ArticleJCI insight2021
TNFRSF13B genotypes control immune-mediated pathology by regulating the functions of innate B cells.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Single-cell dissection of pleural and systemic immunity uncovers pathogen-specific immune reprogramming in tuberculosis versus lung adenocarcinoma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Mucosal B Cell Expansion and Maturation Contribute to Colitis Pathogenesis.Inflammatory bowel diseases · 2026Article
- Atopic Dermatitis with Ichthyosis, Recurrent Fungal and Viral Infections: A Case of ConcurrentClinical, cosmetic and investigational dermatology · 2026Article
- Detecting and characterizing copy number variation in a large commercial U.S. Holstein cattle population.BMC genomics · 2025Article
- Charge-based immunoreceptor signalling in health and disease.Nature reviews. Immunology · 2025Review
- Comprehensive Analysis of Prognostic Alternative Splicing Signatures in Tumor Immune Infiltration in Bladder Cancer.Recent patents on anti-cancer drug discovery · 2025Article
- Complement C3d enables cell-mediated immunity capable of distinguishing spontaneously transformed from nontransformed cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Somatic Cell Fusion in Host Defense and Adaptation.Results and problems in cell differentiation · 2024Article
- TNFRSF13B in B cell responses to organ transplantation.Human immunology · 2023Article
- Accommodation in allogeneic and xenogeneic organ transplantation: Prevalence, impact, and implications for monitoring and for therapeutics.Human immunology · 2023Article
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Authors and funding
15 authors.
Funding
Abstract
Host genes define the severity of inflammation and immunity but specific loci doing so are unknown. Here we show that TNF receptor superfamily member 13B (TNFRSF13B) variants, which enhance defense against certain pathogens, also control immune-mediated injury of transplants, by regulating innate B cells' functions. Analysis of TNFRSF13B in human kidney transplant recipients revealed that 33% of those with antibody-mediated rejection (AMR) but fewer than 6% of those with stable graft function had TNFRSF13B missense mutations. To explore mechanisms underlying aggressive immune responses, we investigated alloimmunity and rejection in mice. Cardiac allografts in Tnfrsf13b-mutant mice underwent early and severe AMR. The dominance and precocity of AMR in Tnfrsf13b-deficient mice were not caused by increased alloantibodies. Rather, Tnfrsf13b mutations decreased "natural" IgM and compromised complement regulation, leading to complement deposition in allografted hearts and autogenous kidneys. Thus, WT TNFRSF13B and Tnfrsf13b support innate B cell functions that limit complement-associated inflammation; in contrast, common variants of these genes intensify inflammatory responses that help clear microbial infections but allow inadvertent tissue injury to ensue. The wide variation in inflammatory reactions associated with TNFRSF13B diversity suggests polymorphisms could underlie variation in host defense and explosive inflammatory responses that sometimes enhance morbidity associated with immune responses.
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