Session Type: Abstract Submissions (ACR)
A hallmark of systemic autoimmune diseases, such as systemic lupus erythematotsus (SLE), is the increased expression of interferon (IFN) type I inducible genes, the so-called IFN type I signature. Recently, a novel T helper 17 subset (Th17 cells), which produces IL-17A, IL-17F, and IL-22, has also been implicated in autoimmune diseases. We investigated a possible link between these two pro-inflammatory immune pathways in SLE.
25 SLE patients and 15 healthy controls (HC) were included. SLE patients were divided into an IFN type I signature negative (n=9) and positive (n=16) group as assessed by mRNA expression of IFN type I inducible genes. Peripheral expression of Th17 cytokines IL-17A, IL-17F and IL-22 by CD4+CCR6+ memory T cells was measured by flow cytometry and compared between IFN type I signature positive and negative patients and HC.
Increased fraction of IL-17A and IL-17A/IL-17F double producing CCR6+ cells was found in IFN type I positive patients compared with IFN type I negative patients and HC. The expression of IL-17A and IL-17F within CCR6+ cells correlated significantly with IFN scores. In addition, we found a significant correlation between BAFF and IL-21 producing CCR6+ cells.
Here we show for the first time a correlation between IFN type I activation and expression of the Th17 cytokines in SLE patients. These data give new insight into the pathogenesis of SLE with possible implications for treatment.
O. B. J. Corneth,
C. G. van Helden-Meeuwsen,
R. J. E. M. Dolhain,
N. I. Maria,
S. M. J. Paulissen,
J. P. van Hamburg,
P. L. Van Daele,
V. A. Dalm,
M. van Hagen,
M. A. Versnel,
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