JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation.

ABSTRACT:

Background

We previously reported that JAK-STAT-pathway mediated regulation of IFN-regulatory factor genes could play an important role in SLE pathogenesis. Here, we evaluated the efficacy of the JAK inhibitor tofacitinib (TOFA) for controlling IFN signalling via the JAK-STAT pathway and as a therapeutic for SLE.

Results

We treated NZB/NZW F1 mice with TOFA and assessed alterations in their disease, pathological, and immunological conditions. Gene-expression results obtained from CD4⁺ T cells (SLE mice) and CD3⁺ T cells (human SLE patients) were measured by DNA microarray and qRT-PCR. TOFA treatment resulted in reduced levels of anti-dsDNA antibodies, decreased proteinuria, and amelioration of nephritis as compared with those observed in control animals

SUBMITTER: Ikeda K 

PROVIDER: S-EPMC5568047 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature