ArticlePloS one2014
Uptake and presentation of myelin basic protein by normal human B cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- The validity of animal models to explore the pathogenic role of the complement system in multiple sclerosis: A review.Frontiers in molecular neuroscience · 2022Review
- Absence of B Cells in Brainstem and White Matter Lesions Associates With Less Severe Disease and Absence of Oligoclonal Bands in MS.Neurology(R) neuroimmunology & neuroinflammation · 2021Article
- Analysis of complement deposition and processing on Chlamydia trachomatis.Medical microbiology and immunology · 2021Article
- Approaches for Controlling Antibody-Mediated Allograft Rejection Through Targeting B Cells.Frontiers in immunology · 2021Review
- Regulation of Decay Accelerating Factor Primes Human Germinal Center B Cells for Phagocytosis.Frontiers in immunology · 2020Article
- The complex functioning of the complement system in xenotransplantation.Xenotransplantation · 2019Review
- An Overview of the Intrinsic Role of Citrullination in Autoimmune Disorders.Journal of immunology research · 2019Review
- Complement as a regulator of adaptive immunity.Seminars in immunopathology · 2018Review
- Targeting B cells in relapsing-remitting multiple sclerosis: from pathophysiology to optimal clinical management.Therapeutic advances in neurological disorders · 2017Review
- Myelin Basic Protein Citrullination in Multiple Sclerosis: A Potential Therapeutic Target for the Pathology.Neurochemical research · 2016Review
- Increased levels of peptidylarginine deiminase 2 in synovial fluid from anti-CCP-positive rheumatoid arthritis patients: Association with disease activity and inflammatory markers.Rheumatology (Oxford, England) · 2016Article
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Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B cells may play both pathogenic and protective roles in T-cell mediated autoimmune diseases such as multiple sclerosis (MS). These functions relate to the ability of B cells to bind and present antigens. Under serum-free conditions we observed that 3-4% of circulating B cells from healthy donors were capable of binding the MS-associated self-antigen myelin basic protein (MBP) and of presenting the immunodominant peptide MBP85-99, as determined by staining with the mAb MK16 recognising the peptide presented by HLA-DR15-positive cells. In the presence of serum, however, the majority of B cells bound MBP in a complement-dependent manner, and almost half of the B cells became engaged in presentation of MBP85-99. Even though complement receptor 1 (CR1, CD35) and CR2 (CD21) both contributed to binding of MBP to B cells, only CR2 was important for the subsequent presentation of MBP85-99. A high proportion of MBP85-99 presenting B cells expressed CD27, and showed increased expression of CD86 compared to non-presenting B cells. MBP-pulsed B cells induced a low frequency of IL-10-producing CD4+ T cells in 3 out of 6 donors, indicating an immunoregulatory role of B cells presenting MBP-derived peptides. The mechanisms described here refute the general assumption that B-cell presentation of self-antigens requires uptake via specific B-cell receptors, and may be important for maintenance of tolerance as well as for driving T-cell responses in autoimmune diseases.
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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.