rM GM-CSF
- Known as:
- rM GM-CSF
- Catalog number:
- AK8233-0100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Akro
- Gene target:
- GM-CSF
Related genes to: rM GM-CSF
- Gene:
- CSF2 NIH gene
- Name:
- colony stimulating factor 2
- Previous symbol:
- -
- Synonyms:
- GM-CSF, GMCSF
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2018-12-12
Related products to: rM GM-CSF
Related articles to: rM GM-CSF
- Expression of the Csf1r gene is regulated by a conserved enhancer, the fms-intronic regulatory element (FIRE). In mice with a germ-line deletion of FIRE (Fireko) CSF1R expression is undetectable in bone marrow progenitors and classical monocytes but monocytopoiesis and non-classical monocyte maturation are unaffected. The loss of CSF1R is overcome in part by CSF2 in vitro and inflammatory recruitment in vivo. Fireko mice lack microglia and subpopulations of tissue-resident macrophages in peritoneum, kidney, heart, adipose, liver, skeletal muscle, pancreas, pituitary, adrenal and gonads. Heterozygous mutation impacts CSF1-induced proliferation and postnatal expansion of tissue macrophages. Physiological functions of heart and kidney were not affected by the absence of macrophages. In a model of renal injury macrophage recruitment and histopathology in WT and Fireko mice were indistinguishable but there was a male-specific increase in serum creatinine and urea in the Fireko. Tissue-resident macrophages depleted in Fireko mice, including microglia, were replaced by donor-derived cells following intraperitoneal transfer of wild-type bone marrow at weaning. The Fireko mouse provides a platform to dissect functions of tissue resident macrophages in development, homeostasis and pathology. - Source: PubMed
Publication date: 2026/06/26
Liu YajunJacquelin SebastienTaylor IsisGreen Emma KPatkar Omkar LKeshvari SaharRanpura GinellO'Brien Conan J OJessen ElineMaxwell EmmaAllavena RachelGallerand AlexandreIvanov StoyanAdamson AntonyHumphreys Neil ESummers Kim MIrvine Katharine MHume David A - Autoimmune myocarditis frequently progresses to inflammatory cardiomyopathy through dysregulated immune-stromal interactions. This study employs single-nuclei RNA-sequencing (snRNA-seq) to profile 46,233 cardiac nuclei from the experimental autoimmune myocarditis (EAM) mouse model at four timepoints: day 0 (healthy), day 14 (inflammation), day 21 (acute inflammation), and day 40 (late cardiac remodelling). Single-nuclei RNA profiling identified 18 transcriptionally distinct cell populations. Global cell-cell communication analysis revealed a dramatic peak of intercellular signalling at day 14 (5907 interactions), with fibroblast subpopulations and macrophages as dominant hubs, followed by partial resolution at day 21 (2264 interactions) and renewed remodelling at day 40 (4862 interactions). Subclustering of the macrophage compartment identified five subpopulations: Mac-TLF, Mac-MHCII, Mac-rMHCII, Mac-ResL, and Classical Monocytes. Tissue-resident macrophages (Mac-TLF, CCR2-) dominated at healthy state (~55%) but were rapidly depleted at day 14, coinciding with a dramatic influx of recruited CCR2 macrophages (Mac-rMHCII), which expanded to over 70% of the compartment and maintained dominance through day 40. At inflammation (day 14), the expanded Mac-rMHCII subpopulation displayed a strongly pro-inflammatory signature (, , , ), and the overall macrophage compartment was enriched for cytokine response, Fc-gamma receptor, and Notch signalling pathways, while downregulating homeostatic and mitochondrial metabolic programmes, potentially contributing to impaired efferocytosis and cardiomyocyte dysfunction. Macrophage-centred communication networks expanded markedly at day 14 (1047 interactions), with resting fibroblasts (FB-R) as the primary signalling partner, driving pro-inflammatory stromal activation marked by upregulation of , , and . Intra-macrophage subcluster communication also intensified at this timepoint (447 interactions). These findings delineate the temporal and functional heterogeneity of cardiac macrophages during EAM progression and identify key immune-stromal interactions driving pathological cardiac remodelling. The coexistence of pro-inflammatory and transitional reparative macrophage subsets highlights the limitations of broad immunosuppression and supports precision strategies targeting CCR2-mediated recruitment, the SPP1 signalling axis, and macrophage-fibroblast crosstalk as therapeutic avenues in myocarditis and its progression. - Source: PubMed
Publication date: 2026/06/19
Stefanska MonikaKot MartaKoterba DamianZeyland Joanna - Head and neck squamous cell carcinoma (HNSC) exhibits substantial prognostic and microenvironmental heterogeneity. However, the integrated prognostic relevance of synergistic immune and inflammatory signatures in HNSC remains fully elucidated. - Source: PubMed
Publication date: 2026/06/19
Li JieSun ShuxianJi ZiyuWang JiaTang SichenShen ShuijieShi Xiaoya - It is documented that antigens can induce immune responses able to regulate complex diseases. Conversely, the dysregulated inflammatory response in leprosy increases morbidity and leads to reactional episodes, impairing the disease pathogenesis. The goal of this study was to evaluate the potential of the (Sm29) antigen in regulating the immune response in leprosy through a transcriptome study across clinical reactional forms: reversal reaction (RR), and erythema nodosum leprosum (ENL), and without reaction (WR). - Source: PubMed
Publication date: 2026/06/01
Karoline Silva Joycede Farias Lucas NevesLago TainãCardoso Luciana Dos SantosKhouri RicardoMachado Paulo RobertoCastellucci Léa Cristina - Depletion of CD4 cells during an anti-tumor immune response promotes tumor regression and accelerates proliferation of tumor-antigen-specific CD8 T cells in draining lymph nodes (dLNs). However, the effect of the depletion on inter-organ kinetics of antigen presentation and qualitative changes in dendritic cells (DCs) are not yet understood. Here, we established a novel approach for simultaneous detection of cellular movement and cell cycle phase by KikGR/Fucci mice and used it to examine migratory and LN resident DC (LNDC) dynamics after CD4 cell depletion. We found that CD4 cell depletion enhanced migration of CD11c MHC class II migratory DCs from tumor to dLNs and induced activation-associated phenotypic changes, such as increased MHC class II expression. Despite reduced overall cellularity in tumor dLNs, LNDC numbers were relatively maintained. Within the LNDC compartment, CD4 depletion increased the relative abundance of a CD8αCD11b subset and promoted influx and cell-cycle activity among newly recruited LNDCs. Publicly available single-cell RNA sequencing data further delineated ligand-receptor expression relationships, including and axes, within tumor dLNs. These findings reveal remodeling of DC migration, activation, and LNDC turnover within tumor dLNs in the context of CD4 cell depletion, which enhanced anti-tumor immunity. - Source: PubMed
Publication date: 2026/06/10
Moriya TaikiHashimoto MayukoUeda MizukiAoyagi TatsuyaKawaguchi AyakoTakahashi KentaroTsukasa KobayashiDoi KazukiHemmi HiroakiKaisho TsuneyasuUeha SatoshiMatsushima KojiKusumoto YutakaChtanova TatyanaTomura Michio