ITGB2 Antibody
- Known as:
- ITGB2 Antibody
- Catalog number:
- XW-7798
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- ITGB2 Antibody
Related genes to: ITGB2 Antibody
- Gene:
- ITGB2 NIH gene
- Name:
- integrin subunit beta 2
- Previous symbol:
- CD18, MFI7
- Synonyms:
- LFA-1, MAC-1
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: ITGB2 Antibody
Related articles to: ITGB2 Antibody
- Primary sclerosing cholangitis (PSC) is a chronic, idiopathic cholestatic liver disease characterized by inflammation and fibrosis of the bile ducts, yet the cellular crosstalk driving periductal fibrosis remains poorly defined. This study applied a multi-omics approach integrating spatial transcriptomics, RNA-seq, and proteomics to characterize fibrotic periductal regions and their cell-cell communications. Macrophages (MP) subsets, including monocyte-drived-(Mo)MP and lipid-associated-macrophage (LAM)-like, co-localized with cholangiocytes, lymphocytes, and hepatic stellate cells (HSC1). Cell niche analysis identified periductal regions with elevated fibrotic signals, where cell-cell communication analysis revealed potential MP-HSC interactions involving 17 fibrotic driver genes in MP, including ITGB2, GRN, and CCL21, and 6 fibrotic effector genes in HSC. In validation analyses, bulk RNA-seq data showed higher driver and effector gene expression in PSC with established fibrosis compared to early-stage PSC or healthy control (HC). Plasma proteins encoded by MP driver genes were elevated in PSC and in patients with elevated (≥3.29 kPa) liver stiffness on MR elastography. Furthermore, immunofluorescence and SHG imaging showed enrichment of CD68+/CD18+(ITGB2) macrophages in fibrotic regions of PSC liver biopsies. These findings revealed enrichment of MoMP and LAM-like macrophages in fibrotic regions and suggest that they likely contribute to fibrotic activation of nearby HSCs in PSC. - Source: PubMed
Publication date: 2026/04/23
Wang YunguanAdeleke DavidXie XiangfeiYang Zi FWang XiangyaLoi GiuliaYang Vom Hofe AnnikaSingh ManaviMalik AsthaKudira RameshCastro-Rojas CydPfuhler LivaAlquraish MosabSylvestre PamelaDillman Jonathan RTrout Andrew TMiraldi Emily RMiethke Alexander G - Leukocyte adhesion deficiency-I (LAD-I) is a rare autosomal-recessive inborn error of immunity caused by mutations in encoding CD18, which is essential for leukocyte endothelial adhesion and tissue migration. LAD-I is predominantly characterized by frequent life-threatening infections and hyperinflammatory complications, with high rates of pediatric mortality and morbidity without allogeneic hematopoietic stem cell transplantation. Historically, diagnosis and severity classification were based on polymorphonuclear leukocyte CD18 expression. Given improved knowledge of prognostic factors and an evolving treatment landscape, contemporary guidance for severity classification and management is needed. - Source: PubMed
Publication date: 2026/03/14
Heimall JenniferGonzález-Granado Luis IgnacioBooth ClaireIp WinnieKuo Caroline YBakhtiar ShahrzadIkincioğullari AydanFerrua FrancescaChitty-Lopez MariaBailey MirandaCarter PatriceMatthews EmilyLee JenniferProckop SusanGennery Andrew RLeiding Jennifer W - High-grade serous ovarian cancer (HGSOC) is the most lethal histological subtype of ovarian cancer, exhibiting significant heterogeneity and limited therapeutic options. A comprehensive characterisation of proteomic landscape across disease stages is needed to identify actionable biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/18
Tu MengyanTang SangsangZhang QiaoGuo TianchenCen YixuanXu XiaomengWu ShenglongChen XinLu WeiguoDing ChenXu Junfen - Immune checkpoint blockade (ICB) targeting PD-1/PD-L1 axis has transformed breast cancer treatment, yet how therapy reshapes the tumor microenvironment (TME) through cell-cell communication (CCC) remains unclear. Existing CCC inference methods relying on correlations have difficulty distinguishing genuine signaling from confounded associations. Here, we present a causal inference framework that uses single-cell data and leverages treatment as an instrumental variable to identify genuine CCC networks, referred to as scIVCCC, which infers causal signal transduction across cell types. Applying scIVCCC to single-cell RNA-seq data from 31 breast cancer patients before and after anti-PD-1 therapy, we constructed causal CCC networks linking exhausted T cells to tumor-associated macrophages (TAMs). Our analysis reveals a dual role of T cell-macrophage crosstalk: CD4+ and CD8+ exhausted T cells drive anti-tumor M1-like TAMs activation via TNF-TNFRSF1A, TNFSF14-LTBR, and ICAM1-ITGAL/ITGB2. Conversely, they also induce immunosuppressive M2-like polarization through pathways such as TNF-TNFRSF1B (TNFR2), TNFSF14-TNFRSF14 (HVEM), and RPS19-C5AR1, which likely contribute to therapeutic resistance. Our causal modeling suggests that receptors within these networks, such as C5AR1, TNFR2, and CSF1R, may serve as potential candidates for combination therapies to enhance anti-PD-1 efficacy. Collectively, these findings demonstrate that scIVCCC offers a robust framework for dissecting treatment-induced CCC dynamics and prioritizing actionable targets for clinical translation. - Source: PubMed
Qiu AodongZhang HanRamsey Joseph DAndrews BryanSun BoyangRen ShuangxiaLu MengyaoZhang KunCooper Gregory FLu BinfengChen LujiaLu Xinghua - Leukocyte Adhesion Deficiency (LAD) is a rare primary immunodeficiency characterized by impaired leukocyte adhesion and migration, resulting in recurrent bacterial infections, poor wound healing, and delayed umbilical cord separation. We report a 42-day-old female infant who presented with recurrent skin infections and delayed cord detachment in the absence of fever and purulent discharge. Flow cytometry showed markedly reduced CD18 expression (1.8%), and genetic analysis confirmed a homozygous ITGB2 mutation (c.844C>T; p.Arg282Trp), consistent with LAD Type I. Neutrophil oxidative burst was normal, excluding chronic granulomatous disease. Early diagnosis allowed timely initiation of prophylactic antibiotics and close follow-up to prevent complications. This case emphasizes the diagnostic importance of recognizing infection without pus and delayed umbilical separation as hallmark features of LAD. - Source: PubMed
Publication date: 2026/04/14
Goli RasoulKarimi NasrinHassanzadeh AkoRezaei SomayehArad MansourShahmirza NoushinAtharifar Reza