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Related Concept Videos

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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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The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
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ICER is requisite for Th17 differentiation.

Nobuya Yoshida1, Denis Comte1,2, Masayuki Mizui1

  • 1Division of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.

Nature Communications
|September 30, 2016
PubMed
Summary

Inducible cAMP early repressor (ICER) drives Th17 cell development and autoimmunity. Blocking ICER in mice protected against autoimmune diseases, suggesting ICER as a therapeutic target.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Autoimmunity

Background:

  • Inducible cAMP early repressor (ICER) is a known transcriptional repressor.
  • The role of ICER in T helper 17 (Th17) cell differentiation and its contribution to autoimmune diseases remain largely unexplored.

Purpose of the Study:

  • To investigate the role of ICER in Th17 cell biology and its involvement in the pathogenesis of autoimmune diseases.
  • To determine if ICER could serve as a therapeutic target for autoimmune conditions.

Main Methods:

  • Investigated ICER expression in Th17 cells via the IL-6-STAT3 pathway.
  • Analyzed ICER binding to the Il17a promoter and its effect on RORγt accumulation.
  • Utilized in vitro differentiation of naive ICER/CREM-deficient CD4+ T cells.
  • Employed ICER/CREM-deficient B6.lpr mice models for autoimmunity studies, including anti-glomerular basement membrane-induced glomerulonephritis and experimental encephalomyelitis.
  • Examined ICER expression in CD4+ T cells from patients with systemic lupus erythematosus.

Main Results:

  • ICER is predominantly expressed in Th17 cells, facilitated by the IL-6-STAT3 pathway.
  • ICER binds to the Il17a promoter, promoting RORγt accumulation and Th17 cell differentiation.
  • Impaired Th17 differentiation in ICER/CREM-deficient cells was rescued by ICER overexpression.
  • ICER/CREM-deficient mice showed protection against developing autoimmunity, including glomerulonephritis and experimental encephalomyelitis.
  • Elevated ICER levels were observed in CD4+ T cells from systemic lupus erythematosus patients.

Conclusions:

  • ICER plays a critical role in Th17 cell-dependent autoimmunity.
  • ICER influences both organ-specific and systemic autoimmune diseases.
  • ICER represents a potential therapeutic target for managing autoimmune disorders.