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Related Concept Videos

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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EPS and iPS Cells in Disease Research

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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Related Experiment Video

Updated: Jul 4, 2026

Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture
10:31

Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture

Published on: April 8, 2016

Uncovering a Dual Th17/Type 2 Transcriptomic Endotype in Psoriasis.

Chung-Han Chen1, Meng-Sui Lee2, Wen-Yu Chang3

  • 1Department of Dermatology, National Taiwan University Hospital and National Taiwan University College of Medicine.

Journal of the American Academy of Dermatology
|July 2, 2026
PubMed
Summary

Taiwanese psoriasis shows a dual immune response involving Th17 and Type 2 pathways, with high IL-36 activation. This finding highlights the need for tailored psoriasis treatments in this population.

Keywords:
Interleukin-36PsoriasisTh17/Th2 dual endotypeTranscriptomics

Related Experiment Videos

Last Updated: Jul 4, 2026

Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture
10:31

Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture

Published on: April 8, 2016

Area of Science:

  • Dermatology and Immunology
  • Transcriptomics
  • Molecular Biology

Background:

  • The IL-23/Th17 axis is central to psoriasis, but ethnic variations in its molecular profile are not well understood.
  • Psoriasis pathogenesis involves complex immune dysregulation, necessitating deeper molecular characterization across diverse populations.

Purpose of the Study:

  • To define the immunological and pathogenic transcriptomic profiles of a Taiwanese psoriasis cohort.
  • To identify molecular differences and potential biomarkers for psoriasis severity in Taiwanese individuals.

Main Methods:

  • Bulk RNA-sequencing of lesional skin (LS), non-lesional skin (NL), and normal skin (N) from psoriasis patients and healthy controls.
  • Differential gene expression (DEG) analysis, Gene Set Enrichment Analysis (GSEA), and correlation analysis with Psoriasis Area and Severity Index (PASI) scores.
  • ELISA validation of serum cytokine levels in a larger cohort of psoriasis patients and controls.

Main Results:

  • Identified 4,694 differentially expressed genes (DEGs) in lesional vs. normal skin, confirming Th17 pathway activation (IL-17A/C, IL-23A).
  • Revealed a significant dual immune dysregulation with upregulation of Type 2 (Th2) signatures (IL-4R, CCL17, TSLP) and extreme IL-36 family activation (IL-36G).
  • Observed downregulation of skin barrier genes (KRT77, GJB4) and identified IL-36RN and AREG/CDSN as potential psoriasis severity biomarkers.

Conclusions:

  • Taiwanese psoriasis exhibits a unique dual Th17/Type 2 endotype with pronounced IL-36 pathway activation.
  • Transcriptomic findings suggest the need for ethnicity-specific therapeutic strategies for psoriasis.
  • Limitations include a small sample size and focus on a single ethnic group, with findings representing associations rather than direct causality.