CCR3 (C-Terminus) Peptide
- Known as:
- CCR3 (C-Terminus) Peptide
- Catalog number:
- 1105P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CCR3 (C-Terminus) Peptide
Related genes to: CCR3 (C-Terminus) Peptide
- Gene:
- CCR3 NIH gene
- Name:
- C-C motif chemokine receptor 3
- Previous symbol:
- CMKBR3
- Synonyms:
- CC-CKR-3, CKR3, CD193
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-30
- Date modifiied:
- 2016-10-05
Related products to: CCR3 (C-Terminus) Peptide
Related articles to: CCR3 (C-Terminus) Peptide
- Nucleated erythroid cells (NECs) are emerging as important immunoregulators at the feto-maternal interface, yet their chemokine profiles and functional dynamics across pregnancy remain poorly understood. Using a murine allogeneic pregnancy model (CBA × C57Bl/6), we isolated placental and splenic TER-119 NECs at mid- (E12.5) and late (E19.5) gestation. Chemokine production (13-plex), chemokine receptor expression (qPCR), immunosuppressive molecules (PD-L1, TGF-β, and ROS), T-cell proliferation (CFSE), and immune cell migration (Transwell) were assessed. CD45 placental NECs were the main producers of PD-L1, TGF-β, and ROS, with maximal expression at E19.5, suggesting their potential contribution to the immunosuppressive functions observed in the total TER-119 population. Chemokine production showed a striking shift in CCL17 and CXCL9 from the spleen to the placenta as pregnancy advanced (E12.5 → E19.5). Splenic NECs displayed dominant expressions of CCR3 and CXCR4. Unexpectedly, CCL2 and CCL4 blockade enhanced immune cell migration toward placental NECs at E19.5. Placental nucleated erythroid cells potently suppressed T-cell proliferation at E12.5, and this suppressive capacity remained stable until full term. Placental NECs undergo dynamic chemokine reprogramming while maintaining stable T-cell suppression. The paradoxical enhancement of migration after CCL2/CCL4 blockade suggests a complex chemokine network warranting further investigation. These findings provide new insights into the immunobiology of pregnancy and may have implications for understanding pregnancy complications. - Source: PubMed
Publication date: 2026/08/08
Shevchenko Julia ANazarov Kirill VGizbrekht Alina ASavostyanova Tatyana AZakhareva Alena PSennikov Sergey V - Allergic rhinitis (AR) is a prevalent chronic upper airway inflammatory disorder. Olfactory dysfunction (OD) in AR patients represents a frequent and burdensome complication that significantly compromises quality of life. While the pathogenesis of AR-associated OD remains incompletely characterized, emerging evidence points to olfactory bulb (OB) microglial neuroinflammation as a crucial contributor. C-C motif chemokine ligand 7 (CCL7) is consistently upregulated in AR nasal mucosa and has been documented to drive microglial inflammation. However, its expression and function in OB microglia remain undefined. This study aimed to investigate the specific role of CCL7 in OB microglia and its potential contribution to AR-associated OD, with the goal of providing new mechanistic insights and potential intervention targets. - Source: PubMed
Publication date: 2026/08/10
Yang TingShen HuiZhao TingtingMou YakuiHu YueSong XiaoyuWang YaoChen YujiaoWang HanruiRen ChaoSong Xicheng - Diffuse midline gliomas (DMGs) are highly aggressive, WHO grade 4 glial tumors that arise in midline central nervous system structures and are defined by K27M mutations in histone H3 genes. These K27M mutations shape intratumoral myeloid cell composition in DMG. In H3.1K27M DMGs, genetic ablation of monocyte recruitment reshapes the tumor microenvironment (TME) by reducing monocyte-derived macrophages (MDMs) and increasing microglia and neutrophil presence, with overall survival remaining unchanged, indicating compensatory myeloid remodeling is occurring. Here, by using CRISPR/Cas9-based genome editing, we generated a mouse model deficient for CCR1/CCR2/CCR3/CCR5 (Δ1235). Using this strain, we effectively abolished monocyte and MDM infiltration and reversed compensatory recruitment of CCR1+ neutrophils. Abolishing MDMs in tumors skewed remaining neutrophils and microglia toward a homeostatic state, reduced expression of immune checkpoint molecules on T cells, and extended the survival of H3.1K27M DMG-bearing mice. In contrast, H3.3K27M DMG showed independence from MDM recruitment, suggesting reliance on other TME-driven signaling. Last, H3.1K27M DMGs exhibited reduced microglia presence and a dose-dependent increase in MDM infiltration postirradiation. MDM depletion did not further enhance radiation efficacy, potentially due to compensatory recruitment of classical neutrophils. Collectively, these data reveal histone mutation-specific myeloid dependencies in DMG, highlighting MDM-independent mechanisms in H3.3K27M tumors and MDM-dependent pathways in H3.1K27M tumors. - Source: PubMed
Publication date: 2026/08/13
Puigdelloses Vallcorba MontserratRawat KavitaSoni NishantDiMauro AngelaChu Jacqueline DThomason WesFurtado Glaucia CStrahl MayaWu JunyanJoshi TanviAngione AngeloPiñero GonzaloBecher Oren JRoss James LTsankov Alexander MLira Sergio AHambardzumyan Dolores - [This retracts the article DOI: 10.1002/ccr3.72524.]. - Source: PubMed
Publication date: 2026/08/06
- Intradermal injections of anti-canine immunoglobulin E (IgE) in healthy dogs have been utilized in preclinical drug testing to evaluate the efficacy of anti-allergic drugs used to treat canine atopic dermatitis (AD). However, the molecular effects of established canine anti-allergic drugs on this acute canine IgE-mediated atopic model remain largely uninvestigated. The objective of this study was to characterize the effect of proactive oclacitinib and prednisolone treatments on the immune and skin barrier transcriptome of IgE-mediated late-phase reactions (LPRs) in an acute model of canine AD. Sixteen healthy adult research-bred beagles were randomized to receive either oclacitinib or prednisolone orally for six days, followed by an intradermal anti-canine IgE injection. Biopsies were collected 24 h post-injection for RNA isolation and sequencing; previously analyzed transcriptomes (healthy skin, saline-injected skin, IgE lesions without drug modulation) from the same colony of dogs served as controls. Administration of prednisolone and oclacitinib prior to intradermal anti-IgE injections reduced the number of differentially expressed genes (DEGs) in 24 h samples to 1251 and 1471, respectively. Both treatments resulted in a decrease in expression of several significantly upregulated T helper-(Th)1 (e.g., , , ), Th2 (e.g., , , , , , ), chemokine and receptor (e.g., , , , , ) genes in comparison to the untreated IgE-mediated lesions. Interestingly, only prednisolone treatment significantly reduced upregulation, an important gene in the Th2 immune response. In conclusion, both prednisolone and oclacitinib reduced the transcriptomic changes observed in the acute lesions of the canine IgE-induced atopic dermatitis model, with prednisolone inducing a broader inhibitory immune response. - Source: PubMed
Publication date: 2026/07/13
Leon RenatoBlubaugh AmandaStarr HaleyBanovic Frane