Ask about this productRelated genes to: BLNK antibody
- Gene:
- BLNK NIH gene
- Name:
- B cell linker
- Previous symbol:
- -
- Synonyms:
- SLP65, Ly57, SLP-65, BLNK-s, BASH, bca
- Chromosome:
- 10q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-16
- Date modifiied:
- 2019-04-23
Related products to: BLNK antibody
Related articles to: BLNK antibody
- Autoimmune nodopathies (AINs) are rare acquired autoimmune neuropathies with distinct clinical features and circulating autoantibodies, often of the immunoglobulin G4 (IgG4) subclass, targeting proteins at the node of Ranvier. Defects in B cell tolerance checkpoints have been implicated in several autoimmune diseases, including MuSK-positive myasthenia gravis, another IgG4 autoantibody-mediated disease. Here, we investigated whether tolerance defects exist in neurofascin-155-mediated AIN (NF155-AIN), using a well-established assay, by generating recombinant antibodies from new emigrant (NE) and mature naive (MN) B cells from three NF155-AIN patients, and tested them for polyreactivity and autoreactivity. Additionally, we analyzed the transcriptome of peripheral blood mononuclear cells, with a particular focus on naive B cells and CD4+ T cells at the single-cell level, and characterized cell-cell interactions. NF155-AIN patients have an elevated frequency of polyreactive B cells in the NE (37.4% compared to 9.7% in healthy controls (HCs), = 0.03) and MN (31.5% compared to 10.5% in HCs, = 0.03) compartments, consistent with a breach in early B cell tolerance checkpoints. In this unbiased exploratory transcriptomics analysis, we observed potentially abnormal B cell receptor (BCR) signaling characterized by low CD79B, CSK, BLNK, and BTK expression, and possible impaired CD4+ T cell regulatory function. Moreover, comparison with chronic inflammatory demyelinating polyneuropathy, a related autoimmune neuropathy, suggested that these differences are specific to NF155-AIN. A breach in early B cell tolerance checkpoints, with defective BCR signaling, and disrupted T cell-B cell interactions in NF155-AIN, may contribute to the development of pathogenic autoreactivity. - Source: PubMed
Publication date: 2026/04/20
Roy BhaskarObaid Abeer HWang ZhenjianKovacs Kristof GOhashi SarahKalayci F Naz CemreJoo DanielMasi GianvitoCoppola CarminaDas SameeranHernandez Amanda LMartin-Aguilar LorenaLleixà CintaNowak Richard JQuerol LuisO'Connor Kevin C - Chronic lung allograft dysfunction (CLAD) leads to declining respiratory function and high mortality, representing the main barrier to long-term survival in lung transplantation (LT). We performed the first genome-wide association study (GWAS) investigating donor's and recipient's genetic factors associated with CLAD. - Source: PubMed
Publication date: 2026/03/19
Brocard SimonMauduit VincentMorin MartinBoussamet LéoSilva Nayane Dos Santos BritoDurand AxelleHalitim PierreRenaud-Picard BenjaminCoiffard BenjaminDemant XavierFalque LoïcLe Pavec JéromeRoux AntoineVilleneuve ThomasKnoop ChristianeMerveilleux ClaireSalpin MathildeCarlier NicolasGourraud Pierre AntoineMagnan AntoineLair DavidBerthelot LaurelineSüdholt MarioVince NicolasTissot AdrienLimou Sophie - Accumulating evidence indicates that Alzheimer disease (AD) is caused by dysregulated microglial phagocytosis. The main risk factor for AD is age, and ageing reduces microglial phagocytosis of amyloid-β (Aβ) plaques, while increasing microglial phagocytosis of synapses and neurons. Most of the known genetic risk for AD can be linked to microglial phagocytosis, including ABCA1, ABI3, ACE, ADAM17, APOE, APP, BIN1, BLNK, CD2AP, CD33, CLU, CR1, CTSB, CTSH, EED, GRN, INPP5D, LILRB2, PICALM, PLCG2, PSEN1, PTK2B, SIGLEC11, SORL1, SPI1, TMEM106B and TREM2. Moreover, the only disease-modifying treatments for AD - anti-Aβ antibodies - work by increasing microglial phagocytosis of Aβ aggregates. Microglial phagocytosis of Aβ via TREM2, LRP1, CD33, TAM receptors and anti-Aβ antibodies appears to reduce AD pathology by pruning and compacting plaques, restricting subsequent tau pathology, whereas microglial phagocytosis of synapses and neurons seems detrimental in the later stages of AD, via complement, P2Y receptor and TREM2. However, the roles of microglial phagocytosis in AD are complex and multifaceted, and improved treatments are likely to require a deeper understanding of these roles. - Source: PubMed
Publication date: 2025/11/28
Brown Guy CSt George-Hyslop PeterPaolicelli Rosa CLemke Greg - Alzheimer's disease (AD) has greater prevalence in women and lacks effective treatments. Integrating multimodal data using machine learning (ML) may help improve diagnostics and prognostics. - Source: PubMed
Publication date: 2025/10/03
Mohamed Ismail NasimMiller MaggieCrossland HannahSharif Jalil-AhmadChapple J PaulWahlestedt ClaesShkura KirillVolmar Claude-HenrySlabaugh GregoryTimmons James A - Classic Hodgkin lymphoma (cHL) is a malignant tumor in children. At present, some patients cannot be cured with first-line treatment, and many cured patients die prematurely because of the late toxic effects of treatment. In addition, effective early survival prediction biomarkers are lacking. The aim of this study was to explore the predictive value of B-cell linker protein (BLNK) in cHL. Sixty-three patients from the Fourth Hospital of Hebei Medical University were included in the study from January 2008 to March 2024 (training set). Immunohistochemistry was used to measure the expression of BLNK. Eleven patients with < 10% BLNK-positive cells (BLNK-negative, BLNK-) and 52 patients with 10 ~ 49% BLNK-positive cells (BLNK-positive, BLNK+) were included. The correlations between BLNK expression and clinicopathological features were analyzed. Univariate and multivariate Cox analyses were used to determine the independent prognostic variables of overall survival (OS) and progression-free survival (PFS). Construction and validation of nomogram to predict PFS of cHL patients. In addition, we included 29 patients with cHL who were admitted between January 2000 and December 2007 as a validation set to explore the robustness of the above prediction model. The OS and PFS of cHL patients in the BLNK+ group were significantly longer than those of patients in the BLNK- group. BLNK expression, the presence of bulky disease, the B lymphocyte count, LDH levels and the neutrophil count were determined to be independent prognostic factors by multivariable Cox regression analysis of PFS. A nomogram model was constructed based on these factors. The discriminative ability of the nomogram was good; the C-index was 0.844 (0.761, 0.926) in the training set and 0.824 (0.717, 0.931) in the validation set. The results of the calibration curve suggested strong agreement between the forecast and actual observations in both the training set and the validation set. Subgroup analysis successfully identified a treatment-sensitive population of cHL patients to predict prognosis according to the BLNK level. In the subgroups without giant tumor lesions, an age≥9 years, St. Jude Stages III-IV, chemotherapy regimens (1/2), a CRP concentration >7.5 mg/L, a B lymphocyte count >5.7 × 10^6/L, a lymphocyte count ≤ 3.68 × 10^9/L, and a platelet count ≤ 387 × 10^9/L had a greater effect on PFS in the BLNK-negative group. An age ≥9 years, St. Jude Stages III-IV, the absence of a giant tumor lesion, a chemotherapy regimen (2), a CRP concentration >10.2 mg/L, a B lymphocyte count >18.5 × 10^6/L, an IgG concentration >6.91 g/L, a neutrophil count ≤ 5.6 × 10^9/L, a lymphocyte count >0.49 × 10^9/L, a platelet count >298.5 × 10^9/L, a PLR >199.31, and an NLR >3.17 had a greater effect on OS in the BLNK-negative group. Decreased BLNK expression predicts prolonged PFS among patients with cHL. The validated nomogram integrating BLNK and clinical parameters provides potential predictive value for PFS of cHL. No Clinical trial registration. - Source: PubMed
Publication date: 2025/10/24
Yan YiweiHou YuanyuanZhu XiuliChen JianZhang WentingDiao YuqiaoLu XiaofeiJiang Lian