide antibodies, and only PADs (translated proteins from PADI genes) can provide peptidyl citrulline via the modification of protein substrates. The aim of this study was to evaluate the importance of the PADI4 gene in the progression of RA. Methods We generated Padi4 knockout ($ Padi4^{−/−} $) DBA1J mice. The $ Padi4^{−/−} $ DBA1J and wild-type mice were immunized with bovine type II collagen (CII) to develop collagen-induced arthritis (CIA). The expression of various inflammatory cytokines and Padi genes in immune cells was detected by the real-time TaqMan assay. Cytokine concentrations in sera were measured by enzyme-linked immunosorbent assays. Localization of the PAD4 and PAD2 proteins was indicated by immunohistochemistry. Results We demonstrated that the clinical disease score was significantly decreased in the $ Padi4^{−/−} $ mice and Padi4 expression was induced by CII immunization. In the $ Padi4^{−/−} $ mice, serum anti-type II collagen (CII) immunoglobulin M (IgM), IgG, and inflammatory cytokine levels were significantly decreased compared with those in the wild-type mice. Padi2 expression was induced in the immune cells of the $ Padi4^{−/−} $ mice as a compensation for the defect in Padi4. Conclusions Padi4 affected disease severity in the CIA mice and was involved in the enhancement of the collagen-initiated inflammatory responses. Peptidylarginine deiminase type 4 (dpeaa)DE-He213 Rheumatoid arthritis (dpeaa)DE-He213 Collagen-induced arthritis mice (dpeaa)DE-He213 TNF-α (dpeaa)DE-He213 Citrullination (dpeaa)DE-He213 Kochi, Yuta aut Shoda, Hirofumi aut Seri, Yu aut Fujio, Keishi aut Sawada, Tetsuji aut Yamada, Ryo aut Yamamoto, Kazuhiko aut Enthalten in BMC musculoskeletal disorders London : BioMed Central, 2000 17(2016), 1 vom: 05. Mai (DE-627)326643745 (DE-600)2041355-5 1471-2474 nnns volume:17 year:2016 number:1 day:05 month:05 https://dx.doi.org/10.1186/s12891-016-1055-2 kostenfrei 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2016 1 05 05
allfieldsGer	10.1186/s12891-016-1055-2 doi (DE-627)SPR028036425 (SPR)s12891-016-1055-2-e DE-627 ger DE-627 rakwb eng Suzuki, Akari verfasserin aut Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Suzuki et al. 2016 Background Peptidylarginine deiminase type 4 (PADI4) has been identified as a susceptibility gene for rheumatoid arthritis (RA) by genome-wide association studies. PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in RA because it is a target antigen for anti-citrullinated peptide antibodies, and only PADs (translated proteins from PADI genes) can provide peptidyl citrulline via the modification of protein substrates. The aim of this study was to evaluate the importance of the PADI4 gene in the progression of RA. Methods We generated Padi4 knockout ($ Padi4^{−/−} $) DBA1J mice. The $ Padi4^{−/−} $ DBA1J and wild-type mice were immunized with bovine type II collagen (CII) to develop collagen-induced arthritis (CIA). The expression of various inflammatory cytokines and Padi genes in immune cells was detected by the real-time TaqMan assay. Cytokine concentrations in sera were measured by enzyme-linked immunosorbent assays. Localization of the PAD4 and PAD2 proteins was indicated by immunohistochemistry. Results We demonstrated that the clinical disease score was significantly decreased in the $ Padi4^{−/−} $ mice and Padi4 expression was induced by CII immunization. In the $ Padi4^{−/−} $ mice, serum anti-type II collagen (CII) immunoglobulin M (IgM), IgG, and inflammatory cytokine levels were significantly decreased compared with those in the wild-type mice. Padi2 expression was induced in the immune cells of the $ Padi4^{−/−} $ mice as a compensation for the defect in Padi4. Conclusions Padi4 affected disease severity in the CIA mice and was involved in the enhancement of the collagen-initiated inflammatory responses. Peptidylarginine deiminase type 4 (dpeaa)DE-He213 Rheumatoid arthritis (dpeaa)DE-He213 Collagen-induced arthritis mice (dpeaa)DE-He213 TNF-α (dpeaa)DE-He213 Citrullination (dpeaa)DE-He213 Kochi, Yuta aut Shoda, Hirofumi aut Seri, Yu aut Fujio, Keishi aut Sawada, Tetsuji aut Yamada, Ryo aut Yamamoto, Kazuhiko aut Enthalten in BMC musculoskeletal disorders London : BioMed Central, 2000 17(2016), 1 vom: 05. Mai (DE-627)326643745 (DE-600)2041355-5 1471-2474 nnns volume:17 year:2016 number:1 day:05 month:05 https://dx.doi.org/10.1186/s12891-016-1055-2 kostenfrei 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2016 1 05 05
allfieldsSound	10.1186/s12891-016-1055-2 doi (DE-627)SPR028036425 (SPR)s12891-016-1055-2-e DE-627 ger DE-627 rakwb eng Suzuki, Akari verfasserin aut Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Suzuki et al. 2016 Background Peptidylarginine deiminase type 4 (PADI4) has been identified as a susceptibility gene for rheumatoid arthritis (RA) by genome-wide association studies. PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in RA because it is a target antigen for anti-citrullinated peptide antibodies, and only PADs (translated proteins from PADI genes) can provide peptidyl citrulline via the modification of protein substrates. The aim of this study was to evaluate the importance of the PADI4 gene in the progression of RA. Methods We generated Padi4 knockout ($ Padi4^{−/−} $) DBA1J mice. The $ Padi4^{−/−} $ DBA1J and wild-type mice were immunized with bovine type II collagen (CII) to develop collagen-induced arthritis (CIA). The expression of various inflammatory cytokines and Padi genes in immune cells was detected by the real-time TaqMan assay. Cytokine concentrations in sera were measured by enzyme-linked immunosorbent assays. Localization of the PAD4 and PAD2 proteins was indicated by immunohistochemistry. Results We demonstrated that the clinical disease score was significantly decreased in the $ Padi4^{−/−} $ mice and Padi4 expression was induced by CII immunization. In the $ Padi4^{−/−} $ mice, serum anti-type II collagen (CII) immunoglobulin M (IgM), IgG, and inflammatory cytokine levels were significantly decreased compared with those in the wild-type mice. Padi2 expression was induced in the immune cells of the $ Padi4^{−/−} $ mice as a compensation for the defect in Padi4. Conclusions Padi4 affected disease severity in the CIA mice and was involved in the enhancement of the collagen-initiated inflammatory responses. Peptidylarginine deiminase type 4 (dpeaa)DE-He213 Rheumatoid arthritis (dpeaa)DE-He213 Collagen-induced arthritis mice (dpeaa)DE-He213 TNF-α (dpeaa)DE-He213 Citrullination (dpeaa)DE-He213 Kochi, Yuta aut Shoda, Hirofumi aut Seri, Yu aut Fujio, Keishi aut Sawada, Tetsuji aut Yamada, Ryo aut Yamamoto, Kazuhiko aut Enthalten in BMC musculoskeletal disorders London : BioMed Central, 2000 17(2016), 1 vom: 05. Mai (DE-627)326643745 (DE-600)2041355-5 1471-2474 nnns volume:17 year:2016 number:1 day:05 month:05 https://dx.doi.org/10.1186/s12891-016-1055-2 kostenfrei 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2016 1 05 05
language	English
source	Enthalten in BMC musculoskeletal disorders 17(2016), 1 vom: 05. Mai volume:17 year:2016 number:1 day:05 month:05
sourceStr	Enthalten in BMC musculoskeletal disorders 17(2016), 1 vom: 05. Mai volume:17 year:2016 number:1 day:05 month:05
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Peptidylarginine deiminase type 4 Rheumatoid arthritis Collagen-induced arthritis mice TNF-α Citrullination
isfreeaccess_bool	true
container_title	BMC musculoskeletal disorders
authorswithroles_txt_mv	Suzuki, Akari @@aut@@ Kochi, Yuta @@aut@@ Shoda, Hirofumi @@aut@@ Seri, Yu @@aut@@ Fujio, Keishi @@aut@@ Sawada, Tetsuji @@aut@@ Yamada, Ryo @@aut@@ Yamamoto, Kazuhiko @@aut@@
publishDateDaySort_date	2016-05-05T00:00:00Z
hierarchy_top_id	326643745
id	SPR028036425
language_de	englisch
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PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in RA because it is a target antigen for anti-citrullinated peptide antibodies, and only PADs (translated proteins from PADI genes) can provide peptidyl citrulline via the modification of protein substrates. The aim of this study was to evaluate the importance of the PADI4 gene in the progression of RA. Methods We generated Padi4 knockout ($ Padi4^{−/−} $) DBA1J mice. The $ Padi4^{−/−} $ DBA1J and wild-type mice were immunized with bovine type II collagen (CII) to develop collagen-induced arthritis (CIA). The expression of various inflammatory cytokines and Padi genes in immune cells was detected by the real-time TaqMan assay. Cytokine concentrations in sera were measured by enzyme-linked immunosorbent assays. Localization of the PAD4 and PAD2 proteins was indicated by immunohistochemistry. Results We demonstrated that the clinical disease score was significantly decreased in the $ Padi4^{−/−} $ mice and Padi4 expression was induced by CII immunization. In the $ Padi4^{−/−} $ mice, serum anti-type II collagen (CII) immunoglobulin M (IgM), IgG, and inflammatory cytokine levels were significantly decreased compared with those in the wild-type mice. Padi2 expression was induced in the immune cells of the $ Padi4^{−/−} $ mice as a compensation for the defect in Padi4. 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author	Suzuki, Akari
spellingShingle	Suzuki, Akari misc Peptidylarginine deiminase type 4 misc Rheumatoid arthritis misc Collagen-induced arthritis mice misc TNF-α misc Citrullination Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice
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topic_title	Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice Peptidylarginine deiminase type 4 (dpeaa)DE-He213 Rheumatoid arthritis (dpeaa)DE-He213 Collagen-induced arthritis mice (dpeaa)DE-He213 TNF-α (dpeaa)DE-He213 Citrullination (dpeaa)DE-He213
topic	misc Peptidylarginine deiminase type 4 misc Rheumatoid arthritis misc Collagen-induced arthritis mice misc TNF-α misc Citrullination
topic_unstemmed	misc Peptidylarginine deiminase type 4 misc Rheumatoid arthritis misc Collagen-induced arthritis mice misc TNF-α misc Citrullination
topic_browse	misc Peptidylarginine deiminase type 4 misc Rheumatoid arthritis misc Collagen-induced arthritis mice misc TNF-α misc Citrullination
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title	Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice
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title_full	Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice
author_sort	Suzuki, Akari
journal	BMC musculoskeletal disorders
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author_browse	Suzuki, Akari Kochi, Yuta Shoda, Hirofumi Seri, Yu Fujio, Keishi Sawada, Tetsuji Yamada, Ryo Yamamoto, Kazuhiko
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title_sort	decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice
title_auth	Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice
abstract	Background Peptidylarginine deiminase type 4 (PADI4) has been identified as a susceptibility gene for rheumatoid arthritis (RA) by genome-wide association studies. PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in RA because it is a target antigen for anti-citrullinated peptide antibodies, and only PADs (translated proteins from PADI genes) can provide peptidyl citrulline via the modification of protein substrates. The aim of this study was to evaluate the importance of the PADI4 gene in the progression of RA. Methods We generated Padi4 knockout ($ Padi4^{−/−} $) DBA1J mice. The $ Padi4^{−/−} $ DBA1J and wild-type mice were immunized with bovine type II collagen (CII) to develop collagen-induced arthritis (CIA). The expression of various inflammatory cytokines and Padi genes in immune cells was detected by the real-time TaqMan assay. Cytokine concentrations in sera were measured by enzyme-linked immunosorbent assays. Localization of the PAD4 and PAD2 proteins was indicated by immunohistochemistry. Results We demonstrated that the clinical disease score was significantly decreased in the $ Padi4^{−/−} $ mice and Padi4 expression was induced by CII immunization. In the $ Padi4^{−/−} $ mice, serum anti-type II collagen (CII) immunoglobulin M (IgM), IgG, and inflammatory cytokine levels were significantly decreased compared with those in the wild-type mice. Padi2 expression was induced in the immune cells of the $ Padi4^{−/−} $ mice as a compensation for the defect in Padi4. Conclusions Padi4 affected disease severity in the CIA mice and was involved in the enhancement of the collagen-initiated inflammatory responses. © Suzuki et al. 2016
abstractGer	Background Peptidylarginine deiminase type 4 (PADI4) has been identified as a susceptibility gene for rheumatoid arthritis (RA) by genome-wide association studies. PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in RA because it is a target antigen for anti-citrullinated peptide antibodies, and only PADs (translated proteins from PADI genes) can provide peptidyl citrulline via the modification of protein substrates. The aim of this study was to evaluate the importance of the PADI4 gene in the progression of RA. Methods We generated Padi4 knockout ($ Padi4^{−/−} $) DBA1J mice. The $ Padi4^{−/−} $ DBA1J and wild-type mice were immunized with bovine type II collagen (CII) to develop collagen-induced arthritis (CIA). The expression of various inflammatory cytokines and Padi genes in immune cells was detected by the real-time TaqMan assay. Cytokine concentrations in sera were measured by enzyme-linked immunosorbent assays. Localization of the PAD4 and PAD2 proteins was indicated by immunohistochemistry. Results We demonstrated that the clinical disease score was significantly decreased in the $ Padi4^{−/−} $ mice and Padi4 expression was induced by CII immunization. In the $ Padi4^{−/−} $ mice, serum anti-type II collagen (CII) immunoglobulin M (IgM), IgG, and inflammatory cytokine levels were significantly decreased compared with those in the wild-type mice. Padi2 expression was induced in the immune cells of the $ Padi4^{−/−} $ mice as a compensation for the defect in Padi4. Conclusions Padi4 affected disease severity in the CIA mice and was involved in the enhancement of the collagen-initiated inflammatory responses. © Suzuki et al. 2016
abstract_unstemmed	Background Peptidylarginine deiminase type 4 (PADI4) has been identified as a susceptibility gene for rheumatoid arthritis (RA) by genome-wide association studies. PADI4 is highly expressed in the bone marrow, macrophages, neutrophils, and monocytes. Peptidyl citrulline is an interesting molecule in RA because it is a target antigen for anti-citrullinated peptide antibodies, and only PADs (translated proteins from PADI genes) can provide peptidyl citrulline via the modification of protein substrates. The aim of this study was to evaluate the importance of the PADI4 gene in the progression of RA. Methods We generated Padi4 knockout ($ Padi4^{−/−} $) DBA1J mice. The $ Padi4^{−/−} $ DBA1J and wild-type mice were immunized with bovine type II collagen (CII) to develop collagen-induced arthritis (CIA). The expression of various inflammatory cytokines and Padi genes in immune cells was detected by the real-time TaqMan assay. Cytokine concentrations in sera were measured by enzyme-linked immunosorbent assays. Localization of the PAD4 and PAD2 proteins was indicated by immunohistochemistry. Results We demonstrated that the clinical disease score was significantly decreased in the $ Padi4^{−/−} $ mice and Padi4 expression was induced by CII immunization. In the $ Padi4^{−/−} $ mice, serum anti-type II collagen (CII) immunoglobulin M (IgM), IgG, and inflammatory cytokine levels were significantly decreased compared with those in the wild-type mice. Padi2 expression was induced in the immune cells of the $ Padi4^{−/−} $ mice as a compensation for the defect in Padi4. Conclusions Padi4 affected disease severity in the CIA mice and was involved in the enhancement of the collagen-initiated inflammatory responses. © Suzuki et al. 2016
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title_short	Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice
url	https://dx.doi.org/10.1186/s12891-016-1055-2
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Decreased severity of experimental autoimmune arthritis in peptidylarginine deiminase type 4 knockout mice

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