The small-molecule inhibitor verteporfin suppressed the disease severity in autoimmune mouse models and IL-17A production in T cells from patients with SLE.
Here we demonstrate that IL-17-producing Treg cells (Th17-like cells) increased in peripheral blood of patients with Systemic Lupus Erythematosus (SLE).
These results confirm that the IL-17A -737T/C, -444A/G, -197G/A, and -121G/A SNPs are not risk factors for RA, but the IL-17A TAGA haplotype is a risk factor for SLE.
Hence, IL-17 measurement has no role in SLE disease activity assessments and future studies are needed to search for other reliable activity biomarkers.
In addition, higher levels of plasma IL-10, IFN-γ, TNF-α, and IL-17 along with higher frequencies of circulating plasma and memory B cells were observed in the SLE patients.
Depression in SLE patients increased the release of pro-inflammatory cytokine (IL-6 and IL-17) that in turn generating more autoantibodies and showed strong recognition to 16α-OHE<sub>1</sub>-A.
The results of the study indicate that the activity of CaMK4 could be responsible for glycolysis, which contributes to the production of IL-17, and CaMK4 may contribute to aberrant expression of GLUT1 in T cells from patients with active SLE.
ADSC treatment reduced Akt, mTOR, p70S6K, HIF-1α, and that this inhibition can avert IL-17-induced inflammation, suggesting that ADSC may be a promising treatment for SLE.
Effector CD4<sup>+</sup> T cells with increased IL-17A and reduced IL-2 production contribute to tissue inflammation and organ damage in systemic lupus erythematosus (SLE).
SLE NETs were decorated with tissue factor (TF) and interleukin-17A (IL-17A), which promoted thrombin generation and the fibrotic potential of cultured skin fibroblasts.
Biologic therapies and small-molecule drugs that target IL-17 production are required for the achievement of a favorable clinical effect in SLE patients.
Phosphatase PP2A expression levels are positively correlated to the clinical severity of systemic lupus erythematosus (SLE) and IL17A cytokine overproduction, indicating a potential role of PP2A in controlling T<sub>H</sub>17 differentiation and inflammation.
Increased HERV-E clone 4-1 expression contributes to DNA hypomethylation and IL-17 release from CD4<sup>+</sup> T cells via miR-302d/MBD2 in systemic lupus erythematosus.
We also found that plasma level of IL-17A was positively correlated with SLE disease activities index (SLEDAI) scores and an equation among the level of C3, IgA, IL-17A and SLEDAI scores.