ReviewFrontiers in immunology2022
Anaphylatoxins spark the flame in early autoimmunity.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Immune-mediated platelet refractoriness: Mechanisms, diagnostics, and therapeutic breakthroughs.Transfusion medicine (Oxford, England) · 2026Review
- The immune dysregulation of fibrosis: insights into immune-fibrotic crosstalk and potential therapeutic targets.Frontiers in immunology · 2026Review
- Activation of B1 B cells by F. tularensis atypical LPS depends on classical complement and C3a.PLoS pathogens · 2025Article
- Safety Assessment of Stem Cell-Based Therapies: Current Standards and Advancing Frameworks.Cells · 2025Review
- Unique Features and Collateral Immune Effects of mRNA-LNP COVID-19 Vaccines: Plausible Mechanisms of Adverse Events and Complications.Pharmaceutics · 2025Review
- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Inhibition of Alternative and Terminal Complement Pathway Components Modulate the Immune Response Against Bacteria and Fungi in Whole Blood.Scandinavian journal of immunology · 2025Article
- Review
- Th2 predominance and decreased NK cells in patients with hereditary angioedema.Frontiers in immunology · 2025Article
- Evolving understanding of Guillain-Barré syndrome pathophysiology and the central role of the classical complement pathway in axonal injury.Frontiers in neurology · 2025Article
- sMR and PTX3 levels associate with COVID-19 outcome and survival but not with Long COVID.iScience · 2024Article
- Association of Complement Factors With Disability Progression in Primary Progressive Multiple Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
- Review
- Decrease in multiple complement proteins associated with development of islet autoimmunity and type 1 diabetes.iScience · 2024Article
- Pseudo-allergic reactions induced by Chinese medicine injections: a review.Chinese medicine · 2023Review
- Mast Cells and Basophils in IgE-Independent Anaphylaxis.International journal of molecular sciences · 2023Review
- The complement system and human autoimmune diseases.Journal of autoimmunity · 2023Review
- Structural biology of complement receptors.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system (CS) is an ancient and highly conserved part of the innate immune system with important functions in immune defense. The multiple fragments bind to specific receptors on innate and adaptive immune cells, the activation of which translates the initial humoral innate immune response (IR) into cellular innate and adaptive immunity. Dysregulation of the CS has been associated with the development of several autoimmune disorders such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), ANCA-associated vasculitis, and autoimmune bullous dermatoses (AIBDs), where complement drives the inflammatory response in the effector phase. The role of the CS in autoimmunity is complex. On the one hand, complement deficiencies were identified as risk factors to develop autoimmune disorders. On the other hand, activation of complement can drive autoimmune responses. The anaphylatoxins C3a and C5a are potent mediators and regulators of inflammation during the effector phase of autoimmunity through engagement of specific anaphylatoxin receptors, i.e., C3aR, C5aR1, and C5aR2 either on or in immune cells. In addition to their role in innate IRs, anaphylatoxins regulate humoral and cellular adaptive IRs including B-cell and T-cell activation, differentiation, and survival. They regulate B- and T-lymphocyte responses either directly or indirectly through the activation of anaphylatoxin receptors
Indexed as
Identifiers
What OpenQuestion holds
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.