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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...
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...

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Related Experiment Video

Updated: Jun 23, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

Adiposity-Associated Monocyte Costimulatory Programming in Rheumatoid Arthritis Identified by Single-Cell

Shalini N Swamy, Hua Zhong, Kylie Williams

    Medrxiv : the Preprint Server for Health Sciences
    |June 22, 2026
    PubMed
    Summary
    This summary is machine-generated.

    Obesity amplifies immune activation in rheumatoid arthritis (RA) by enhancing monocyte costimulatory pathways. This metabolic dysregulation may worsen RA disease activity and outcomes.

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    Area of Science:

    • Immunology
    • Rheumatology
    • Metabolic disease

    Background:

    • Rheumatoid arthritis (RA) is a chronic inflammatory disease with significant morbidity.
    • Obesity is linked to increased RA disease activity and poorer long-term outcomes.
    • Understanding the link between adiposity and immune dysregulation is crucial for refining RA treatments.

    Purpose of the Study:

    • To investigate how adiposity influences monocyte programming in rheumatoid arthritis.
    • To determine if obesity enhances monocyte costimulatory signaling, promoting adaptive immune activation in RA.

    Main Methods:

    • Single-cell RNA sequencing of circulating monocytes from 16 RA patients and 15 controls.
    • Analysis of transcriptomic profiles to identify monocyte populations and pathway enrichment.
    • Statistical evaluation of associations between disease status, body mass index (BMI), and immune activation pathways.

    Main Results:

    • RA monocytes showed enrichment in antigen processing and presentation pathways.
    • Higher BMI in RA patients correlated with increased enrichment of T-cell costimulatory pathways.
    • Specific costimulatory molecules (CD86, ICOSLG, TNFSF4) showed patterns consistent with inducible signaling.

    Conclusions:

    • Metabolic dysregulation, particularly obesity, amplifies monocyte-mediated immune activation in RA.
    • This amplified immune activation may contribute to more severe RA disease activity and outcomes.