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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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T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...
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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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Related Experiment Video

Updated: Aug 1, 2025

Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation
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Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation

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Intrinsic STAT4 Expression Controls Effector CD4 T Cell Migration and Th17 Pathogenicity.

Ashlyn A Buzzelli1, Ian L McWilliams1, Boyoung Shin1

  • 1Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL.

Journal of Immunology (Baltimore, Md. : 1950)
|April 24, 2023
PubMed
Summary
This summary is machine-generated.

Signal transducer and activator of transcription 4 (STAT4) is crucial for CD4 T cell migration and pathogenicity in autoimmune central nervous system (CNS) inflammation. STAT4 controls gene expression in Th17 cells, driving autoimmune responses.

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Area of Science:

  • Immunology
  • Neuroimmunology
  • Molecular Biology

Background:

  • Effector CD4 T cells drive autoimmune chronic inflammatory diseases.
  • STAT4 genetic variations link to autoimmune disorder susceptibility.
  • The role of STAT4 in Th17 cell pathogenicity is unclear.

Purpose of the Study:

  • To investigate the role of STAT4 in CD4 T cell-mediated autoimmune CNS inflammation.
  • To elucidate the function of STAT4 in Th17 cell pathogenicity.

Main Methods:

  • Mouse models of autoimmune CNS inflammation.
  • Transcriptional profiling of Th17 cells.
  • Analysis of CD4 T cell migration.

Main Results:

  • CD4 T cell-intrinsic STAT4 is essential for inducing autoimmune CNS inflammation in mice.
  • STAT4 regulates CD4 T cell migration to the inflamed CNS.
  • STAT4 controls >200 genes in Th17 cells, including those involved in IL-23-stimulated pathogenicity.

Conclusions:

  • STAT4 plays a critical role in Th17 cell pathogenicity.
  • STAT4 is required for Th17 cells to induce autoimmune inflammation.
  • STAT4 represents a novel therapeutic target for Th17-mediated autoimmune diseases.