Showing papers by "Corinne Miceli-Richard published in 2011"
TL;DR: This study and meta-analysis of the literature confirmed the absence of any functional consequences of the TNF-α -308G/A promoter polymorphism, either alone, or in various haplotype combinations in healthy subjects.
Abstract: The functional consequences of TNF-α promoter SNPs are still controversial and, to date, the functional consequences of TNF-α haplotype combinations in healthy subjects have not been assessed. In order to assess functional consequences of each TNF-α polymorphism and of their haplotype combination, TNF-α expression and secretion by LPS-stimulated monocytes from 50 healthy subjects were assessed. Monocytes were isolated and cultured for four hours, after 100 ng/mL LPS stimulation. mRNA expression was quantified using the real-time polymerase chain reaction, and TNF-α levels were measured by enzyme-linked immunosorbent assay. Each subject was genotyped for TNF-α -857 C/T, -238 G/A, -308 G/A polymorphisms. In order to confirm definitively the functional consequences of these TNF-α polymorphisms, we then performed a systematic review of the literature for TNF-α SNPs, and then a meta-analysis of the functional studies of the TNF-α -308 G/A SNP. No association between TNF-α mRNA or protein level expression, and TNF-α -238G/A, -308G/A, -857C/T polymorphisms, studied either independently or in haplotype combinations, was revealed. Using a meta-analysis for the TNF-α -308 G/A polymorphism, we confirmed the absence of any association between TNF-α mRNA and protein levels, and TNF-α -308 G/A genotypes. This study and meta-analysis of the literature confirmed the absence of any functional consequences of the TNF-α -308G/A promoter polymorphism, either alone, or in various haplotype combinations in healthy subjects.
70 citations
TL;DR: Assessment of the effect of different viruses on various cell types – SGECs but also dendritic cells (DCs) and monocytes – in the induction of BAFF provides additional data suggesting that both dsRNA virus stimulation of DCs and single-stranded RNA virus infection ofSGECs or monocytes can induce BAFF expression, but through a PKR-independent mechanism for these 3 cell types.
Abstract: B cell-activating factor of the TNF family (BAFF) plays a key role in promoting B lymphocyte activation and survival. We previously showed in primary Sjogren’s syndrome that salivary gland epithelial
36 citations
3 citations
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TL;DR: La decouverte de mutations de CARD15 comme etant a l’origine de ce syndrome a permis d’elargir le spectre des manifestations cliniques associees a ces mutations, faisant of ce syndrome une affection tres proche au plan clinique de the sarcoidose.
Abstract: Resume Le syndrome de Blau est une affection granulomateuse rare a transmission autosomale dominante. Les signes cardinaux de cette affection sont une triade regroupant arthrites, eruptions cutanees et uveites. Cependant, la decouverte de mutations de CARD15 comme etant a l’origine de ce syndrome a permis d’elargir le spectre des manifestations cliniques associees a ces mutations, faisant de ce syndrome une affection tres proche au plan clinique de la sarcoidose. CARD15 code pour une proteine de l’immunite innee reconnaissant des structures peptidiques issues d’agents bacteriens a Gram positif ou negatif. Neanmoins, les mutations en cause dans le syndrome de Blau ne sont pas localisees dans le site de reconnaissance par CARD15 de ces agents bacteriens mais sont localisees dans une region du gene conduisant a une oligomerisation spontanee de CARD15 et ainsi une activation de la voie NFkB, observation ayant fait integrer le syndrome de Blau dans le spectre des maladies auto-inflammatoires.