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Marc Ittah

Researcher at University of Paris-Sud

Publications -  17
Citations -  2262

Marc Ittah is an academic researcher from University of Paris-Sud. The author has contributed to research in topics: B-cell activating factor & Interferon. The author has an hindex of 16, co-authored 17 publications receiving 2109 citations.

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Activation of IFN pathways and plasmacytoid dendritic cell recruitment in target organs of primary Sjögren’s syndrome

TL;DR: The results support the pathogenic interaction between the innate and adaptive immune system in pSS, and the persistence of the IFN signature might be related to a vicious circle, in which the environment interacts with genetic factors to drive the stimulation of salivary TLRs.
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Tolerance and efficacy of rituximab and changes in serum B cell biomarkers in patients with systemic complications of primary Sjögren’s syndrome

TL;DR: Good efficacy and fair tolerance of rituximab for systemic symptoms in patients with primary Sjögren’s syndrome are shown, and RTX allows for a marked reduction in corticosteroid use.
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B cell-activating factor of the tumor necrosis factor family (BAFF) is expressed under stimulation by interferon in salivary gland epithelial cells in primary Sjögren's syndrome.

TL;DR: Demonstrating the capacity of SGECs to express and secrete BAFF after IFN stimulation adds further information to the pivotal role of these epithelial cells in the pathogenesis of pSS, possibly after stimulation by innate immunity.
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Increased levels of circulating microparticles in primary Sjögren's syndrome, systemic lupus erythematosus and rheumatoid arthritis and relation with disease activity

TL;DR: Plasma MP level is elevated in primary Sjögren's syndrome, as well as in SLE and RA, and could be used as a biomarker reflecting systemic cell activation, and increase of platelet-derived MPs, sCD40L and sCD62P, highlights platelet activation in pSS.
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Increase of B cell-activating factor of the TNF family (BAFF) after rituximab treatment: insights into a new regulating system of BAFF production

TL;DR: Two distinct mechanisms are probably involved in the increase in BAFF level after B cell depletion: (1) the decrease in its receptors leading to a release of BAFF; (2) a delayed regulation of BAff mRNA transcription.