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Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification
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Elevated interleukin-32 expression in granulomatosis with polyangiitis.

Suyoung Bae1, Yong-Gil Kim, Jida Choi

  • 1Laboratory of Cytokine Immunology, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 143-701 Korea.

Rheumatology (Oxford, England)
|August 2, 2012
PubMed
Summary

Interleukin-32 (IL-32) levels are elevated in granulomatosis with polyangiitis (GPA) patients and correlate with disease activity. IL-32 may play a role in GPA

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Area of Science:

  • Immunology
  • Rheumatology
  • Molecular Biology

Background:

  • Granulomatosis with polyangiitis (GPA) is a systemic vasculitis.
  • Proteinase 3 (PR3) is a key autoantigen in GPA.
  • Interleukin-32 (IL-32) is a novel cytokine implicated in inflammation.

Purpose of the Study:

  • To investigate the role of IL-32 in GPA.
  • To assess the relationship between IL-32 levels and disease activity in GPA patients.
  • To explore the interaction between PR3 and IL-32.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) was used to measure IL-32, PR3, TNF-α, and IL-6 levels.
  • Northern blot analysis quantified IL-32 mRNA in leukocytes.
  • Immunofluorescence (IF) staining examined the intracellular colocalization of IL-32 and PR3.

Main Results:

  • IL-32 and PR3 levels were significantly elevated in GPA patients compared to healthy individuals.
  • IL-32 mRNA levels were markedly increased in GPA patient leukocytes.
  • Intracellular colocalization of IL-32 and PR3 was confirmed in GPA leukocytes.

Conclusions:

  • Elevated IL-32 levels are associated with GPA.
  • IL-32 levels may reflect treatment response in GPA patients.
  • IL-32 could serve as a potential biomarker and contribute to the pathogenesis of GPA.