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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

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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.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
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EPS and iPS Cells in Disease Research01:21

EPS and iPS Cells in Disease Research

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Embryonic and induced pluripotent stem cells are excellent models for disease research because of their ability to self-renew and differentiate into most cell types. Somatic cells from a patient are isolated and reprogrammed into induced pluripotent stem cells or iPSCs. These iPSCs are later differentiated into the desired cell type, which mirrors the diseased cell of the patient. In this way, disease models have been created for investigating diseases such as Down syndrome, type I diabetes,...
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iPS Cell Differentiation01:22

iPS Cell Differentiation

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The ability of induced pluripotent stem cells or iPSCs to differentiate into most body cell types has stimulated repair and regenerative medicine research over the past few decades. iPSC-derived blood cells, hepatocytes, beta islet cells, cardiomyocytes, neurons, and other cell types can repair injuries or regenerate damaged tissue in diseases such as diabetes and neurodegenerative disorders.
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Regulation of Hematopoietic Stem Cells01:01

Regulation of Hematopoietic Stem Cells

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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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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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Related Experiment Video

Updated: Feb 17, 2026

Author Spotlight: Insights and Innovations in Gene Expression Manipulation Techniques for Choroid Plexus Research
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Author Spotlight: Insights and Innovations in Gene Expression Manipulation Techniques for Choroid Plexus Research

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Systemic CSF1R Targeting Depletes Pathogenic MPS Bubs and Ameliorates Psoriasis via PPARα-mediated Resolution.

Zhen-Jia Lin1,2, Ying Li1, Yangyinhui Yu1

  • 1Department of Human Anatomy and Physiology and Pain Research Center, Zhongshan School of Medicine and Guangdong Province Key Laboratory of Brain Function and Disease, Sun Yat-sen University, No.74, 2nd Zhongshan Road, Yuexiu District, Guangzhou 510080, China.

Theranostics
|February 16, 2026
PubMed
Summary

Systemic targeting of colony-stimulating factor 1 receptor (CSF1R) disrupts pathogenic mononuclear phagocyte system (MPS) hubs in psoriasis. This approach releases PPAR-alpha, resolving inflammation and offering a novel therapeutic strategy.

Keywords:
CSF1RPPARαinflammationmononuclear phagocyte system (MPS)psoriasis

Related Experiment Videos

Last Updated: Feb 17, 2026

Author Spotlight: Insights and Innovations in Gene Expression Manipulation Techniques for Choroid Plexus Research
04:43

Author Spotlight: Insights and Innovations in Gene Expression Manipulation Techniques for Choroid Plexus Research

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Area of Science:

  • Immunology
  • Dermatology
  • Molecular Biology

Background:

  • Psoriasis involves persistent mononuclear phagocyte system (MPS) activation.
  • The specific roles of colony-stimulating factor 1 receptor (CSF1R) in pathogenic MPS subsets are unclear.

Purpose of the Study:

  • Identify pathogenic CSF1R-high MPS subsets in psoriasis.
  • Characterize their ligand-receptor interactions.
  • Define the CSF1R-PPARα axis in disease pathogenesis.

Main Methods:

  • Integrated human single-cell and spatial transcriptomics.
  • Utilized murine imiquimod-induced psoriasis models.
  • Employed genetic and pharmacologic interventions.

Main Results:

  • A pathogenic CSF1R-high MPS population expanded, forming cytokine hubs (TNF-α, IL-1β, IL-23).
  • CSF1 upregulation amplified MPS activation via autocrine loops.
  • Systemic CSF1R blockade dismantled skin-blood MPS circuits and suppressed cytokines more effectively than local blockade.
  • CSF1R activation suppressed PPARα; CSF1R inhibition's anti-inflammatory effect required PPARα, indicating a downstream role.
  • CSF1R suppression activates PPARα-mediated resolution programs.

Conclusions:

  • A unidirectional CSF1R-PPARα pathogenic axis drives psoriasis inflammation.
  • Systemic CSF1R targeting is necessary to disrupt this circuit.
  • This provides a mechanistic basis for novel psoriasis treatments.