Zobrazeno 1 - 10
of 134
pro vyhledávání: '"Familial chilblain lupus"'
Autor:
Anne Eugster, Denise Müller, Anne Gompf, Susanne Reinhardt, Annett Lindner, Michelle Ashton, Nick Zimmermann, Stefan Beissert, Ezio Bonifacio, Claudia Günther
Publikováno v:
Frontiers in Immunology, Vol 13 (2022)
Externí odkaz:
https://doaj.org/article/7203cfb05b9f4baeb29fa431d030cfb6
Autor:
Anne Eugster, Denise Müller, Anne Gompf, Susanne Reinhardt, Annett Lindner, Michelle Ashton, Nick Zimmermann, Stefan Beissert, Ezio Bonifacio, Claudia Günther
Publikováno v:
Frontiers in Immunology, Vol 13 (2022)
Heterozygous TREX1 mutations are associated with monogenic familial chilblain lupus and represent a risk factor for developing systemic lupus erythematosus. These interferonopathies originate from chronic type I interferon stimulation due to sensing
Externí odkaz:
https://doaj.org/article/817b4a005bfd4d63a3713bff11c81cea
Autor:
Shiyu Zhang, Jiaxing Song, Yuyan Yang, Huilei Miao, Lu Yang, Yuehua Liu, Xue Zhang, Yaping Liu, Tao Wang
Publikováno v:
Pediatric Rheumatology Online Journal, Vol 19, Iss 1, Pp 1-8 (2021)
Abstract Background Type I interferonopathies are a group of rare autoimmune diseases characterised by excessive activation of type I interferon that leads to disturbances in immune function. Three prime repair exonuclease 1 (TREX1) is an important e
Externí odkaz:
https://doaj.org/article/cc5cd8cdd6f4424c86122fb35818ebf9
Publikováno v:
Pediatric Rheumatology Online Journal, Vol 18, Iss 1, Pp 1-7 (2020)
Abstract Background Familial chilblain lupus (FCL) is a rare, chronic form of cutaneous lupus erythematosus, which is characterized by painful bluish-red inflammatory cutaneous lesions in acral locations. Mutations in TREX1, SAMHD1 and STING have bee
Externí odkaz:
https://doaj.org/article/7d096424476c4470a14578344fc0372b
Autor:
Eugster, A., Müller, D., Gompf, A., Reinhardt, S., Lindner, A., Ashton, M.P., Zimmermann, N., Beissert, S., Bonifacio, E., Günther, C.
Publikováno v:
Front. Immunol. 13:897500 (2022)
Heterozygous TREX1 mutations are associated with monogenic familial chilblain lupus and represent a risk factor for developing systemic lupus erythematosus. These interferonopathies originate from chronic type I interferon stimulation due to sensing
Autor:
Tao Wang, Yuyan Yang, Xue Zhang, Yuehua Liu, Yaping Liu, Jiaxing Song, Lu Yang, Huilei Miao, Shiyu Zhang
Publikováno v:
Pediatric Rheumatology Online Journal, Vol 19, Iss 1, Pp 1-8 (2021)
Pediatric Rheumatology Online Journal
Pediatric Rheumatology Online Journal
Background Type I interferonopathies are a group of rare autoimmune diseases characterised by excessive activation of type I interferon that leads to disturbances in immune function. Three prime repair exonuclease 1 (TREX1) is an important exonucleas
Autor:
Gómez-Arias, Pedro Jesús, Gómez-García, Francisco, Hernández-Parada, Jorge, Montilla-López, Ana María, Ruano, Juan, Parra-Peralbo, Esmeralda
Importance Type I interferon (IFN)-mediated monogenic autoinflammatory disorders (interferonopathies) are childhood-onset rare multisystemic diseases with limited treatment options. The Janus kinase (JAK) inhibitors are promising potential therapeuti
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=od______2636::38b6799c1f83164a5bacecbcf6dee16c
https://hdl.handle.net/10668/4440
https://hdl.handle.net/10668/4440
Autor:
Juan Ruano, Francisco Gómez-García, Esmeralda Parra-Peralbo, Pedro Jesús Gómez-Arias, Ana María Montilla-López, Jorge Hernández-Parada
Publikováno v:
Dermatology and Therapy
Importance Type I interferon (IFN)-mediated monogenic autoinflammatory disorders (interferonopathies) are childhood-onset rare multisystemic diseases with limited treatment options. The Janus kinase (JAK) inhibitors are promising potential therapeuti
Publikováno v:
Pediatric Rheumatology Online Journal, Vol 18, Iss 1, Pp 1-7 (2020)
Pediatric Rheumatology Online Journal
Pediatric Rheumatology Online Journal
Background Familial chilblain lupus (FCL) is a rare, chronic form of cutaneous lupus erythematosus, which is characterized by painful bluish-red inflammatory cutaneous lesions in acral locations. Mutations in TREX1, SAMHD1 and STING have been describ
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