Dysregulation of Type 1 Interferon Signaling in Systemic Sclerosis: a Promising Therapeutic Target?

ABSTRACT:

Purpose of review

There are several lines of evidence at the genetic and gene expression levels linking type I interferon (IFN) activation to systemic sclerosis (SSc) pathogenesis. Herein, we summarize the potential role of type I IFN signaling components as therapeutic targets.

Recent findings

All type I IFN cytokines signal through the interferon-α/β receptor (IFNAR). Early phase studies indicate that anifrolumab (a human monoclonal antibody against IFNAR subunit 1) has an acceptable safety profile and can attenuate transforming growth factor beta (TGF-β)-mediated fibrosis in SSc skin, supporting its further clinical development. Janus kinase (JAK) signaling pathways are downstream from IFNAR. Building on their efficacy in hereditary interferonopathies, JAK inhibitors have

SUBMITTER: Wu M 

PROVIDER: S-EPMC9187215 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature