SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases

The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered wi...
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Autor*in:	Regina Larionova [verfasserIn] K. Byvaltsev [verfasserIn] Оlga Kravtsova [verfasserIn] Elena Takha [verfasserIn] Sergei Petrov [verfasserIn] Gevorg Kazarian [verfasserIn] Anna Valeeva [verfasserIn] Eduard Shuralev [verfasserIn] Malik Mukminov [verfasserIn] Yves Renaudineau [verfasserIn] Marina Arleevskaya [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	SARS-Cov2 Infection Rheumatoid arthritis Systemic lupus erythematosus Risk factors Inflammation

Übergeordnetes Werk:	In: Journal of Translational Autoimmunity - Elsevier, 2020, 5(2022), Seite 100154-
Übergeordnetes Werk:	volume:5 ; year:2022 ; pages:100154-

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.jtauto.2022.100154

Katalog-ID:	DOAJ083335358

Internformat


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520			\|a The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN–I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development.
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650		4	\|a Rheumatoid arthritis
650		4	\|a Systemic lupus erythematosus
650		4	\|a Risk factors
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653		0	\|a Immunologic diseases. Allergy
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700	0		\|a Yves Renaudineau \|e verfasserin \|4 aut
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allfields	10.1016/j.jtauto.2022.100154 doi (DE-627)DOAJ083335358 (DE-599)DOAJ0fd7fd7a2146472e9a5a2072d5e0bc9f DE-627 ger DE-627 rakwb eng RC581-607 Regina Larionova verfasserin aut SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN–I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development. SARS-Cov2 Infection Rheumatoid arthritis Systemic lupus erythematosus Risk factors Inflammation Immunologic diseases. Allergy K. Byvaltsev verfasserin aut Оlga Kravtsova verfasserin aut Elena Takha verfasserin aut Sergei Petrov verfasserin aut Gevorg Kazarian verfasserin aut Anna Valeeva verfasserin aut Eduard Shuralev verfasserin aut Malik Mukminov verfasserin aut Yves Renaudineau verfasserin aut Marina Arleevskaya verfasserin aut In Journal of Translational Autoimmunity Elsevier, 2020 5(2022), Seite 100154- (DE-627)1691028606 25899090 nnns volume:5 year:2022 pages:100154- https://doi.org/10.1016/j.jtauto.2022.100154 kostenfrei https://doaj.org/article/0fd7fd7a2146472e9a5a2072d5e0bc9f kostenfrei http://www.sciencedirect.com/science/article/pii/S2589909022000156 kostenfrei https://doaj.org/toc/2589-9090 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 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_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 5 2022 100154-
spelling	10.1016/j.jtauto.2022.100154 doi (DE-627)DOAJ083335358 (DE-599)DOAJ0fd7fd7a2146472e9a5a2072d5e0bc9f DE-627 ger DE-627 rakwb eng RC581-607 Regina Larionova verfasserin aut SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN–I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development. SARS-Cov2 Infection Rheumatoid arthritis Systemic lupus erythematosus Risk factors Inflammation Immunologic diseases. Allergy K. Byvaltsev verfasserin aut Оlga Kravtsova verfasserin aut Elena Takha verfasserin aut Sergei Petrov verfasserin aut Gevorg Kazarian verfasserin aut Anna Valeeva verfasserin aut Eduard Shuralev verfasserin aut Malik Mukminov verfasserin aut Yves Renaudineau verfasserin aut Marina Arleevskaya verfasserin aut In Journal of Translational Autoimmunity Elsevier, 2020 5(2022), Seite 100154- (DE-627)1691028606 25899090 nnns volume:5 year:2022 pages:100154- https://doi.org/10.1016/j.jtauto.2022.100154 kostenfrei https://doaj.org/article/0fd7fd7a2146472e9a5a2072d5e0bc9f kostenfrei http://www.sciencedirect.com/science/article/pii/S2589909022000156 kostenfrei https://doaj.org/toc/2589-9090 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 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_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 5 2022 100154-
allfields_unstemmed	10.1016/j.jtauto.2022.100154 doi (DE-627)DOAJ083335358 (DE-599)DOAJ0fd7fd7a2146472e9a5a2072d5e0bc9f DE-627 ger DE-627 rakwb eng RC581-607 Regina Larionova verfasserin aut SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN–I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development. SARS-Cov2 Infection Rheumatoid arthritis Systemic lupus erythematosus Risk factors Inflammation Immunologic diseases. Allergy K. Byvaltsev verfasserin aut Оlga Kravtsova verfasserin aut Elena Takha verfasserin aut Sergei Petrov verfasserin aut Gevorg Kazarian verfasserin aut Anna Valeeva verfasserin aut Eduard Shuralev verfasserin aut Malik Mukminov verfasserin aut Yves Renaudineau verfasserin aut Marina Arleevskaya verfasserin aut In Journal of Translational Autoimmunity Elsevier, 2020 5(2022), Seite 100154- (DE-627)1691028606 25899090 nnns volume:5 year:2022 pages:100154- https://doi.org/10.1016/j.jtauto.2022.100154 kostenfrei https://doaj.org/article/0fd7fd7a2146472e9a5a2072d5e0bc9f kostenfrei http://www.sciencedirect.com/science/article/pii/S2589909022000156 kostenfrei https://doaj.org/toc/2589-9090 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 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_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 5 2022 100154-
allfieldsGer	10.1016/j.jtauto.2022.100154 doi (DE-627)DOAJ083335358 (DE-599)DOAJ0fd7fd7a2146472e9a5a2072d5e0bc9f DE-627 ger DE-627 rakwb eng RC581-607 Regina Larionova verfasserin aut SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN–I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development. SARS-Cov2 Infection Rheumatoid arthritis Systemic lupus erythematosus Risk factors Inflammation Immunologic diseases. Allergy K. Byvaltsev verfasserin aut Оlga Kravtsova verfasserin aut Elena Takha verfasserin aut Sergei Petrov verfasserin aut Gevorg Kazarian verfasserin aut Anna Valeeva verfasserin aut Eduard Shuralev verfasserin aut Malik Mukminov verfasserin aut Yves Renaudineau verfasserin aut Marina Arleevskaya verfasserin aut In Journal of Translational Autoimmunity Elsevier, 2020 5(2022), Seite 100154- (DE-627)1691028606 25899090 nnns volume:5 year:2022 pages:100154- https://doi.org/10.1016/j.jtauto.2022.100154 kostenfrei https://doaj.org/article/0fd7fd7a2146472e9a5a2072d5e0bc9f kostenfrei http://www.sciencedirect.com/science/article/pii/S2589909022000156 kostenfrei https://doaj.org/toc/2589-9090 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 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_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 5 2022 100154-
allfieldsSound	10.1016/j.jtauto.2022.100154 doi (DE-627)DOAJ083335358 (DE-599)DOAJ0fd7fd7a2146472e9a5a2072d5e0bc9f DE-627 ger DE-627 rakwb eng RC581-607 Regina Larionova verfasserin aut SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN–I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development. SARS-Cov2 Infection Rheumatoid arthritis Systemic lupus erythematosus Risk factors Inflammation Immunologic diseases. Allergy K. Byvaltsev verfasserin aut Оlga Kravtsova verfasserin aut Elena Takha verfasserin aut Sergei Petrov verfasserin aut Gevorg Kazarian verfasserin aut Anna Valeeva verfasserin aut Eduard Shuralev verfasserin aut Malik Mukminov verfasserin aut Yves Renaudineau verfasserin aut Marina Arleevskaya verfasserin aut In Journal of Translational Autoimmunity Elsevier, 2020 5(2022), Seite 100154- (DE-627)1691028606 25899090 nnns volume:5 year:2022 pages:100154- https://doi.org/10.1016/j.jtauto.2022.100154 kostenfrei https://doaj.org/article/0fd7fd7a2146472e9a5a2072d5e0bc9f kostenfrei http://www.sciencedirect.com/science/article/pii/S2589909022000156 kostenfrei https://doaj.org/toc/2589-9090 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 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_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 5 2022 100154-
language	English
source	In Journal of Translational Autoimmunity 5(2022), Seite 100154- volume:5 year:2022 pages:100154-
sourceStr	In Journal of Translational Autoimmunity 5(2022), Seite 100154- volume:5 year:2022 pages:100154-
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	SARS-Cov2 Infection Rheumatoid arthritis Systemic lupus erythematosus Risk factors Inflammation Immunologic diseases. Allergy
isfreeaccess_bool	true
container_title	Journal of Translational Autoimmunity
authorswithroles_txt_mv	Regina Larionova @@aut@@ K. Byvaltsev @@aut@@ Оlga Kravtsova @@aut@@ Elena Takha @@aut@@ Sergei Petrov @@aut@@ Gevorg Kazarian @@aut@@ Anna Valeeva @@aut@@ Eduard Shuralev @@aut@@ Malik Mukminov @@aut@@ Yves Renaudineau @@aut@@ Marina Arleevskaya @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	1691028606
id	DOAJ083335358
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">DOAJ083335358</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230311020825.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230311s2022 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.jtauto.2022.100154</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ083335358</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ0fd7fd7a2146472e9a5a2072d5e0bc9f</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC581-607</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Regina Larionova</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). 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callnumber-first	R - Medicine
author	Regina Larionova
spellingShingle	Regina Larionova misc RC581-607 misc SARS-Cov2 misc Infection misc Rheumatoid arthritis misc Systemic lupus erythematosus misc Risk factors misc Inflammation misc Immunologic diseases. Allergy SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases
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topic_title	RC581-607 SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases SARS-Cov2 Infection Rheumatoid arthritis Systemic lupus erythematosus Risk factors Inflammation
topic	misc RC581-607 misc SARS-Cov2 misc Infection misc Rheumatoid arthritis misc Systemic lupus erythematosus misc Risk factors misc Inflammation misc Immunologic diseases. Allergy
topic_unstemmed	misc RC581-607 misc SARS-Cov2 misc Infection misc Rheumatoid arthritis misc Systemic lupus erythematosus misc Risk factors misc Inflammation misc Immunologic diseases. Allergy
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title	SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases
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title_full	SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases
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author_browse	Regina Larionova K. Byvaltsev Оlga Kravtsova Elena Takha Sergei Petrov Gevorg Kazarian Anna Valeeva Eduard Shuralev Malik Mukminov Yves Renaudineau Marina Arleevskaya
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title_sort	sars-cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases
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title_auth	SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases
abstract	The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN–I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development.
abstractGer	The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN–I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development.
abstract_unstemmed	The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN–I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development.
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title_short	SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases
url	https://doi.org/10.1016/j.jtauto.2022.100154 https://doaj.org/article/0fd7fd7a2146472e9a5a2072d5e0bc9f http://www.sciencedirect.com/science/article/pii/S2589909022000156 https://doaj.org/toc/2589-9090
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SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases

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