ArticleThe Journal of experimental medicine2018
BCAP links IL-1R to the PI3K-mTOR pathway and regulates pathogenic Th17 cell differentiation.
Article in The Journal of experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 56 citations in OpenAlex.
- Perspective: Personalized Management of Oxidative and Nitrosative Stress in Post-Exercise Recovery with a Particular Emphasis on the Potential of Micro-Immunotherapy.Sports (Basel, Switzerland) · 2026Review
- Orchestrating neuroinflammation: A symphony of Interleukin-1 and cell type-specific Interleukin-1 receptor type 1 signaling in the brain.Brain behavior and immunity integrative · 2026Article
- Targeting IL-17 Presents a Promising Strategy for Treating Diseases Related to the Dysregulation of Lipid Homeostasis.Mediators of inflammation · 2026Review
- Absence of BCAP in myeloid cells abrogates M2 macrophage differentiation and promotes anti-tumor immunity.iScience · 2025Article
- Interleukin Networks in GVHD: Mechanistic Crosstalk, Therapeutic Targeting, and Emerging Paradigms.International journal of molecular sciences · 2025Review
- BCAP Is an Interferon-Stimulated Gene That Enhances Type I Interferon Activity in Response to Lipopolysaccharide.International journal of molecular sciences · 2025Article
- Targeting persistently activated inflammatory microenvironment to promote chronic wound healing.Frontiers in immunology · 2025Review
- IL-18R supported CAR T cells targeting oncofetal tenascin C for the immunotherapy of pediatric sarcoma and brain tumors.Journal for immunotherapy of cancer · 2024Article
- B cell adapter for PI 3-kinase (BCAP) coordinates antigen internalization and trafficking through the B cell receptor.Science advances · 2024Article
- Pattern-Recognition Receptors and Immunometabolic Reprogramming: What We Know and What to Explore.Journal of innate immunity · 2024Review
- Transcriptome Analysis Revealed Potential Genes of Skeletal Muscle Thermogenesis in Mashen Pigs and Large White Pigs under Cold Stress.International journal of molecular sciences · 2023Article
- IEC-intrinsic IL-1R signaling holds dual roles in regulating intestinal homeostasis and inflammation.The Journal of experimental medicine · 2023Article
- Neuroinflammation in epileptogenesis: from pathophysiology to therapeutic strategies.Frontiers in immunology · 2023Review
- ATF5 promotes malignant T cell survival through the PI3K/AKT/mTOR pathway in cutaneous T cell lymphoma.Frontiers in immunology · 2023Article
- Molecular Characterization of a B Cell Adaptor for Phosphoinositide 3-Kinase Homolog in Lamprey (International journal of molecular sciences · 2022Article
- Proteomic analysis and identification reveal the anti-inflammatory mechanism of clofazimine on lipopolysaccharide-induced acute lung injury in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Article
- Interleukin-18 cytokine in immunity, inflammation, and autoimmunity: Biological role in induction, regulation, and treatment.Frontiers in immunology · 2022Review
- Interleukin-18 in metabolism: From mice physiology to human diseases.Frontiers in endocrinology · 2022Review
- Targeting Glutamine Metabolism Ameliorates Autoimmune HepatitisFrontiers in immunology · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The toll-like receptor (TLR) and interleukin (IL)-1 family of receptors share several signaling components, including the most upstream adapter, MyD88. We previously reported the discovery of B cell adapter for phosphoinositide 3-kinase (BCAP) as a novel toll-IL-1 receptor homology domain-containing adapter that regulates inflammatory responses downstream of TLR signaling. Here we find that BCAP plays a critical role downstream of both IL-1 and IL-18 receptors to regulate T helper (Th) 17 and Th1 cell differentiation, respectively. Absence of T cell intrinsic BCAP did not alter development of naturally arising Th1 and Th17 lineages but led to defects in differentiation to pathogenic Th17 lineage cells. Consequently, mice that lack BCAP in T cells had reduced susceptibility to experimental autoimmune encephalomyelitis. More importantly, we found that BCAP is critical for IL-1R-induced phosphoinositide 3-kinase-Akt-mechanistic target of rapamycin (mTOR) activation, and minimal inhibition of mTOR completely abrogated IL-1β-induced differentiation of pathogenic Th17 cells, mimicking BCAP deficiency. This study establishes BCAP as a critical link between IL-1R and the metabolic status of activated T cells that ultimately regulates the differentiation of inflammatory Th17 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.