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Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
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Single-cell Analysis of Immunophenotype and Cytokine Production in Peripheral Whole Blood via Mass Cytometry
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Distinct interferon signatures and cytokine patterns define additional systemic autoinflammatory diseases.

Adriana A de Jesus1, Yangfeng Hou2, Stephen Brooks3

  • 1Translational Autoinflammatory Diseases Section (TADS), NIAID/NIH, Bethesda, Maryland, USA.

The Journal of Clinical Investigation
|December 25, 2019
PubMed
Summary

This study identifies an interferon signature (IRG-S) in undifferentiated systemic autoinflammatory diseases (USAIDs), revealing new subtypes like IL-18-mediated PAP and recurrent MAS, NEMO-NDAS, and SAMD9L-SAAD for targeted therapies.

Keywords:
Genetic diseasesImmunologyInflammationInnate immunityMonogenic diseases

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Area of Science:

  • Immunology
  • Genetics
  • Rheumatology

Background:

  • Undifferentiated systemic autoinflammatory diseases (USAIDs) pose diagnostic and therapeutic challenges.
  • Chronic interferon (IFN) signaling and cytokine dysregulation may indicate treatable conditions.

Purpose of the Study:

  • To screen USAID patients for an interferon signature (IRG-S) and identify associated clinical features and genetic underpinnings.
  • To expand diagnostic capabilities for USAIDs through molecular and genetic profiling.

Main Methods:

  • Sixty-six USAID patients were evaluated using a type-I IFN-response-gene score (IRG-S), cytokine profiling, and next-generation sequencing.
  • Clinical features and genetic mutations were correlated with IRG-S levels.

Main Results:

  • 55% of patients exhibited an elevated IRG-S, associated with increased prevalence of neutrophilic panniculitis, basal ganglia calcifications, interstitial lung disease, and myositis.
  • Identified novel autoinflammatory disease subtypes: IL-18-mediated pulmonary alveolar proteinosis and recurrent macrophage activation syndrome (IL-18PAP-MAS), NEMO deleted exon 5-autoinflammatory syndrome (NEMO-NDAS), and SAMD9L-associated autoinflammatory disease (SAMD9L-SAAD).
  • Discovered mutations in LRBA, IKBKG, and SAMD9L, suggesting distinct NF-κB activation pathways in some patients.

Conclusions:

  • Elevated IRG-S is a valuable biomarker in USAIDs, aiding in diagnosis and identifying distinct disease entities.
  • The IRG-S expands the diagnostic toolkit for USAIDs, pointing to diverse regulatory pathways of interferon response.
  • This research facilitates the identification of patients eligible for targeted treatments based on their molecular and clinical profiles.