Literature DB >> 24013646

The JAK inhibitor, tofacitinib, reduces the T cell stimulatory capacity of human monocyte-derived dendritic cells.

Satoshi Kubo1, Kunihiro Yamaoka1, Masahiro Kondo1, Kaoru Yamagata1, Jidong Zhao1, Shigeru Iwata1, Yoshiya Tanaka1.   

Abstract

OBJECTIVE: Tofacitinib, which is a Janus kinase (JAK) inhibitor, has shown clinical effects in the treatment of rheumatoid arthritis. JAKs are important kinases in lymphocyte differentiation; however, their function in dendritic cells (DCs) is unknown. In this study, the function of JAKs in DCs was investigated with tofacitinib.
METHODS: The effects of tofacitinib on the maturation of human monocyte-derived DCs induced by lipopolysaccharide (LPS) stimulation were investigated. In addition, its effects on T cell stimulatory capability was investigated by coculturing with naïve CD45RA-positive T cells.
RESULTS: Tofacitinib decreased expression of CD80/CD86 in a concentration-dependent manner in LPS-stimulated DCs; however, it did not affect HLA-DR expression. Tofacitinib suppressed tumour necrosis factor, interleukin (IL)-6 and IL-1β production without affecting transforming growth factor (TGF)-β and IL-10 production. Meanwhile, CD80/CD86 expression in DCs was enhanced by type I interferon (IFN) stimulation, and the LPS-induced CD80/CD86 expression was inhibited by an antibody to type I IFN receptor. Furthermore, tofacitinib suppressed production of type I IFN and activation of interferon regulatory factor (IRF)-7, which is a transcription factor involved in CD80/CD86 and type I IFN expression. Tofacitinib also decreased the T cell stimulatory capability of DCs and increased expression of indoleamine 2,3-dioxygenase (IDO)-1 and IDO-2.
CONCLUSIONS: Tofacitinib, a JAK1/JAK3 inhibitor, affected the activities of human DCs. It decreased CD80/CD86 expression and T cell stimulatory capability through suppression of type I IFN signalling. These results suggest a novel mode of action for tofacitinib and a pivotal role for JAKs in the differentiation of DCs. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

Entities:  

Keywords:  Cytokines; DMARDs (synthetic); Pharmacokinetics; Rheumatoid Arthritis; Systemic Lupus Erythematosus

Mesh:

Substances:

Year:  2013        PMID: 24013646     DOI: 10.1136/annrheumdis-2013-203756

Source DB:  PubMed          Journal:  Ann Rheum Dis        ISSN: 0003-4967            Impact factor:   19.103


  43 in total

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3.  Comparative efficacy and safety of baricitinib 2 mg and 4 mg in patients with active rheumatoid arthritis : A Bayesian network meta-analysis of randomized controlled trials.

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5.  Reversibility of peripheral blood leukocyte phenotypic and functional changes after exposure to and withdrawal from tofacitinib, a Janus kinase inhibitor, in healthy volunteers.

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Review 6.  Infectious Complications of Biological and Small Molecule Targeted Immunomodulatory Therapies.

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Review 7.  Comparative Efficacy and Safety of Peficitinib 25, 50, 100, and 150 mg in Patients with Active Rheumatoid Arthritis: A Bayesian Network Meta-Analysis of Randomized Controlled Trials.

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9.  Tofacitinib for refractory ocular mucous membrane pemphigoid.

Authors:  Hayley James; Grace L Paley; Richard Brasington; Philip L Custer; Todd P Margolis; Michael A Paley
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Review 10.  Untwining Anti-Tumor and Immunosuppressive Effects of JAK Inhibitors-A Strategy for Hematological Malignancies?

Authors:  Klara Klein; Dagmar Stoiber; Veronika Sexl; Agnieszka Witalisz-Siepracka
Journal:  Cancers (Basel)       Date:  2021-05-26       Impact factor: 6.639

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