ArticleOncotarget2018
Decreased expression levels of complement regulator CD55 contribute to the development of bullous pemphigoid.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Immune regulation by CD55 in chronic beryllium disease.American journal of respiratory cell and molecular biology · 2026Article
- Failure of early B cell tolerance and possible BCR signaling dysregulation underlie NF155-mediated autoimmune nodopathies.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Decay-Accelerating Factor Differentially Associates With Complement-Mediated Damage in Synovium After Meniscus Tear as Compared to Anterior Cruciate Ligament Injury.Immune network · 2024Article
- Role of PDGFRANature communications · 2023Article
- CD55 in cancer: Complementing functions in a non-canonical manner.Cancer letters · 2022Review
- Differential expression of C5aR1 and C5aR2 in innate and adaptive immune cells located in early skin lesions of bullous pemphigoid patients.Frontiers in immunology · 2022Article
- Kaposi's Sarcoma-Associated Herpesvirus and Host Interaction by the Complement System.Pathogens (Basel, Switzerland) · 2020Review
- Role of Regulatory Immune Cells and Molecules in Autoimmune Bullous Dermatoses.Frontiers in immunology · 2019Review
- Blister Fluid Induces MMP-9-Associated M2-Type Macrophages in Bullous Pemphigoid.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bullous pemphigoid is a common autoimmune blistering disease of the elderly associated with autoantibody-mediated complement activation, and complement dysregulation is critical for its pathogenesis. As a crucial regulator of the complement system, CD55 has been widely studied in autoimmune diseases. Here, we investigated the involvement of CD55 in bullous pemphigoid, as little is known regarding its role in this disease. We found that CD55 levels were significantly lower in the lesions of patients with bullous pemphigoid (n = 8) compared to those in skin samples from healthy controls (n = 6). Interestingly, CD55 depletion in HaCaT human keratinocytes enhanced autoantibody-mediated complement activation. Moreover, complement activation was blocked by exogenous recombinant CD55 protein in both skin sections and keratinocytes exposed to pathogenic antibodies from patients with bullous pemphigoid. Notably, a significant increase in the expression of TNF-α and IFN-γ, administration of which downregulated CD55 levels in HaCaT cells, was observed in the sera of patients with bullous pemphigoid (n = 38) compared to that in healthy controls (n = 19). We found that ERK1/2 is involved in both TNF-α- and IFN-γ-induced CD55 downregulation. Thus, CD55 deficiency is a crucial factor in bullous pemphigoid pathogenesis, suggesting that increasing CD55 levels may exert a therapeutic effect.
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