Fiche publication
Date publication
décembre 2015
Journal
Scientific reports
Auteurs
Membres identifiés du Cancéropôle Est :
Pr AUBIN François
,
Pr VABRES Pierre
,
Pr ANTONICELLI Franck
Tous les auteurs :
Plée J, Le Jan S, Giustiniani J, Barbe C, Joly P, Bedane C, Vabres P, Truchetet F, Aubin F, Antonicelli F, Bernard P
Lien Pubmed
Résumé
Bullous pemphigoid (BP) is an inflammatory autoimmune bullous disease involving cytokines and proteases in the process of blister formation. Recently, IL-17 and IL-23 were evidenced in lesional skin and serum of BP patients at time of diagnosis, but their involvement in disease outcome has still not been investigated yet. We then analysed IL-17 and IL-23 serum levels during the first months of follow-up upon treatment. Compared with age- and sex- matched controls, high levels of IL-23 were observed at baseline in BP patients serum (P < 0.01), while IL-17 levels was not. However, some BP patients expressed high IL-17 serum level, independently of disease severity. In these patients, those with ongoing remission reduced IL-17 concentration upon treatment (P < 0.001), whereas IL-17 level remained elevated in patients who relapsed. Meanwhile, IL-23 serum levels increased during the first month of treatment in BP patients who later relapsed (P < 0.01) and MMP-9 serum level was not controlled. Accordingly, we found that both IL-17 and IL-23 increased MMP-9 secretion from leukocytes in-vitro. Then, we showed that elevated IL-17/IL-23 serum concentrations helped to discriminate BP patients who later relapsed. Such uncontrolled inflammatory response raises the question whether these molecules could become biological target for BP patients resistant to steroid treatment.
Mots clés
Aged, Aged, 80 and over, Autoantibodies, blood, Biomarkers, Cytokines, blood, Female, Follow-Up Studies, Humans, Interleukin-17, blood, Interleukin-23, blood, Male, Matrix Metalloproteinase 9, secretion, Patient Outcome Assessment, Pemphigoid, Bullous, blood, Prognosis, Recurrence
Référence
Sci Rep. 2015 Dec;5:18001