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Videos de Conceptos Relacionados

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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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...
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Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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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...
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Regulation of Angiogenesis and Blood Supply01:24

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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Inflammatory Response01:28

Inflammatory Response

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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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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.
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Updated: Jan 10, 2026

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries
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Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

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La inhibición de la señalización JAK-STAT suprime las respuestas inmunes patógenas en la vasculitis vascular media y

Hui Zhang1, Ryu Watanabe1, Gerald J Berry2

  • 1Department of Medicine, Division of Immunology and Rheumatology (H.Z., R.W., J.J.G., C.M.W.).

Circulation
|December 20, 2017
PubMed
Resumen

Tofacitinib, un inhibidor de la Janus quinasa (JAK), suprime eficazmente la inflamación crónica en la arteritis de células gigantes al dirigirse a las células T y reducir el daño vascular. Este tratamiento minimiza las células T de memoria residentes en el tejido e inhibe las vías clave que impulsan la vasculitis.

Palabras clave:
Las cinasas de JanusFactores de transcripción STATLos linfocitos TLas citocinasArteriitis por células gigantesinflamaciónEnfermedad de las venas

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Área de la Ciencia:

  • Inmunología
  • Medicina cardiovascular
  • Reumatología

Sus antecedentes:

  • La arteritis de células gigantes (GCA) es una vasculitis autoinmune crónica que afecta a las arterias grandes, lo que lleva a complicaciones como aneurismas y oclusiones.
  • La inflamación persistente en el GCA involucra células T efectoras y células T de memoria residentes en el tejido, lo que contribuye a la vasculitis crónica a pesar del tratamiento con corticosteroides.
  • La inflamación impulsa la neoangiogénesis microvascular y la hiperplasia íntima, comprometiendo la integridad arterial.

Objetivo del estudio:

  • Investigar si las células T lesionadas, incluidas las células T de memoria residentes en el tejido, mantienen una inflamación persistente en el GCA.
  • Para determinar la sensibilidad de estas células T al tofacitinib, un inhibidor de Janus kinase (JAK) dirigido a JAK3 y JAK1.

Principales métodos:

  • Las arterias humanas de pacientes con GCA fueron injertadas en ratones inmunodeficientes y reconstituidas con células inmunes del paciente.
  • Los ratones con arterias inflamadas fueron tratados con tofacitinib o con un control de vehículo.
  • La inflamación vascular, la expresión de genes y proteínas y las poblaciones de células inmunes se analizaron utilizando RT-PCR, inmunohistoquímica y citometría de flujo.

Principales resultados:

  • Tofacitinib suprime significativamente la inmunidad innata y adaptativa dentro de la pared arterial.
  • Las células T lesionales mostraron una reducción de la proliferación y la producción de moléculas efectoras (IFN-γ, IL-17, IL-21) tras el tratamiento con tofacitinib.
  • Tofacitinib inhibió la angiogénesis adventicial, redujo la hiperplasia íntima y disminuyó las células T de memoria CD4 + CD103 + residentes en el tejido.

Conclusiones:

  • La señalización de citocinas a través de JAK3 y JAK1 es crucial para la inflamación crónica en las arterias grandes afectadas por GCA.
  • El inhibidor JAK tofacitinib suprime eficazmente las células T de memoria residentes en el tejido y las vías vasculitogénicas clave en el GCA.
  • Tofacitinib demuestra potencial como agente terapéutico para el manejo de la inflamación arterial crónica en el GCA.