ArticleFrontiers in immunology2021
Human Complement C4B Allotypes and Deficiencies in Selected Cases With Autoimmune Diseases.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Persistent cutaneous lupus erythematosus: A pathway toward systemic disease?Journal of translational autoimmunity · 2026Review
- Association of C4d with disease activity in anti-neutrophil cytoplasmic antibody-associated vasculitis: evidence for classical/lectin complement pathway activation.Arthritis research & therapy · 2025Article
- Low C4A copy numbers and higher HERV gene insertion contributes to increased risk of SLE, with absence of association with disease phenotype and disease activity.Immunologic research · 2024Article
- Translating Molecular Approaches to Oligodendrocyte-Mediated Neurological Circuit Modulation.Brain sciences · 2024Review
- ptx3aCell reports · 2024Article
- Investigation of the association between circulating inflammatory proteins and encephalitis risk in Europeans by two-sample Mendelian randomization analysis.Frontiers in neurology · 2024Article
- Article
- Review
- The complement system and human autoimmune diseases.Journal of autoimmunity · 2023Review
- Low copy numbers of complementAnnals of the rheumatic diseases · 2023Article
- Risk and protection of different rare protein-coding variants of complement component C4A in age-related macular degeneration.Frontiers in genetics · 2023Article
- Complement C4-deficient mice have a high mortality rate during PTZ-induced epileptic seizures, which correlates with cognitive problems and the deficiency in the expression of Egr1 and other immediate early genes.Frontiers in cellular neuroscience · 2023Article
- Article
Corrections and comments
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Authors and funding
20 authors at 10 institutions in 5 countries.
Funding
Abstract
Human complement C4 is one of the most diverse but heritable effectors for humoral immunity. To help understand the roles of C4 in the defense and pathogenesis of autoimmune and inflammatory diseases, we determined the bases of polymorphisms including the frequent genetic deficiency of C4A and/or C4B isotypes. We demonstrated the diversities of C4A and C4B proteins and their gene copy number variations (CNVs) in healthy subjects and patients with autoimmune disease, such as type 1 diabetes, systemic lupus erythematosus (SLE) and encephalitis. We identified subjects with (a) the fastest migrating C4B allotype, B7, or (b) a deficiency of C4B protein caused by genetic mutation in addition to gene copy-number variation. Those variants and mutants were characterized, sequenced and specific techniques for detection developed. Novel findings were made in four case series. First, the amino acid sequence determinant for C4B7 was likely the R729Q variation at the anaphylatoxin-like region. Second, in healthy White subject MS630, a C-nucleotide deletion at codon-755 led to frameshift mutations in his single
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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.