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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...
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 rapamycin-insensitive companion...
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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 are of three kinds RI, RII, and RIII. The RI...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

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Related Experiment Videos

Dermatomyositis is characterized by TYK2-dependent STAT3 activation.

M Fornaro1, S Del Vescovo1, F Cacciapaglia2,3

  • 1Unit of Rheumatology, Department of Precision and Regenerative Medicine, Area Jonica (DiMePRe-J), University of Bari, Bari, Italy.

Clinical and Experimental Immunology
|July 8, 2026
PubMed
Summary

Dermatomyositis involves Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway activation. This study found TYK2 inhibition selectively reduced STAT3 activation in dermatomyositis patients, suggesting TYK2 as a therapeutic target.

Keywords:
JAK inhibitorsJAK/STAT pathwaydermatomyositis

Related Experiment Videos

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Dermatomyositis (DM) pathogenesis involves cytokine pathways and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) axis.
  • The specific roles of individual JAK family members in DM remain incompletely understood.
  • Understanding JAK/STAT pathway contributions is crucial for developing targeted therapies for autoimmune diseases.

Purpose of the Study:

  • To investigate the contribution of individual Janus kinase (JAK) family members to signal transducer and activator of transcription 3 (STAT3) activation in dermatomyositis (DM).
  • To compare JAK/STAT pathway activation patterns in DM with those in rheumatoid arthritis (RA), systemic sclerosis (SSc), and healthy donors (HD).
  • To identify potential therapeutic targets within the JAK family for DM treatment.

Main Methods:

  • Peripheral blood mononuclear cells (PBMCs) were isolated from patients with active DM, RA, SSc, and HDs.
  • Phosphorylated STAT3 (pSTAT3) levels were measured using flow cytometry in CD4+ and CD14+ cells.
  • Selective inhibition of JAK1, JAK2, JAK3, and TYK2 was performed using specific inhibitors (abrocitinib, gandotinib, decernotinib, deucravacitinib) to assess their impact on pSTAT3.

Main Results:

  • Patients with active DM exhibited significantly higher basal pSTAT3 levels in CD4+ cells compared to HDs and SSc patients.
  • DM patients showed elevated pSTAT3 in CD14+ cells compared to HDs.
  • Selective TYK2 inhibition, but not other JAK inhibitors, significantly reduced pSTAT3 levels in both CD4+ and CD14+ cells in DM patients, unlike in RA, SSc, or HDs.

Conclusions:

  • A distinct pattern of TYK2-dependent STAT3 activation is identified in circulating immune cells of dermatomyositis patients.
  • This finding differentiates DM from other autoimmune conditions like RA and SSc.
  • TYK2 emerges as a potential targeted therapeutic strategy for managing dermatomyositis.