Related Experiment Video

Updated: Jan 13, 2026

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors
12:40

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

Published on: December 7, 2014

15.2K

Ruxolitinib Suppresses Interferon-γ-Induced JAK/STAT Activation in Oral Keratinocytes

Kim N Stolte1, Anna Fedorova1, Sameh Attia1

  • 1Department of Periodontology, Oral Medicine and Oral Surgery, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Berlin, Germany.

Clinical and Experimental Dental Research
|January 10, 2026
PubMed
Abstract

Insights

The Janus kinase (JAK)/Signal Transducer and Activator of Transcription (STAT) pathway is key in oral inflammation. Ruxolitinib effectively inhibited interferon-gamma (IFN-γ)-induced STAT1 activation and HLA-DRB1 expression in oral keratinocytes, suggesting therapeutic potential.

Area of Science:

  • Oral immunology
  • Molecular biology
  • Inflammation research

Background:

  • The Janus kinase (JAK)/Signal Transducer and Activator of Transcription (STAT) pathway is implicated in oral inflammatory conditions like oral lichen planus and periodontitis.
  • Interferon-gamma (IFN-γ), a pro-inflammatory cytokine, activates the JAK/STAT pathway, contributing to oral inflammation.

Purpose of the Study:

  • To investigate the effect of the JAK1/2 inhibitor ruxolitinib on IFN-γ-induced inflammation in human oral keratinocytes.
  • To assess the impact of ruxolitinib on STAT1 activation and human leukocyte antigen (HLA)-DRB1 expression.

Main Methods:

  • Human oral keratinocytes (OKG4) were stimulated with IFN-γ to induce inflammation.
  • Ruxolitinib was used to inhibit IFN-γ signaling.
  • Western blotting, immunofluorescence microscopy, and cell viability assays were employed to analyze protein expression and cell health.

Main Results:

  • IFN-γ significantly upregulated phosphorylated STAT1 (pSTAT1) and HLA-DRB1 expression in oral keratinocytes.
  • Co-treatment with ruxolitinib effectively suppressed IFN-γ-induced pSTAT1 and HLA-DRB1 upregulation to baseline levels.
  • Ruxolitinib demonstrated no adverse effects on oral keratinocyte viability.

Conclusions:

  • IFN-γ triggers sustained STAT1 activation and HLA-DRB1 upregulation in oral keratinocytes.
  • Ruxolitinib effectively inhibits these IFN-γ-mediated inflammatory responses.
  • Targeting the JAK/STAT pathway with agents like ruxolitinib holds promise for treating oral inflammatory diseases.
Keywords:
Janus kinase inhibitorsJanus kinasesinterferon‐gammalichen planusoral

More Related Videos

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF311:44

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

Published on: January 24, 2016

12.4K
Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production08:32

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

10.9K

Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
11.9K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
10.4K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.3K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
9.8K
Experimental RNAi02:15

Experimental RNAi

RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
7.2K