ArticleThe American journal of pathology2010
The tetraspanin CD37 protects against glomerular IgA deposition and renal pathology.
Article in The American journal of pathology, 2010. 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, 21 citations in OpenAlex.
- The role of tetraspanins in organ fibrosis: mechanisms and therapeutic perspectives.Journal of translational medicine · 2025Review
- Identification of Messenger RNA Signatures in Age-Dependent Renal Impairment.Diagnostics (Basel, Switzerland) · 2023Article
- History of IgA Nephropathy Mouse Models.Journal of clinical medicine · 2021Review
- CD37 in B Cell Derived Tumors-More than Just a Docking Point for Monoclonal Antibodies.International journal of molecular sciences · 2020Review
- Expression and Function of Tetraspanins and Their Interacting Partners in B Cells.Frontiers in immunology · 2018Review
- Modulating Host Signaling Pathways to Promote Resistance to Infection byFrontiers in cellular and infection microbiology · 2017Review
- Article
- Protection from systemic Candida albicans infection by inactivation of the Sts phosphatases.Infection and immunity · 2015Article
- Kidney Diseases Enhance Expression of Tetraspanin-8: A Possible Protective Effect against Tubular Injury.Nephron extra · 2014Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tetraspanin protein CD37 is a leukocyte-specific transmembrane protein that is highly expressed on B cells. CD37-deficient (CD37(-/-)) mice exhibit a 15-fold increased level of immunoglobulin A (IgA) in serum and elevated numbers of IgA+ plasma cells in lymphoid organs. Here, we report that CD37(-/-) mice spontaneously develop renal pathology with characteristics of human IgA nephropathy. In young naïve CD37(-/-) mice, mild IgA deposition in glomeruli was observed. However, CD37(-/-) mice developed high titers of IgA immune complexes in serum during aging, which was associated with increased glomerular IgA deposition. Severe mesangial proliferation, fibrosis, and hyalinosis were apparent in aged CD37(-/-) mice, whereas albuminuria was mild. To further evaluate the role of CD37 in glomerular disease, we induced anti-glomerular basement membrane (GBM) nephritis in mice. CD37(-/-) mice developed higher IgA serum levels and glomerular deposits of anti-GBM IgA compared with wild-type mice. Importantly, glomerular macrophage and neutrophil influx was significantly higher in CD37(-/-) mice during both the heterologous and autologous phase of anti-GBM nephritis. Taken together, tetraspanin CD37 controls the formation of IgA-containing immune complexes and glomerular IgA deposition, which induces influx of inflammatory myeloid cells. Therefore, CD37 may protect against the development of IgA nephropathy.
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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.