ArticleThe Journal of experimental medicine2014
Consequences of the recurrent MYD88(L265P) somatic mutation for B cell tolerance.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 81 citations in OpenAlex.
- Mechanisms of resistance to BTK inhibitors in B cell malignancies and emerging targeted strategies.Molecular therapy. Oncology · 2026Review
- Frequency and Relevance of MYD88European journal of neurology · 2025Article
- Targeting BCL2 in Waldenström macroglobulinemia: from biology to treatment management.Frontiers in oncology · 2025Review
- The Prevalence of MYD88 L265P and TNFAIP3 Mutations and Their Correlations with Clinico-Hematological Profile in Egyptian Patients with Diffuse Large B Cell Lymphoma.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Transcriptome Analysis of Diffuse Large B-Cell Lymphoma Cells Inducibly Expressing MyD88 L265P Mutation Identifies Upregulated CD44, LGALS3, NFKBIZ, and BATF as Downstream Targets of Oncogenic NF-κB Signaling.International journal of molecular sciences · 2023Article
- The NF-κB multidimer system model: A knowledge base to explore diverse biological contexts.Science signaling · 2023Review
- An Aged/Autoimmune B-cell Program Defines the Early Transformation of Extranodal Lymphomas.Cancer discovery · 2023Article
- Article
- Review
- Nucleic Acid Biomarkers in Waldenström Macroglobulinemia and IgM-MGUS: Current Insights and Clinical Relevance.Diagnostics (Basel, Switzerland) · 2022Review
- Aberrant Extrafollicular B Cells, Immune Dysfunction, Myeloid Inflammation, and MyD88-Mutant Progenitors Precede Waldenstrom Macroglobulinemia.Blood cancer discovery · 2021Article
- MYD88 L265P elicits mutation-specific ubiquitination to drive NF-κB activation and lymphomagenesis.Blood · 2021Article
- An Autochthonous Mouse Model of Myd88- and BCL2-Driven Diffuse Large B-cell Lymphoma Reveals Actionable Molecular Vulnerabilities.Blood cancer discovery · 2021Article
- Continuous MYD88 Activation Is Associated With Expansion and Then Transformation of IgM Differentiating Plasma Cells.Frontiers in immunology · 2021Article
- Lymphoplasmacytic lymphoma in a patient with Birt-Hogg-Dubé syndrome.International journal of hematology · 2020Article
- Intramacrophage ROS Primes the Innate Immune System via JAK/STAT and Toll Activation.Cell reports · 2020Article
- Oncogenic Mutations of MYD88 and CD79B in Diffuse Large B-Cell Lymphoma and Implications for Clinical Practice.Cancers · 2020Review
- TLR-mediated activation of Waldenström macroglobulinemia B cells reveals an uncoupling from plasma cell differentiation.Blood advances · 2020Article
- Immuno-Modulation of Hematopoietic Stem and Progenitor Cells in Inflammation.Frontiers in immunology · 2020Review
- B-Cell-Specific Myd88 L252P Expression Causes a Premalignant Gammopathy Resembling IgM MGUS.Frontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
MYD88(L265P) has recently been discovered as an extraordinarily frequent somatic mutation in benign monoclonal IgM gammopathy, Waldenström's macroglobulinemia, and diffuse large B cell lymphoma. In this study, we analyze the consequences for antigen-activated primary B cells of acquiring MYD88(L265P). The mutation induced rapid B cell division in the absence of exogenous TLR ligands and was inhibited by Unc93b1(3d) mutation and chloroquine or TLR9 deficiency, indicating continued dependence on upstream TLR9 activation. Proliferation and NF-κB activation induced by MYD88(L265P) were nevertheless rapidly countered by the induction of TNFAIP3, an NF-κB inhibitor frequently inactivated in MYD88(L265P)-bearing lymphomas, and extinguished by Bim-dependent apoptosis. MYD88(L265P) caused self-reactive B cells to accumulate in vivo only when apoptosis was opposed by Bcl2 overexpression. These results reveal checkpoints that fortify TLR responses against aberrant B cell proliferation in response to ubiquitous TLR and BCR self-ligands and suggest that tolerance failure requires the accumulation of multiple somatic mutations.
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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.