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Autoimmune Regulator Deficiency Results in a Decrease in STAT1 Levels in Human Monocytes.

Ofer Zimmerman1, Lindsey B Rosen1, Muthulekha Swamydas1

  • 1Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Immunology, National Institutes of Health, Bethesda, MD, United States.

Frontiers in Immunology
|August 4, 2017
PubMed
Summary
This summary is machine-generated.

Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) patients have lower STAT1 protein and phosphorylation levels in monocytes, unlike STAT1 gain-of-function mutations. This finding contrasts with previous research on immune regulation in APECED.

Keywords:
AIREAPECEDCD14+ monocytesIFN-γSTAT1chronic mucocutaneous candidiasisphosphorylation

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Area of Science:

  • Immunology
  • Genetics
  • Molecular Biology

Background:

  • Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a rare primary immunodeficiency linked to AIRE mutations, causing chronic mucocutaneous candidiasis and autoimmunity.
  • STAT1 gain-of-function mutations also lead to similar symptoms, with elevated STAT1 activity.
  • AIRE interacts with protein inhibitor of activated STAT1, suggesting a regulatory link to STAT1.

Purpose of the Study:

  • To investigate whether APECED patients exhibit altered STAT1 protein and phosphorylation levels in CD14+ monocytes.
  • To compare STAT1 signaling in APECED patients with that in healthy controls and patients with STAT1 gain-of-function mutations.

Main Methods:

  • Peripheral blood mononuclear cells were isolated from 8 APECED patients and 13 healthy controls.
  • Levels of STAT1 protein, STAT1 tyrosine phosphorylation (pSTAT1), and STAT1 mRNA were assessed at rest and after interferon-gamma (IFN-γ) stimulation.
  • Monocyte surface expression of IFN-γ receptor 2 and autoantibodies to type I IFN were also analyzed.

Main Results:

  • APECED patients showed a significant ~20% decrease in mean STAT1 protein levels in CD14+ monocytes, both at rest and after IFN-γ stimulation.
  • The mean peak level of IFN-γ-induced pSTAT1 was also significantly ~20% lower in APECED patients compared to healthy controls.
  • This decrease correlated with autoantibodies to type I IFN and reduced IFN-γ receptor 2 expression, not with decreased STAT1 mRNA or anti-IFN-γ autoantibodies.

Conclusions:

  • APECED patients exhibit a moderate but significant decrease in total STAT1 protein and lower peak pSTAT1 levels following IFN-γ stimulation.
  • This contrasts with STAT1 gain-of-function mutations, suggesting a distinct mechanism of immune dysregulation in APECED.
  • The findings highlight a novel aspect of STAT1 pathway modulation in APECED, potentially linked to type I IFN autoimmunity.