Janus Kinase Inhibitor Baricitinib Modulates Human Innate and Adaptive Immune System

• DOI: 10.3389/fimmu.2018.01510
• Publication Date: 2018-06-28T00:15:12Z
• Authors: Satoshi Kubo; Shingo Nakayamada; Kei Sakata; Yukihiro Kitanaga; Xiaoxue Ma; Seunghyun Lee; Akina Ishii; Kaoru Yamagata; Kazuhisa Nakano; Yoshiya Tanaka
• Keywords: CD86; CD80

The purpose of this study was to elucidate the mechanism action baricitinib on JAK/STAT signaling, which involves in human innate and adaptive immune system. effects were evaluated using monocyte-derived dendritic cells (MoDCs), plasmacytoid (pDCs), B T cells. Baricitinib concentration-dependently suppressed expression CD80/CD86 MoDCs production type-I IFN by pDCs. also differentiation into plasmablasts cell receptor stimuli, inhibited IL-6 from Human CD4+ proliferated after stimulation with anti-CD3 anti-CD28 antibody; however, such proliferation a concentration-dependent manner. In addition, Th1 IL-12 Th17 TGF-β1, IL-6, IL-1β IL-23 stimulation. Tofacitinib showed similar these experiments. naive cells, IFN-α IFN-γ induced phosphorylation STAT1, as well tofacitinib. Furthermore, IL-6-induced STAT1 STAT3 JAK inhibitors. conclusion, results indicated that suppresses plasmablasts, immunity, stimulatory capacity DCs. Thus, inhibitors can be potentially clinically effective not only rheumatoid arthritis but other immune-related diseases.