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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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Related Experiment Video

Updated: Aug 11, 2025

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis
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The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis

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AIM2 and Psoriasis.

Yuxi Zhang1,2,3,4, Xiaoqing Xu1,2,3,4, Hui Cheng1,2,3,4

  • 1Department of Dermatology, The First Affiliated Hospital, Anhui Medical University, Hefei, Anhui, China.

Frontiers in Immunology
|February 6, 2023
PubMed
Summary
This summary is machine-generated.

Absent in melanoma 2 (AIM2) is a key gene in psoriasis development, influencing inflammation and immune cell function. Understanding AIM2

Keywords:
AIM2epigeneticinflammasomekeratinocytespsoriasistrained immunity

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Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture
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Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture
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Area of Science:

  • Dermatology and Immunology
  • Molecular Biology
  • Genetics

Background:

  • Psoriasis is a global chronic inflammatory skin disease with significant impacts on patient quality of life.
  • Its pathogenesis involves environmental, genetic, epigenetic factors, and immune/non-immune cell dysregulation.
  • Absent in melanoma 2 (AIM2) is a psoriasis susceptibility locus found in psoriatic keratinocytes.

Purpose of the Study:

  • To review the characteristics of AIM2.
  • To elucidate the mechanisms by which AIM2 mediates psoriasis development.
  • To explore AIM2's role in psoriasis recurrence via trained immunity.

Main Methods:

  • Literature review of studies on AIM2 and psoriasis.
  • Analysis of AIM2's inflammasome-dependent and -independent functions.
  • Examination of AIM2's involvement in immune regulation and cell programming.

Main Results:

  • AIM2 activation releases IL-1β and IL-18, driving inflammation.
  • AIM2 regulates regulatory T(Treg) cell function and keratinocyte cell death/proliferation.
  • AIM2 may contribute to psoriasis recurrence through trained immunity.

Conclusions:

  • AIM2 is a critical factor in psoriasis pathogenesis and progression.
  • AIM2's multifaceted roles in inflammation and immune modulation are central to the disease.
  • Targeting AIM2 pathways could offer novel therapeutic strategies for psoriasis.