BTLA
- Known as:
- BTLA
- Catalog number:
- Y214083
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BTLA
Related genes to: BTLA
- Gene:
- BTLA NIH gene
- Name:
- B and T lymphocyte associated
- Previous symbol:
- -
- Synonyms:
- BTLA1, CD272
- Chromosome:
- 3q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-08-20
- Date modifiied:
- 2014-11-19
Related products to: BTLA
Related articles to: BTLA
- Continuous exposure to antigens drives the activation of circulating T follicular helper (cTfh) cells, promoting high-affinity antibody production. However, sustained stimulation may impair their function through the upregulation of immunoregulatory markers like B and T lymphocyte attenuator (BTLA) and Lymphocyte-activation gene 3 (LAG-3). This study investigated the role of cTfh cells and their subsets in Plasmodium falciparum-associated placental malaria (PM). In a cross-sectional study conducted in Yaounde, Cameroon (March 2022-May 2023), peripheral, placental, and cord blood samples were collected from 49 women at delivery. Hemoglobin (Hb) levels were recorded, and peripheral blood mononuclear cells (PBMCs), intervillous blood mononuclear cell (IVBMCs), and cord blood mononuclear cells (CBMCs) were isolated for multiparametric flow cytometry analysis of cTfh cells and subsets (ICOS and ICOS cTfh subsets). PM was associated with increased cTfh cell frequencies in both PBMC and IVBMC. PM-negative (PM-) women displayed higher ICOS cTfh cell frequencies, while PM-positive (PM+) women had elevated ICOS cTfh cells that correlated with parasitemia levels. BTLA expression was downregulated in bulk cTfh and ICOS cTfh cells during PM. Interestingly, cTfh frequencies in IVBMC positively correlated with baby weight, while cTfh frequencies in PBMC and IVBMC negatively associated with maternal Hb. Furthermore, BTLA and LAG-3 expression in IVBMC negatively correlated with birth weight. Together, these findings highlight altered cTfh cell profiles during PM, influencing maternal and neonatal outcomes. - Source: PubMed
Zambo Bitye Bernard MarieMbianda Nana Chris MarcoKwanou Tchakounte Bodin DarcisseFogang BalotinKenfack Tekougang Zangue BereniceMedouen Ndeumou Reine Seumko'oAyong LawrenceMegnekou Rosette - Bladder cancer (BC) is a common malignancy with high recurrence and substantial monitoring costs. Limitations of current diagnostic tools: cystoscopy is invasive and expensive, urine cytology lacks sensitivity and existing urine biomarkers cannot replace cystoscopy, underscoring the need for improved non-invasive methods. Immune checkpoints (ICs) regulate immune activity, and newer ICs: T-cell immunoglobulin and mucin domain 3 (TIM-3), galectin-9 (Gal-9), B- and T-lymphocyte attenuator (BTLA), herpesvirus entry mediator (HVEM), cluster of differentiation 160 (CD160), and lymphocyte-activation gene 3 (LAG-3), are involved in cancer immune evasion. This study demonstrated that levels of soluble ICs (sICs) are markedly elevated in patients with early-stage BC. Serum levels of sTIM-3, sGal-9, sBTLA, sHVEM, sCD160, and sLAG-3 were quantified in BC and controls. sTIM-3, sGal-9, and sBTLA were significantly elevated in BC, while their concentrations didn’t vary by tumor stage or grade, supporting diagnostic rather than prognostic utility. Whereas sHVEM, sCD160, and sLAG-3 showed no diagnostic value. Age, sex, and body mass index (BMI) had minimal influence on sIC levels. Receiver operating characteristic (ROC) analyses showed strong performance: sGal-9 was the best classifier (area under the curve (AUC) = 0.98; 91% sensitivity; 100% specificity), followed by sTIM-3 (AUC = 0.91) and sBTLA (AUC = 0.78). sHVEM, sCD160, sLAG-3 performed poorly. A multivariate model incorporating sGal-9, sTIM-3, and sBTLA achieved a cross-validated AUC = 0.982, with sGal-9 remaining independently predictive. Correlation analyses revealed two clusters: sGal-9/sTIM-3/sBTLA and sHVEM/sCD160, that relationships align with known receptor-ligand biology and may reflect shedding during T-cell exhaustion. Overall, sGal-9, supported by sTIM-3 and sBTLA, constitutes promising serum biomarker panel associated with early-stage BC, however, as these markers are not disease-specific and may be affected by inflammatory or other pathological conditions, further validation is required. - Source: PubMed
Publication date: 2026/04/14
Andrzejczak AnnaKrajewski WojciechJaskuła EmiliaChorbińska JoannaTomkiewicz AnnaSarat KrystianMroczek RobertMałkiewicz BartoszSzydełko TomaszKarabon Lidia - Immunosuppressive tumor microenvironment (TME) inactivates CD8+ cytotoxic lymphocytes (CTLs). Here, we identify SPTBN2 spectrin as a key immunosuppressive regulator induced in CTLs in response to nutritional deficit. In human pancreatic and colorectal cancers, SPTBN2 expression negatively correlated with CTL infiltration and patients' survival. In TME of mouse pancreatic and colorectal adenocarcinomas, SPTBN2 inactivated intratumoral CTLs, stimulated tumor growth and conferred cross-resistance to anti-cancer therapies. SPTBN2 knockout protected CAR T-cells from trogocytosis and increased their memory state. SPTBN2 maintained levels of cell surface proteins such as BTLA that undermine CAR T-cell cytotoxicity and promote exhaustion. Re-expression of BTLA largely reversed phenotypes in SPTBN2-deficient CAR T-cells. In manufactured CAR T cells, SPTBN2 was associated with their clinical failure in pediatric patients with leukemia. Accordingly, ablation of SPTBN2 in CAR T-cells increased their cytotoxicity, in vivo persistence and therapeutic effects indicating that SPTBN2 can be targeted to increase the efficacy of anti-cancer therapies. - Source: PubMed
Publication date: 2026/04/01
Bui Quoc ThangBasavaraja RaghavendraDhamdhere Mayura RHolczbauer ÅgnesParuzzo LucaGuruprasad PuneethScaglione MichaelTang YingyingSun YuchenBeiting Daniel PNash Erik KFazelinia HosseinSpruce Lynn AWang AliceTan KaiGuo WeiConn Crystal SFan YiKoumenis ConstantinosSpiegelman Vladimir SRui HallgeirDiehl J AlanAtherton Matthew JStanger Ben ZBailis WillRuella MarcoFuchs Serge Y - Schizophrenia (SCZ) is a complex psychiatric disorder, and its pathogenic mechanisms are not yet fully understood. The identification of reliable blood biomarkers and molecular subtypes for early diagnosis and effective therapy remains a significant challenge. To address this issue, we utilized a combination of bioinformatics and machine learning (ML) to identify potential biomarkers for SCZ. Our approach involved the integration of 12 different ML algorithms to develop a diagnostic signature based on data from several datasets, including GSE18312, GSE27383, GSE38485, GSE54913, and GSE165604. A nomogram was constructed using these datasets for potential clinical applications. In addition, clustering analysis was performed on SCZ patients using consensus clustering and non-negative matrix factorization (NMF) algorithms. We further evaluated subtype differences in biological functions and immune cells through various methods, such as gene set enrichment analysis (GSEA), gene set variation analysis (GSVA), Proteomaps, and IOBR analyses. Our results identified a diagnostic signature composed of 16 genes (APBB2, CLCN1, SYDE1, PAX5, SNAI1, DAZL, UNC93B1, PLAGL2, HS3ST1, ITPKB, PILRA, BTLA, SWAP70, AZI2, ADM, and AVPR2), which demonstrated robust performance in diagnosing SCZ across eight different datasets. A nomogram based on these genes was created, providing clinical benefits for SCZ patients. Among the identified genes, AZI2 was found to be the most critical, influencing inflammation and immunity. We also identified potential chemical compounds that could target these 16 genes. Unsupervised clustering and NMF algorithms revealed two distinct subtypes of SCZ, each associated with unique immune cell profiles, biological functions, and protein expression levels. In conclusion, this study not only developed a diagnostic signature and a novel nomogram for SCZ but also provided new insights into the subtypes of SCZ. These findings may pave the way for personalized diagnosis and treatment strategies for SCZ patients. - Source: PubMed
Publication date: 2026/03/24
Li ZhijunSun QingLi HaoyuGuan NaiyuNi JingWang JingXu XiaoleiShen YeSun SiyuLi Yan - Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a systemic autoimmune disease characterized by necrotizing small-vessel inflammation, in which dysregulated adaptive immune responses play a central pathogenic role. Beyond the well-established contribution of ANCAs and innate immune activation, increasing evidence highlights profound alterations in T-cell regulation that drive persistent inflammation, autoantibody production, and organ damage. Immune checkpoints (ICs)-a network of co-stimulatory and co-inhibitory pathways that fine-tune lymphocyte activation and maintain peripheral tolerance-have emerged as key regulators in this process. In this review, we summarize current experimental and clinical evidence demonstrating imbalance across multiple immune checkpoint pathways in AAV, including the PD-1/PD-L1/PD-L2 axis, CD28/CTLA-4, ICOS, CD40-CD40L, OX40, LAG-3, TIM-3, BTLA, and CD27. We discuss how impaired inhibitory signaling combined with enhanced co-stimulatory activity promotes sustained T-cell activation, aberrant T-B cell collaboration, and pathogenic ANCA production, contributing to vascular and renal injury. Importantly, both membrane-bound and soluble checkpoint molecules show disease-specific alterations in blood, urine, and renal tissue, correlating with disease activity, renal involvement, treatment response, and relapse risk. These findings position immune checkpoint components as promising biomarkers that may complement conventional clinical and serological markers. Finally, we review the current therapeutic landscape of checkpoint modulation in AAV, including clinical experience with abatacept and emerging evidence supporting PD-1 agonism and other pathway-targeted strategies derived from related autoimmune diseases. Collectively, this work highlights immune checkpoint dysregulation as a central feature of AAV pathophysiology and underscores its potential for advancing precision biomarkers and immune-targeted therapies. - Source: PubMed
Publication date: 2026/03/02
García-Serrano LydiaMartinez-Valenzuela LauraDraibe Juliana