ArticleThe Journal of clinical investigation2005
Role of C5 in the development of airway inflammation, airway hyperresponsiveness, and ongoing airway response.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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
29 citing papers in PubMed.
- Site-targeted proximal complement C3 inhibition, but not C5 blockade, attenuates neurodegeneration in a mouse model of amyotrophic lateral sclerosis: Implications for failed clinical trials.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Review
- Complement and T cell activation in transplantation.Transplantation reviews (Orlando, Fla.) · 2025Review
- Prevalence of Fetal Inflammatory Response Syndrome and Villitis of Unknown Etiology in the Placenta of Saudi Women and Their Association with Baby Sex.Life (Basel, Switzerland) · 2024Article
- The Value of Targeting Complement Components in Asthma.Medicina (Kaunas, Lithuania) · 2020Article
- Complement factor C5 inhibition reduces type 2 responses without affecting group 2 innate lymphoid cells in a house dust mite induced murine asthma model.Respiratory research · 2019Article
- Complement mediators: key regulators of airway tissue remodeling in asthma.Journal of translational medicine · 2015Review
- Properdin Contributes to Allergic Airway Inflammation through Local C3a Generation.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Treatment with the C5a receptor/CD88 antagonist PMX205 reduces inflammation in a murine model of allergic asthma.International immunopharmacology · 2014Article
- Complement anaphylatoxins as immune regulators in cancer.Cancer medicine · 2014Review
- Molecular basis for downregulation of C5a-mediated inflammation by IgG1 immune complexes in allergy and asthma.Current allergy and asthma reports · 2013Review
- Role of complement activation in obliterative bronchiolitis post-lung transplantation.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Bifunctional lipocalin ameliorates murine immune complex-induced acute lung injury.The Journal of biological chemistry · 2013Article
- The complement system in ischemia-reperfusion injuries.Immunobiology · 2012Review
- The critical role of complement alternative pathway regulator factor H in allergen-induced airway hyperresponsiveness and inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Absence of mannose-binding lectin prevents hyperglycemic cardiovascular complications.The American journal of pathology · 2012Article
- The role of complement in the diagnosis and management of allergic rhinitis and allergic asthma.Current allergy and asthma reports · 2011Review
- A complex role for complement in allergic asthma.Expert review of clinical immunology · 2010Review
- The role of the anaphylatoxins in health and disease.Molecular immunology · 2009Review
- Modulation of the antitumor immune response by complement.Nature immunology · 2008Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of complement component C5 in asthma remains controversial. Here we examined the contribution of C5 at 3 critical checkpoints during the course of disease. Using an mAb specific for C5, we were able to evaluate the contribution of C5 during (a) the initiation of airway inflammation, (b) the maintenance of airway hyperresponsiveness (AHR), and (c) sustainment of an ongoing airway response to allergen provocation. Our results indicate that C5 is probably activated intrapulmonarily after infections or exposures to allergen and C5 inhibition has profound effects at all 3 critical checkpoints. In contrast to an earlier report, C5-deficient mice with established airway inflammation did not have elevated AHR to nonspecific stimuli. In the presence of airway inflammation, C5a serves as a direct link between the innate immune system and the development of AHR by engaging directly with its receptors expressed in airways. Through their powerful chemotactic and cell activation properties, both C5a and C5b-9 regulate the downstream inflammatory cascade, which results in a massive migration of inflammatory cells into the bronchial airway lumen and triggers the release of multiple harmful inflammatory mediators. This study suggests that targeting C5 is a potential clinical approach for treating patients with asthma.
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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.