CTLA4_PIG CTLA4 ELISA tesk kit
- Known as:
- CTLA4_PIG CTLA4 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15807
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- CTLA4_PIG CTLA4 ELISA tesk kit
Related genes to: CTLA4_PIG CTLA4 ELISA tesk kit
- Gene:
- CTLA4 NIH gene
- Name:
- cytotoxic T-lymphocyte associated protein 4
- Previous symbol:
- CELIAC3, IDDM12
- Synonyms:
- CD152, CD, GSE, CTLA-4
- Chromosome:
- 2q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2019-04-23
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- Sjögren's disease (SjD) is a systemic autoimmune disorder primarily affecting exocrine glands alongside heterogeneous organ involvement. Historically managed through symptomatic relief and conventional disease-modifying therapies, recent immunological advances have steadily expanded our understanding of its pathogenesis and therapeutic approaches. - Source: PubMed
Publication date: 2026/09/12
Yazisiz Veli - Evidence-based, mechanism-guided therapies are urgently needed for treating monogenic inflammatory bowel disease (mIBD). For such rare diseases, mechanistic insight is essential to guide treatment when conventional clinical trials are often not feasible. We aimed to summarize literature-based evidence and to identify knowledge gaps. - Source: PubMed
Yeh Pai-JuiCharlesworth James E GTaylor HenryAshton James JNash KatrinaLam Kin Hangde Ridder LissyVuijk Stephanie AYe ZiqingHuang YingBildstein TaniaHaller WolframJones Kelsey D JShouval Dror SWeiss BatiaLau Yu LungBui-Thi-Thuy QuynhMuise Aleixo MRichards DuncanTravis SimonTurner DanUhlig Holm H - Preeclampsia (PE) is a pregnancy-specific disorder whose pathogenesis remains incompletely elucidated. The prevailing theory suggests that compromised maternal-fetal immune tolerance is a key contributor. In recent years, inhibitory immune checkpoints have garnered considerable attention as key regulatory factors in maintaining immune homeostasis during pregnancy. Programmed cell death protein 1 (PD-1), T cell immunoglobulin and mucin domain-containing protein 3 (Tim-3), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), T cell immunoreceptor with Ig and ITIM domains (TIGIT), and lymphocyte-activation gene 3 (LAG-3) are well-established inhibitory immune checkpoints in reproductive immunology. Additionally, emerging co-inhibitory molecules such as B- and T-lymphocyte attenuator (BTLA) and V-domain Ig suppressor of T cell activation (VISTA) have been increasingly implicated in the regulation of maternal-fetal immune tolerance. This review focuses on dissecting the mechanisms of inhibitory immune checkpoints in preeclampsia as well as their functions in maternal-fetal immune regulation. We evaluate their potential as early diagnostic biomarkers and novel targets for immunotherapy, highlight the limitations of existing relevant investigations, and outline critical pathways for subsequent clinical translation, offering insights into precision prophylaxis and treatment of preeclampsia. - Source: PubMed
Publication date: 2026/08/28
Liu MiDuan GuikaiLai XiaominLin BingyingLi XiangYang JieCao ShuChen HaoWang TongChen BingyanHe ZhihuaMa QinglinDuan ChunZhu YanLu YuanbinGao Yuchi - The immunosuppressive tumor microenvironment (TME) remains one of the main obstacles that limit responsiveness to immunotherapy. Recently, lipid nanoparticles carrying messenger RNA (mRNA) have emerged as a promising strategy to modulate the immunosuppressive TME, with the ultimate goal of sustaining anticancer immunity of cytotoxic T lymphocytes (CTLs). However, there are challenges with mRNA-based cytokine/chemokine therapies such as the lack of specific targeting, low therapeutic efficacy, and elevated toxicity, raising concerns about their clinical translation. Here, we have developed an antibody-coated lipid nanoparticle (Ab-LNP) delivery system that targets the protein triggering receptor expressed on myeloid cells 2 (TREM2) expressed by tumor-associated macrophages (TAMs). We demonstrate that codelivery of a Toll-like receptor agonist and CXCL9-encoding mRNA encapsulated in our Ab-LNP successfully ameliorates immunosuppression and improves tumor infiltration and activity of CTLs. Further combination with immune checkpoint inhibitors against PD-L1 and CTLA-4 promoted a CTL-favoring immunological environment and durable memory immunity. Our Ab-LNPs targeting TAMs highlight the potential of reprogramming immunosuppressive TME to enhance CTL activity for improved response to cancer immunotherapy. - Source: PubMed
Publication date: 2026/09/11
Chen RuiXu LetaoStaudacher Alexander HWang XingJia RuoxuanFinnie John WWang XiaoyanWhelan Dawn MBrown Michael PZhao Chun-Xia - Regulatory T cells are well known for their immunomodulatory role but also their regenerative function is increasingly recognized across multiple tissue types including skeletal muscle, lung and the central nervous system (CNS). In the CNS, Tregs have been shown to promote oligodendrocyte precursor cell differentiation and their interaction with microglia supports a pro-regenerative microenvironment in the brain. The suppressive function of Tregs is highly dependent on the epigenetic signature, specifically DNA methylation, of certain network of Treg-related genes including FOXP3, CTLA4, IKZF2, IKZF4 and TNFRSF18 which collectively function to maintain Treg cell lineage and stability. Whether a similar or the same epigenetic program also influences the regenerative capacity of Tregs remains unknown, and the methylation status of regenerative genes such as AREG, NT3, and osteopontin has never been characterized. Understanding the epigenetic regulation of Tregs in this respect is relevant for demyelinating disease such as multiple sclerosis (MS). MS is characterized by chronic neuroinflammation and neurodegeneration associated with remyelination failure. In MS, Treg suppressive function is compromised and epigenetic dysregulation at key Treg loci has been reported. However, the role of those loci in repair is unknown and the methylation status of regenerative genes in MS Tregs has not been studied. This review examines the evidence for Treg-mediated CNS repair, the epigenetic mechanisms controlling Treg identity, and highlights the epigenetic regulation of Treg regenerative genes as a critical gap in the field with potential implications for remyelination failure in MS. - Source: PubMed
Publication date: 2026/08/27
Chenine SarahTiane AssiaBaeten PaulienVerreycken JanneKnippenberg StephanieGerlach OliverBroux Biekevan den Hove Daniel LAVanmierlo Tim