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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.
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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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Related Experiment Video

Updated: Feb 23, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
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IL-23R-activated STAT3/STAT4 is essential for Th1/Th17-mediated CNS autoimmunity.

Priscilla W Lee1,2, Alan J Smith3, Yuhong Yang4

  • 1Department of Microbial Infection and Immunity.

JCI Insight
|September 8, 2017
PubMed
Summary

Cytokines IL-6 and IL-12 induce IL-23 receptor expression, driving pathogenic T cell differentiation in CNS autoimmunity. STAT4 signaling is crucial for this process, impacting autoimmune disease development.

Keywords:
AutoimmunityCytokinesImmunologyMultiple sclerosisT cells

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Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
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Area of Science:

  • Immunology
  • Neuroimmunology
  • Autoimmunity

Background:

  • Factors driving pathogenic T cell differentiation in autoimmune diseases remain unclear.
  • Previous studies using genetically modified mice yielded contradictory findings on molecules involved in autoimmunity.
  • Understanding minimal signals for encephalitogenic T cell development is critical for CNS autoimmunity research.

Purpose of the Study:

  • To define the minimum cytokine signals required for the development of encephalitogenic T cells.
  • To investigate the role of IL-23 signaling and its downstream effectors (STAT3, STAT4) in CNS autoimmunity.
  • To correlate findings in mouse models with human T cells from multiple sclerosis patients.

Main Methods:

  • Differentiating myelin-specific T cells with various cytokine cocktails (IL-6+IL-23, IL-12+IL-23).
  • Assessing pathogenicity by transferring differentiated T cells into recipient mice.
  • Analyzing STAT3 and STAT4 signaling pathways, including receptor expression and phosphorylation.
  • Examining CD4+ memory T cells from multiple sclerosis patients for STAT3/STAT4 activation.

Main Results:

  • IL-6+IL-23 and IL-12+IL-23 cytokine combinations generated encephalitogenic T cells.
  • Both IL-6 and IL-12 induced IL-23 receptor expression on naive T cells (mouse and human).
  • IL-23 signaling involved both STAT3 and STAT4; STAT4 disruption impaired CNS autoimmunity independently of IL-12.
  • STAT4-deficient mice were resistant to CNS autoimmunity, unlike IL-12-deficient mice.
  • Multiple sclerosis patient T cells showed elevated p-STAT3/p-STAT4 levels, with heterodimers upon IL-23 signaling.

Conclusions:

  • IL-23 signaling via STAT3 and STAT4 orchestrates pathogenic T cell generation in CNS autoimmunity.
  • This mechanism operates irrespective of the Th1 or Th17 T cell phenotype.
  • Findings explain differential susceptibility in IL-12 and STAT4 deficient models.
  • Targeting IL-23/STAT4 pathways may offer therapeutic strategies for CNS autoimmune diseases.