Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

ANCA-Associated Vasculitis Pathogenesis: A Commentary.

Eric J Gapud1, Philip Seo1, Brendan Antiochos2

  • 1Division of Rheumatology, Department of Medicine, Johns Hopkins University School of Medicine, 5200 Eastern Avenue, MFL Center Tower, Ste. 5300, Baltimore, MD, 21224, USA.

Current Rheumatology Reports
|April 1, 2017
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Protein•DNA mesh assembly drives dsDNA-specific and duplex length-dependent activation of cGAS.

bioRxiv : the preprint server for biology·2026
Same author

Granulomatosis with polyangiitis following Lyme disease.

The American journal of medicine·2026
Same author

Anti-PAD4 antibodies link autoimmunity to PAD4 with CTL-associated rheumatoid arthritis.

Annals of the rheumatic diseases·2026
Same author

Tracheobronchial Stenosis in Granulomatosis With Polyangiitis: Immunosuppressant Use and Airway Dilation Frequency.

ACR open rheumatology·2026
Same author

Pulmonary manifestations of granulomatosis with polyangiitis and microscopic polyangiitis.

Seminars in arthritis and rheumatism·2026
Same author

Infracordal Stenosis: A Glucocorticoid-Responsive Subtype of Autoimmune Laryngotracheal Stenosis.

The Laryngoscope·2026
Same journal

Intensive Care Management of ANCA-associated Vasculitides: a Narrative Review.

Current rheumatology reports·2026
Same journal

The Role of Musculoskeletal Ultrasound in Psoriatic Arthritis: From Preclinical Detection to Treatment Monitoring.

Current rheumatology reports·2026
Same journal

Correction to: Is Gout and Autoinflammatory Disease?

Current rheumatology reports·2026
Same journal

Risks and Management of Glucocorticoid Therapy for Patients with Rheumatic Disease Having Surgery.

Current rheumatology reports·2026
Same journal

Perioperative Management Considerations for Patients with Systemic Lupus Erythematosus.

Current rheumatology reports·2026
Same journal

Management of IgG4-Related Disease.

Current rheumatology reports·2026
See all related articles

ANCA-associated vasculitides, characterized by anti-neutrophil cytoplasmic antibodies (ANCAs), may involve monocytes and T cells more than previously thought. Revisiting neutrophil-centric views could reveal new therapeutic targets and biomarkers for these rare diseases.

Area of Science:

  • Immunology
  • Rheumatology
  • Pathogenesis of autoimmune diseases

Background:

  • ANCA-associated vasculitides (AAV) are small vessel vasculitides defined by autoantibodies against neutrophil cytoplasmic antigens (ANCAs), primarily PR3 and MPO.
  • Current understanding of AAV pathogenesis heavily emphasizes neutrophil biology due to neutrophils expressing ANCA autoantigens.

Purpose of the Study:

  • To review the current clinical and molecular immunology of AAV.
  • To discuss knowledge gaps in understanding the pathogenic mechanisms of AAV.
  • To re-evaluate the central role of neutrophils in AAV pathogenesis.

Main Methods:

  • Literature review of clinical and molecular immunology studies on AAV.
  • Analysis of genetic, clinical, and cellular biology observations.
Keywords:
AAV pathogenesisANCA-associated vasculitisEosinophilic granulomatosis with polyangiitisGranulomatosis with polyangiitisMicroscopic polyangiitis

Related Experiment Videos

  • Re-evaluation of existing pathogenetic models.
  • Main Results:

    • Genetic, clinical, and cellular data suggest roles for monocytes and T cells in AAV pathogenesis.
    • A purely neutrophil-centric view cannot fully explain all observations in AAV.
    • Alternative immune cell mediators may play under-appreciated roles.

    Conclusions:

    • The pathogenesis of AAV may require a broader focus beyond neutrophils.
    • Re-focusing on monocytes and T cells could uncover novel therapeutic targets.
    • Identifying roles for other immune cells may lead to better biomarkers for disease activity.