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T-helper 17 cell cytokines and interferon type I: partners in crime in systemic lupus erythematosus? #MMPMID24598455
Brkic Z; Corneth OB; van Helden-Meeuwsen CG; Dolhain RJ; Maria NI; Paulissen SM; Davelaar N; van Hamburg JP; van Daele PL; Dalm VA; van Hagen PM; Hazes JM; Versnel MA; Lubberts E
Arthritis Res Ther 2014[Mar]; 16 (2): R62 PMID24598455show ga
INTRODUCTION: A hallmark of systemic autoimmune diseases like systemic lupus erythematosus (SLE) is the increased expression of interferon (IFN) type I inducible genes, so-called IFN type I signature. Recently, T-helper 17 subset (Th17 cells), which produces IL-17A, IL-17F, IL-21, and IL-22, has been implicated in SLE. As CCR6 enriches for Th17 cells, we used this approach to investigate whether CCR6(+) memory T-helper cells producing IL-17A, IL-17F, IL-21, and/or IL-22 are increased in SLE patients and whether this increase is related to the presence of IFN type I signature. METHODS: In total, 25 SLE patients and 15 healthy controls (HCs) were included. SLE patients were divided into IFN type I signature-positive (IFN(+)) (n = 16) and negative (IFN(-)) (n = 9) patients, as assessed by mRNA expression of IFN-inducible genes (IFIGs) in monocytes. Expression of IL-17A, IL-17F, IL-21, and IL-22 by CD4(+)CD45RO(+)CCR6(+) T cells (CCR6(+) cells) was measured with flow cytometry and compared between IFN(+), IFN(-) patients and HCs. RESULTS: Increased percentages of IL-17A and IL-17A/IL-17F double-producing CCR6(+) cells were observed in IFN(+) patients compared with IFN(-) patients and HCs. IL-17A and IL-17F expression within CCR6(+) cells correlated significantly with IFIG expression. In addition, we found significant correlation between B-cell activating factor of the tumor necrosis family (BAFF)-a factor strongly correlating with IFN type I - and IL-21 producing CCR6(+) cells. CONCLUSIONS: We show for the first time higher percentages of IL-17A and IL-17A/IL-17F double-producing CCR6(+) memory T-helper cells in IFN(+) SLE patients, supporting the hypothesis that IFN type I co-acts with Th17 cytokines in SLE pathogenesis.
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Arthritis+Res+Ther 2014 ; 16 (2): R62
