ArticleProceedings of the National Academy of Sciences of the United States of America2017
Cocapture of cognate and bystander antigens can activate autoreactive B cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 66 citations in OpenAlex.
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- The persistent inflammation in COPD: is autoimmunity the core mechanism?European respiratory review : an official journal of the European Respiratory Society · 2024Review
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- Fungal gut microbiota dysbiosis in systemic lupus erythematosus.Frontiers in microbiology · 2023Article
- Acute Inflammatory Diseases of the Central Nervous System After SARS-CoV-2 Vaccination.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- The link between circulating follicular helper T cells and autoimmunity.Nature reviews. Immunology · 2022Review
- B Cell Immunity in Lung Transplant Rejection - Effector Mechanisms and Therapeutic Implications.Frontiers in immunology · 2022Review
- Autoantibodies in neurological disease.Nature reviews. Immunology · 2021Review
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- Autoinflammatory and autoimmune conditions at the crossroad of COVID-19.Journal of autoimmunity · 2020Review
- Host-microbiota interactions in immune-mediated diseases.Nature reviews. Microbiology · 2020Review
- B cell tolerance and antibody production to the celiac disease autoantigen transglutaminase 2.The Journal of experimental medicine · 2020Article
- Using two phases of the CD4 T cell response to blood-stage murine malaria to understand regulation of systemic immunity and placental pathology in Plasmodium falciparum infection.Immunological reviews · 2020Review
- A Link Between Plasma Microbial Translocation, Microbiome, and Autoantibody Development in First-Degree Relatives of Systemic Lupus Erythematosus Patients.Arthritis & rheumatology (Hoboken, N.J.) · 2019Article
- Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms.Viruses · 2019Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoantibodies against myelin oligodendrocyte glycoprotein (MOG) are associated with autoimmune central nervous system diseases like acute disseminated encephalomyelitis (ADEM). For ADEM, it is speculated that a preceding infection is the trigger of the autoimmune response, but the mechanism connecting the infection to the production of MOG antibodies remains a mystery. We reasoned that the ability of B cells to capture cognate antigen from cell membranes, along with small quantities of coexpressed "bystander" antigens, might enable B-cell escape from tolerance. We tested this hypothesis using influenza hemagglutinin as a model viral antigen and transgenic, MOG-specific B cells. Using flow cytometry and live and fixed cell microscopy, we show that MOG-specific B cells take up large amounts of MOG from cell membranes. Uptake of the antigen from the membrane leads to a strong activation of the capturing B cell. When influenza hemagglutinin is also present in the membrane of the target cell, it can be cocaptured with MOG by MOG-specific B cells via the B-cell receptor. Hemagglutinin and MOG are both presented to T cells, which in turn are activated and proliferate. As a consequence, MOG-specific B cells get help from hemagglutinin-specific T cells to produce anti-MOG antibodies. In vivo, the transfer of MOG-specific B cells into recipient mice after the cocapture of MOG and hemagglutinin leads to the production of class-switched anti-MOG antibodies, dependent on the presence of hemagglutinin-specific T cells. This mechanism offers a link between infection and autoimmunity.
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