Ask about this productRelated genes to: FCRL4 antibody
- Gene:
- FCRL4 NIH gene
- Name:
- Fc receptor like 4
- Previous symbol:
- -
- Synonyms:
- FCRH4, IRTA1, IGFP2, CD307d
- Chromosome:
- 1q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-22
- Date modifiied:
- 2016-10-05
Related products to: FCRL4 antibody
Related articles to: FCRL4 antibody
- Our study objective was to identify serum protein signatures associated with progression to rheumatoid arthritis (RA) and response to abatacept in at-risk individuals. - Source: PubMed
Publication date: 2026/02/09
Jasenecova MariannaCoyle CarlMihalovits AlinaRyan SarahPook ElizabethPerucha EsperanzaHarker GabrielleChin MelodyNorton SamCope Andrew P - Fc receptor-like (FCRL) proteins constitute a receptor family that displays overlapping yet distinct features compared to classical Fc receptors. In a healthy immune system, FCRL proteins play a role in promoting and regulating the immune response through their immunoreceptor tyrosine-based motifs. FCRL proteins are expressed mainly by B cells, suggesting a primary role in B-cell responses. For several autoimmune diseases, studies have shown that particularly FCRL4, which binds to dimeric IgA, and FCRL5, which binds to IgG, may have a role in disease pathology and prognosis. These proteins and their transcripts are often enriched in blood and/or affected tissue of patients with a systemic or organ-specific autoimmune disease like rheumatoid arthritis, Sjögren's disease, systemic lupus erythematous, Graves' disease or myasthenia gravis. The expression of FCRL4 and FCRL5 appears to be disease- and context-specific, and influenced by the tissue microenvironment. Yet, the functions of FCRL proteins are still incompletely understood, and more mechanistic studies are necessary to unravel the contribution of FCRL4 and FCRL5 to pathogenic B-cell responses occurring in autoimmune diseases. - Source: PubMed
Publication date: 2026/01/28
Haroun ChristinaKroese Frans G MVerstappen Gwenny M - Nasopharyngeal carcinoma (NPC) is a malignant tumor characterized by extensive immune cell infiltration. However, the function and significance of B cells in NPC have been overlooked. Exploring B cells and their interactions with other immune cells will provide deeper insights into the immune microenvironment of NPC and theories of immunotherapy.We utilized single-cell sequencing data to identify characteristic B cell subtypes of NPC. Subsequently, the presence of the CD20FCRL4 B cell subpopulation was validated in NPC samples using immunohistochemistry and flow cytometry. The interaction between this B cell subpopulation and CD8 T cells was investigated by establishing an in vitro and in vivo co-culture system.Our analysis revealed a subset of CD20FCRL4 B cells that may interact with CD8 T cells through the MHC-I pathway. Furthermore, we observed a co-localized distribution of CD20FCRL4 B cells and CD8 T cells in NPC. Additionally, in vitro experiments demonstrated that IFNγ played a pivotal role in enhancing the delivery of MHC class I-restricted epitope peptides by B cells, potentially due to the upregulation of WDFY4. B cells pre-stimulated with HK-1 lysate and IFNγ, when co-cultured with T cells, can induce the proliferation of CD8 T cells and the formation of immunological memory. Ultimately, this process mediates the cytotoxicity of CD8 T cells against tumor cells both in vitro and in vivo. Notably, we found a positive correlation between the infiltration level of CD20FCRL4 B cells and the expression of PD-1, as well as the response to anti-PD-1 therapy or gemcitabine plus cisplatin combined with anti-PD-1 therapy in NPC.Overall, our study elucidates the potential anti-tumor mechanisms of CD20FCRL4 B cells and provides insights into their role in immunotherapy for NPC. - Source: PubMed
Publication date: 2026/01/08
Zhang BenjianYuan XiaotianGao KeleiYou BoWang YaxuanMeng LaiChen ZirongXie ShaobingLiu YunqingDong ZijianXie ShuminFan RuohaoWang FengjunZhang JunyiXie ZhihaiMo YongzhenZhang HuaJiang Weihong - Sjögren's disease (SjD) is a chronic autoimmune disorder in which sustained B-cell activation drives glandular injury and systemic complications. Epithelial stress and interferon tone amplify B-cell activating factor (BAFF)-dependent survival, skewing selection toward autoreactive clones in both glands and blood. In addition, single-cell B-cell receptor analyses have uncovered interferon-high endotypes with tissue-imprinted oligoclonality and biased isotype and light-chain usage. Within salivary glands, ectopic germinal centers and FcRL4⁺ B cells act as local 'training sites,' integrating Tfh/Tph help, CXCL13 cues, and BAFF/APRIL-NF-κB signaling to sustain plasmablast differentiation. Extrafollicular trajectories - double-negative and age-associated B cells - expand in IFN/TLR7 and IL-21 milieus, while regulatory B-cell restraint is diminished. Emerging data also implicate glycolysis and mTORC1-GLUT1 metabolism in sustaining B-cell hyperactivation. Chronic B-cell receptor signaling and clonal evolution provide a bridge to lymphoma risk. In this review, we outline how these converging pathways define molecular endotypes and propose a precision framework linking them to targeted therapy in SjD. - Source: PubMed
Publication date: 2025/12/23
Chatzis LoukasPalamidas Dimitris AnastasiosDörner Thomas - Disappointing outcomes in Sjögren's disease (SjD) trials underscore the need for reliable, sensitive endpoints. Histological assessment holds promise, but a minimally invasive, repeatable method for salivary gland tissue sampling is lacking. - Source: PubMed
Publication date: 2025/10/23
Achten HelenaGenbrugge EvaDeroo LiselotteCreytens DavidVanhaecke AmberDeprez JokeDumas EmilieVanhoof SophieDe Boeck KristelBauters WouterDochy FrederickRoels DimitriElewaut DirkPeene Isabelle