ReviewFrontiers in immunology2018
The CBM-opathies-A Rapidly Expanding Spectrum of Human Inborn Errors of Immunity Caused by Mutations in the CARD11-BCL10-MALT1 Complex.
Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed.
- B-cell lymphocytosis and reprogramming due to biallelic CARD11 mutations.The Journal of allergy and clinical immunology · 2026Article
- Mechanistic Insights Into Immune Cell Dysregulation Mediated by Novel Heterozygous Variants in CARD11 and MALT1.Journal of clinical immunology · 2026Article
- A novel case of autosomal recessive CARD11 loss-of-function underlying impaired antiviral immunity and a review of literature.Clinical & translational immunology · 2026Article
- Loss of MALT1 Function in a Patient With Combined Immunodeficiency: a Novel Pathogenic Variant and Immunological Insights.Journal of clinical immunology · 2025Article
- Dominant interfering CARD11 variants disrupt JNK signaling to promote GATA3 expression in T cells.The Journal of experimental medicine · 2025Article
- γδ T Cells and Inborn Errors of Immunity.European journal of immunology · 2025Review
- Successful Treatment with Sirolimus of a Patient with a Novel CARD11 Germline Mutation in B-Cell Expansion with Nuclear Factor Kappa B and T-Cell Anergy: Case Report and Literature Review.Journal of clinical immunology · 2025Review
- From syndromic clues to diagnosis: understanding CARD11-driven disorders.Frontiers in immunology · 2025Review
- Leveraging altered lipid metabolism in treating B cell malignancies.Progress in lipid research · 2024Review
- Identification of TFG- and Autophagy-Regulated Proteins and Glycerophospholipids in B Cells.Journal of proteome research · 2024Article
- Epidermodysplasia Verruciformis in CADINS Disease: Expanding the Phenotype.Journal of clinical immunology · 2024Article
- CARD11 regulates the thymic Treg development in an NF-κB-independent manner.Frontiers in immunology · 2024Article
- Specific Mutation Predict Relapse/Refractory Diffuse Large B-Cell Lymphoma.Journal of blood medicine · 2024Article
- MALT1 substrate cleavage: what is it good for?Frontiers in immunology · 2024Review
- B-Cell Receptor Signaling and Beyond: The Role of Igα (CD79a)/Igβ (CD79b) in Normal and Malignant B Cells.International journal of molecular sciences · 2023Review
- Elevated IgE Levels-An Allergy or an Underlying Inborn Error of Immunity in Children with Recurrent Infections?Antibodies (Basel, Switzerland) · 2023Article
- Subcutaneous panniculitis-like T-cell lymphoma in two unrelated individuals with BENTA disease.Clinical immunology (Orlando, Fla.) · 2023Article
- Inborn errors of human B cell development, differentiation, and function.The Journal of experimental medicine · 2023Review
- Mistuned NF-κB signaling in lymphocytes: lessons from relevant inborn errors of immunity.Clinical and experimental immunology · 2023Article
- Autophagy-associated immune dysregulation and hyperplasia in a patient with compound heterozygous mutations inAutophagy · 2023Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The caspase recruitment domain family member 11 (CARD11 or CARMA1)-B cell CLL/lymphoma 10 (BCL10)-MALT1 paracaspase (MALT1) [CBM] signalosome complex serves as a molecular bridge between cell surface antigen receptor signaling and the activation of the NF-κB, JNK, and mTORC1 signaling axes. This positions the CBM complex as a critical regulator of lymphocyte activation, proliferation, survival, and metabolism. Inborn errors in each of the CBM components have now been linked to a diverse group of human primary immunodeficiency diseases termed "CBM-opathies." Clinical manifestations range from severe combined immunodeficiency to selective B cell lymphocytosis, atopic disease, and specific humoral defects. This surprisingly broad spectrum of phenotypes underscores the importance of "tuning" CBM signaling to preserve immune homeostasis. Here, we review the distinct clinical and immunological phenotypes associated with human CBM complex mutations and introduce new avenues for targeted therapeutic intervention.
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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.