ReviewFrontiers in medicine2023
Pathophysiology and clinical manifestations of immune complex vasculitides.
Review in Frontiers in medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Pathological depositions in human disease: converging mechanisms in atherosclerosis, Alzheimer's disease, and related disorders.Molecular biomedicine · 2026Review
- Cardiac computed tomography unmasks cardiac involvement in immune complex vasculitis in a patient with chest pain and shortness of breath.European heart journal. Case reports · 2026Article
- Idiopathic cutaneous immunoglobulin G/immunoglobulin M vasculitis is likely a distinct entity: A European multicentric retrospective study.JAAD international · 2026Article
- Article
- Commentary: Anti-endothelial cell antibodies in pathogenesis of vasculitis.Frontiers in immunology · 2026Article
- Rheumatoid vasculitis presenting in the absence of rheumatoid arthritis: a case-based review.Rheumatology international · 2025Review
- Immunological Disorders: Gradations and the Current Approach in Laboratory Diagnostics.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- The Role of Neutrophils in ANCA-Associated Vasculitis: The Pathogenic Role and Diagnostic Utility of Autoantibodies.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune complex (IC) vasculitides present inflammations of vessel walls associated with perivascular deposition of immunoglobulins (Igs), mostly ICs. They encompass systemic and skin-limited variants of IgA vasculitis (IgAV), cryoglobulinemic vasculitis (CV), rheumatoid, lupus, and hypocomplementemic vasculitides, serum sickness cutaneous IgM/IgG (non-IgA) vasculitis, and recurrent macular (hypergammaglobulinemic or exertion-induced) vasculitis. Serum sickness and CV fulfill the criteria of a type III hypersensitivity immune reaction as large lattices of the IC precipitate at vessel walls and activate polymorphonuclear neutrophils (PMNs). Immunoglobulin-A vasculitis differs with regard to the causes of perivascular deposition of ICs since here many IgA1 molecules are hypoglycosylated (Gd-IgA1), which appears to facilitate their perivascular deposition in skin and mesangium (via e.g. CD71). The reasons for increased generation of immunoglobulins or formation of IC and their perivascular deposition in either skin or systemic organs are different and not fully explored. A common denominator of OC vasculitides is the activation of PMNs near the vessel wall
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.