ArticleThe Journal of experimental medicine1998
Activated complement component 3 (C3) is required for ultraviolet induction of immunosuppression and antigenic tolerance.
Article in The Journal of experimental medicine, 1998. 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, 115 citations in OpenAlex.
- Ultraviolet Radiation-Induced Tolerogenic Dendritic Cells in Skin: Insights and Mechanisms.Cells · 2025Review
- Absence of Langerhans cells resulted in over-influx of neutrophils and increased bacterial burden in skin wounds.Cell death & disease · 2024Article
- Immunity to fungi and vaccine considerations.Cell host & microbe · 2024Review
- Increased expression of complement C3c, iC3b, and cells containing CD11b or CD14 in experimentally induced psoriatic lesion.Clinical and experimental immunology · 2024Article
- C3d-Targeted factor H inhibits tissue complement in disease models and reduces glomerular injury without affecting circulating complement.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Sequential Increase in Complement Factor I, iC3b, and Cells Expressing CD11b or CD14 in Cutaneous Vasculitis.Analytical cellular pathology (Amsterdam) · 2022Article
- Deep sequencing reveals a DAP1 regulatory haplotype that potentiates autoimmunity in systemic lupus erythematosus.Genome biology · 2020Article
- Neutrophil: A New Player in Metastatic Cancers.Frontiers in immunology · 2020Review
- Vitamin D (1,25(OH)The Journal of steroid biochemistry and molecular biology · 2019Article
- Crosstalk Among UV-Induced Inflammatory Mediators, DNA Damage and Epigenetic Regulators Facilitates Suppression of the Immune System.Photochemistry and photobiology · 2017Review
- Complement C3 Exacerbates Imiquimod-Induced Skin Inflammation and Psoriasiform Dermatitis.The Journal of investigative dermatology · 2017Article
- The Skin Microbiome: Is It Affected by UV-induced Immune Suppression?Frontiers in microbiology · 2016Article
- Mac-1 Regulates IL-13 Activity in Macrophages by Directly Interacting with IL-13Rα1.The Journal of biological chemistry · 2015Article
- Intranasal peptide-induced tolerance and linked suppression: consequences of complement deficiency.Immunology · 2015Article
- Decreased ITGAM and FcγRIIIA mRNA expression levels in peripheral blood mononuclear cells from patients with systemic lupus erythematosus.Clinical and experimental medicine · 2014Article
- The immunologic revolution: photoimmunology.The Journal of investigative dermatology · 2012Review
- UV light B-mediated inhibition of skin catalase activity promotes Gr-1+ CD11b+ myeloid cell expansion.The Journal of investigative dermatology · 2012Article
- Polymorphisms of the ITGAM gene confer higher risk of discoid cutaneous than of systemic lupus erythematosus.PloS one · 2010Article
- Integrin CD11b negatively regulates TLR-triggered inflammatory responses by activating Syk and promoting degradation of MyD88 and TRIF via Cbl-b.Nature immunology · 2010Article
- Mice lacking C1q or C3 show accelerated rejection of minor H disparate skin grafts and resistance to induction of tolerance.European journal of immunology · 2010Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Complement component 3 (C3), a critical regulator of innate immunity, may also play a role in the regulation of cognate immunity, such as contact sensitivity responses. Because ultraviolet (UV) radiation also activates C3 in the skin, we determined whether the immunosuppressed state that results when a contact sensitizer is applied through UVB-exposed skin requires the presence and activation of C3. This question was addressed through the use of C3-deficient mice, blockade of C3 cleavage to C3b, and accelerated degradation of iC3b by soluble complement receptor 1 (sCR1). Both C3-modulated systems totally reversed the failure to induce a contact sensitivity response to dinitrofluorobenzene (DNFB) upon primary sensitization at the UV-exposed site, as well as immunologic tolerance to a second DNFB immunization through normal skin. Treatment with sCR1 reduced the infiltration of CD11b+ leukocytes into the epidermis and dermis of UV-irradiated skin but did not reverse the UV-induced depletion of epidermal class II MHC+CD11blo Langerhans cells. These data, taken together with previous results showing abrogation of locally induced UV immunosuppression by in vivo anti-CD11b treatment, suggest a novel mechanism by which ligation of the leukocyte beta2 integrin, CD11b, by iC3b molecules formed from C3 activation in UV-exposed skin, modifies cutaneous CD11b+ cells such that skin antigen-presenting cells are unable to sensitize in a primary immune response, but actively induce antigenic tolerance.
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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.