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Related Concept Videos

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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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.
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Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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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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Related Experiment Video

Updated: Feb 22, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
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Inflammasome lights up in systemic sclerosis.

John Henderson1, Steven O'Reilly2

  • 1Immunology group, Faculty of Health and Life Sciences, Northumbria University, Ellison Building, Newcastle Upon Tyne, Tyne and Wear, NE2 8ST, UK.

Arthritis Research & Therapy
|September 20, 2017
PubMed
Summary
This summary is machine-generated.

Systemic sclerosis (SSc) involves microRNA miR-155, linked to the NLRP3 inflammasome. This discovery connects epigenetic changes and inflammation, offering new therapeutic avenues for SSc.

Keywords:
Caspase-1EpigeneticsFibrosisInflammasomeInterleukin-1MCC950SclerosismicroRNA

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Area of Science:

  • Immunology
  • Epigenetics
  • Fibrosis research

Background:

  • Systemic sclerosis (SSc) is a complex pro-fibrotic disease with unclear origins.
  • Inflammasome signaling pathways are implicated in various inflammatory conditions.
  • MicroRNAs (miRNAs) are recognized as key regulators of gene expression.

Discussion:

  • The study by Artlett et al. highlights the critical role of microRNA miR-155 in SSc pathogenesis.
  • miR-155's activity in SSc is shown to be dependent on the NLRP3 inflammasome.
  • This establishes a novel link between epigenetic regulation (miRNA) and innate immune signaling (inflammasome) in SSc.

Key Insights:

  • MicroRNA miR-155 is a central player in the fibrotic processes of Systemic sclerosis.
  • The NLRP3 inflammasome mediates the pro-fibrotic effects of miR-155 in SSc.
  • This research bridges the gap between epigenetic dysregulation and inflammatory pathways in SSc.

Outlook:

  • The identified miR-155/NLRP3 inflammasome axis presents a promising target for SSc therapies.
  • Developing strategies to modulate miR-155 or NLRP3 could offer new treatment options for SSc patients.
  • Further research into this pathway may elucidate SSc aetiology and identify novel biomarkers.