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1.
J Eur Acad Dermatol Venereol ; 37(5): 1056-1063, 2023 May.
Artigo em Inglês | MEDLINE | ID: mdl-36732052

RESUMO

BACKGROUND: Although ocular adverse events are frequent in AD patients treated with dupilumab, their characterization remains limited due to a lack of prospective studies with a systematic ophthalmological examination. OBJECTIVE: To examine the incidence, characteristics and risk factors of dupilumab-induced ocular adverse events. METHODS: A prospective, multicenter, and real-life study in adult AD patients treated with dupilumab. RESULTS: At baseline, 27 out of 181 patients (14.9%) had conjunctivitis. At week 16 (W16), 25 out of 27 had improved their conjunctivitis and 2 remained stable and 34 out of 181 patients (18.7%) had dupilumab-induced blepharoconjunctivitis: either de novo (n = 32) or worsening of underlying blepharoconjunctivitis (n = 2). Most events (27/34; 79.4%) were moderate. A multivariate analysis showed that head and neck AD (OR = 7.254; 95%CI [1.938-30.07]; p = 0.004), erythroderma (OR = 5.635; 95%CI [1.635-21.50]; p = 0.007) and the presence of dry eye syndrome at baseline (OR = 3.51; 95%CI [3.158-13.90]; p = 0.031) were independent factors associated with dupilumab-induced blepharoconjunctivitis. LIMITATIONS: Our follow-up period was 16 weeks and some late-onset time effects may still occur. CONCLUSION: This study showed that most dupilumab-induced blepharoconjunctivitis cases are de novo. AD severity and conjunctivitis at baseline were not found to be associated risk factors in this study.


Assuntos
Conjuntivite , Dermatite Atópica , Adulto , Humanos , Dermatite Atópica/tratamento farmacológico , Dermatite Atópica/diagnóstico , Estudos Prospectivos , Anticorpos Monoclonais Humanizados/efeitos adversos , Conjuntivite/induzido quimicamente , Conjuntivite/epidemiologia , Índice de Gravidade de Doença , Resultado do Tratamento
2.
Neurosci Lett ; 630: 209-215, 2016 Sep 06.
Artigo em Inglês | MEDLINE | ID: mdl-27478014

RESUMO

The purpose of this study was to investigate the in vitro effect of Suppressor Of Cytokine Signaling 1 (SOCS1) overexpression in retinal pigment epithelium (RPE) cells on their activation by pro-inflammatory cytokines IFNγ, TNFα and IL-17. Retinal pigment epithelium cells (ARPE-19) were stably transfected with the control plasmid pIRES2-AcGFP1 or the plasmid pSOCS1-IRES2-AcGFP1. They were stimulated by IFNγ (150ng/ml), TNFα (30ng/ml) or IL-17 (100ng/ml). The levels of SOCS1 mRNA were measured by real-time PCR. Signal Transducer and Activator of Transcription 1 (STAT1) phosphorylation and IκBα expression were analysed by western Blot (WB). IL-8 secretion was analysed by ELISA and expression of MHCII molecules and ICAM-1/CD54 by flow cytometry. Our data show that SOCS1 mRNA overexpression in RPE cells prevents IFNγ-induced SOCS1 mRNA increase and IFNγ-mediated STAT1 phosphorylation. Moreover, SOCS1 overexpression in RPE cells inhibits IFNγ-induced decrease of IL-8 secretion and prevents IFNγ-induced MHC II and ICAM1/CD54 upregulation. However, SOCS1 overexpression does not affect TNFα-induced IκBα degradation nor block TNFα-induced or IL-17-induced IL-8 secretion. On the contrary, IL-17-induced secretion is increased by SOCS1 overexpression. In conclusion, SOCS1 overexpression in RPE cells inhibits some IFNγ-mediated responses that lead to uveitis development. This notion raises the possibility that SOCS1 overexpression could be a novel target for treating non-infectious uveitis. However, some proinflammatory effects of TNFα and IL-17 stimulation on RPE are not blocked by SOCS1 overexpression.


Assuntos
Citocinas/metabolismo , Epitélio Pigmentado da Retina/metabolismo , Proteína 1 Supressora da Sinalização de Citocina/metabolismo , Uveíte/metabolismo , Células Cultivadas , Antígenos de Histocompatibilidade Classe II/metabolismo , Humanos , Molécula 1 de Adesão Intercelular/metabolismo , Interferon gama/metabolismo , Interleucina-17/metabolismo , Interleucina-8/metabolismo , Inibidor de NF-kappaB alfa/metabolismo , Fosforilação , RNA Mensageiro/metabolismo , Fator de Transcrição STAT1 , Fator de Necrose Tumoral alfa/metabolismo
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