ArticleClinical and experimental immunology2024
Gene expression analysis revealed downregulation of complement receptor 1 in clonal B cells in cold agglutinin disease.
Article in Clinical and experimental immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Anti-MAG Polyneuropathy: Characterization of the Monoclonal Gammopathy and Clonal B-Cell Population.Journal of immunology research · 2026Article
- Diagnosis and management of cold agglutinin disease.Hematology. American Society of Hematology. Education Program · 2025Review
- Genomic and immune profiling of prognostic risk groups in IgM gammopathy reveals novel biomarkers beyondFrontiers in immunology · 2025Article
- Beneath the surface in autoimmune hemolytic anemia: pathogenetic networks, therapeutic advancements and open questions.Frontiers in immunology · 2025Review
- Autoimmune Hemolytic Anemias: Classifications, Pathophysiology, Diagnoses and Management.International journal of molecular sciences · 2024Review
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Cold agglutinin disease (CAD) is a rare B-cell lymphoproliferative disorder of the bone marrow, manifested by autoimmune hemolytic anemia caused by binding of monoclonal IgM autoantibodies to the I antigen. Underlying genetic changes have previously been reported, but their impact on gene expression profile has been unknown. Here, we define differentially expressed genes in CAD B cells. To unravel downstream alteration in cellular pathways, gene expression by RNA sequencing was undertaken. Clonal B-cell samples from 12 CAD patients and IgM-expressing memory B cells from 4 healthy individuals were analyzed. Differential expression analysis and filtering resulted in 93 genes with significant differential expression. Top upregulated genes included SLC4A1, SPTA1, YBX3, TESC, HBD, AHSP, TRAF1, HBA2, RHAG, CA1, SPTB, IL10, UBASH3B, ALAS2, HBA1, CRYM, RGCC, KANK2, and IGHV4-34. They were upregulated at least 8-fold, while complement receptor 1 (CR1/CD35) was downregulated 11-fold in clonal CAD B cells compared to control B cells. Flow cytometry analyses further confirmed reduced CR1 (CD35) protein expression by clonal CAD IgM+ B cells compared to IgM+ memory B cells in controls. CR1 (CD35) is an important negative regulator of B-cell activation and differentiation. Therefore, reduced CR1 (CD35) expression may increase activation, proliferation, and antibody production in CAD-associated clonal B cells.
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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.