CD11b
- Known as:
- CD11b
- Catalog number:
- 10-502-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD11b
Ask about this productRelated genes to: CD11b
- Gene:
- ITGAM NIH gene
- Name:
- integrin subunit alpha M
- Previous symbol:
- CR3A, CD11B
- Synonyms:
- MAC-1, CD11b
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-05
- Date modifiied:
- 2019-04-23
Related products to: CD11b
Related articles to: CD11b
- Systemic lupus erythematosus (SLE) is a complex autoimmune disease with a strong genetic component, and lupus nephritis (LN) represents one of its most common and severe organ-specific manifestations. This review synthesises current evidence on the genetic architecture of SLE and LN, with a particular focus on identifying shared and distinct genetic susceptibility loci and highlighting knowledge and data gaps in highly burdened African populations. Across studies, most risk loci, including , , , , , , , , and , converge on key immune pathways such as antigen presentation, type I IFN signalling, B-cell activation, and immune complex clearance. The findings support a substantial genomic overlap between SLE and LN, with most variants contributing to systemic immune dysregulation rather than kidney-specific susceptibility. A limited number of loci, including , , and , have been implicated in renal involvement, while G1/G2 risk variants are associated with renal disease progression and adverse kidney outcomes among individuals of African ancestry. Despite these advances, relatively few loci have been definitively linked to LN independent of SLE, reflecting both biological overlap and limitations in study design. Moreover, the existing literature is heavily skewed toward European, Asian, and admixed populations, with minimal representation of continental African cohorts. Given the high genetic diversity and disproportionate disease burden in African populations, this represents a critical knowledge gap. Improved inclusion of diverse populations, coupled with high-resolution genomic and functional studies, will be essential to refine causal variant identification and enhance understanding of disease mechanisms. Ultimately, insights into population-specific genetic risk may enable earlier identification of high-risk individuals and support the development of precision medicine strategies for SLE, specifically LN. - Source: PubMed
Publication date: 2026/08/18
Obadic Bianca GKatsukunya Jonathan NDavidson BiancaJones Erika S WHodkinson BridgetFreercks RobertDandara ColletMnika Khuthala - Atherosclerotic cardiovascular disease (ASCVD), including coronary heart disease (CHD), ischemic stroke (IS), and peripheral artery disease (PAD), represents a growing global health burden. Integrins have emerged as potential biomarkers and therapeutic targets. This study aimed to explore the role of integrins as biomarkers for ASCVD and to identify potential drug targets. A total of 33,210 UK Biobank participants were included. Cox proportional hazards models were used to assess associations between circulating integrin levels and ASCVD and its subtypes. Mendelian randomization and colocalization analyses were performed to investigate potential causal relationships and shared genetic variants underlying integrin levels and disease risk. During a median follow-up of 14.04 years, 2468 participants developed ASCVD. In subtype-specific analyses, 1541 CHD events, 1050 IS events, and 590 PAD events were identified. In observational analyses, ITGA11, ITGA2, ITGAM, ITGAV, ITGB1 and ITGB2 were associated with lower ASCVD risk, whereas ITGA5 and ITGBL1 were associated with higher risk. For ASCVD mortality, ITGA11, ITGAM, ITGAV, and ITGB2 showed protective associations, while ITGAX and ITGB6 were linked to increased risk. Sex-stratified analyses revealed distinct patterns, including male-specific risk associations for ITGAX and ITGBL1 and a female-specific protective association for ITGB2. Mendelian randomization supported causal associations for five integrins, with ITGA11 showing consistency with observational findings. Colocalization analysis suggested shared causal variants between ITGAV and both CHD and IS. This study provides both observational and genetic evidence for the critical role of integrins in ASCVD, implicating their potential for assessing disease risk and serving as candidate therapeutic targets. - Source: PubMed
Publication date: 2026/08/15
Niu MengyingFeng YuyaoShu KeqiangYang YixuanChen JunyeLai ZhichaoLiu BaoPeng Bin - Microgliosis and severe coagulation, including fibrinogen deposition, are features of both experimental and human cerebral malaria (CM), a lethal disease. Vascular-associated microglia migrate to coagulated cerebral vessels containing inflammatory monocytes and T cells in experimental CM. We previously showed that microglial depletion exacerbates coagulation and disease severity, including hypothermia, while anticoagulant treatment reduces microgliosis and prevents mortality. These data suggest an overall protective effect of microglia on eCM, and indicate a link between microgliosis, hypothermia, and coagulation. Therefore, mechanisms of migration and activation of microglia, T cells, and monocytes were studied in relation to the role of fibrin(ogen) in eCM. - Source: PubMed
Publication date: 2026/07/24
Domingo Nadia DSolomon Olivia DVillarreal PaulaAussenac FlorentinVanegas DifernandoEndrino Mark JosephMendiola Andrew SPuebla-Clark LucindaGbedande KomiCardona Astrid EAkassoglou KaterinaFlick Matthew JVargas GracieStephens Robin - To identify immune-related molecular targets in polycystic ovary syndrome (PCOS) and evaluate the role of integrin beta-2 (ITGB2) and the potential modulation by rutin. - Source: PubMed
Publication date: 2026/08/10
Yi PengCao YingZhou YanruMao SuqingFu Xianghong - Monocytes play a critical role in regulating immune response to exogenous and endogenous challenge. Recent studies have shown exogenous stimuli can induce metabolic, epigenetic and phenotypic changes in monocytes that reprogramme or 'prime' them to react with an altered response to subsequent stimuli. Obesity is associated with immune dysfunction. However, the ability of endogenous compounds associated with obesity to prime human monocytes and thereby modulate subsequent response remains to be investigated. - Source: PubMed
Publication date: 2026/07/20
Topham Ben JHock Barry DWiggins George A RAshby Louisa VMagon Nicholas JPhillips ElisabethSymonds Emma K CDanielson Kirsty MCurrie Margaret J