CCL22 Antibody (Center) Blocking Peptide
- Known as:
- CCL22 Antibody (Center) Blocking Peptide
- Catalog number:
- BP16351c
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- CCL22 Antibody (Center) Blocking Peptide
Related genes to: CCL22 Antibody (Center) Blocking Peptide
- Gene:
- CCL22 NIH gene
- Name:
- C-C motif chemokine ligand 22
- Previous symbol:
- SCYA22
- Synonyms:
- MDC, STCP-1, ABCD-1, DC/B-CK, A-152E5.1, MGC34554
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2016-10-05
Related products to: CCL22 Antibody (Center) Blocking Peptide
Related articles to: CCL22 Antibody (Center) Blocking Peptide
- Air pollution has been associated with the development and exacerbation of atopic dermatitis (AD), but the molecular signatures connecting pollutant-related targets with AD-associated immune dysregulation remain incompletely characterized. - Source: PubMed
Publication date: 2026/09/03
Gao ChangChen LipingHuang TianfengWang Zi - HIV-exposed uninfected (HEU) infants experience multiple health complications compared to HIV-unexposed (HUU) infants, including immune dysregulation in the first year of life. exposure to maternal inflammation associated with HIV infection is a proposed mechanism of HEU immune dysregulation. This study compared markers of inflammation and immune activation over the first year of life between HEU and HUU infants. - Source: PubMed
Publication date: 2026/09/03
Roseto IsabelleSilveira LoriCurtis KailiCanniff JenniferWeinberg AdrianaSmith Christiana - Understanding alterations in immune homeostasis can help early diagnosis and prevention in rheumatoid arthritis (RA). As joint pain often precedes RA onset, we analysed pain-associated immune mediators in individuals at risk of RA (RISK-RA) and in early untreated RA. Serum CCL22 levels were elevated in both groups, prompting us to further study its sources and effects in RA. - Source: PubMed
Publication date: 2026/09/16
Filipović MašaAfonso MarceloArgyriou AlexandraCîrciumaru AlexandraJoshua VijayRingh MikaelGrönwall CarolineCarlberg KonstantinChen Szu-YingDehara MarinaKrishnamurthy AkilanVivar NancyVan Hulle SenneDecruy TineWähämaa HeidiEkström Tomas JWadsworth Marc HSharma Ravi KumarPadyukov LeonidElewaut DirkVenken KoenAskling JohanWinkler AaronSmith Julia EKlareskog LarsCatrina Anca IHensvold AaseMalmström VivianneChemin KarineRéthi Bence - Eosinophilic chronic rhinosinusitis with nasal polyps (eCRSwNP) is characterized by type 2 inflammation, including M2 macrophage infiltration. Baicalein is a flavonoid with anti-inflammatory properties. This study aimed to investigate the therapeutic effect of baicalein in a papain-induced eosinophilic rhinosinusitis model and to determine whether it acts through arachidonate 15-lipoxygenase (ALOX15)-dependent M2 macrophage function. Clinical nasal samples from controls, non-eosinophilic CRSwNP (neCRSwNP), and eCRSwNP were analyzed for ALOX15 expression and localization. THP-1 cells were differentiated and polarized toward M2 macrophages, and the effects of baicalein on ALOX15 expression, lipid peroxidation, cytokine secretion, and transcriptomic profile were examined. The ALOX15 inhibitor PD146176 was used for target validation. A murine eosinophilic rhinosinusitis model was established by intranasal papain instillation, followed by baicalein treatment. Mucosal inflammation, IgE levels, proteoglycan 2 (PRG2)/ALOX15 expression, and immune cell infiltration were evaluated. ALOX15 was upregulated in eCRSwNP tissues and localized to CD68CD206 M2 macrophages. In vitro, M2 polarization increased ALOX15 expression and lipid peroxidation. Baicalein suppressed ALOX15 expression, lipid peroxidation, and the secretion of CCL22, CCL2, CXCL12, FGF-2, and IL-15. PD146176 produced similar effects, and baicalein showed no additional effect after ALOX15 blockade. RNA sequencing revealed transcriptional remodeling in M2 macrophages after baicalein treatment. In vivo, papain increased ethmoid sinus mucosal thickening, serum IgE, PRG2/ALOX15 positive cells, and infiltration of CD45 immune cells, CD170 eosinophils, F4/80 macrophages, and B220 B cells. Baicalein significantly alleviated all these pathological changes. In conclusion, baicalein attenuates papain-induced eCRSwNP-like inflammation by inhibiting lipid peroxidation and ALOX15-associated M2 macrophage secretory function. The ALOX15/M2 macrophage axis may represent a potential therapeutic target for eCRSwNP. - Source: PubMed
Publication date: 2026/08/26
Wang LeiZhu ZhenzhenLiu YuzhuoAodeng SuritaKang TianhuiWang WeiqingLv Wei - Keratinocytes coordinate re-epithelialization, barrier restoration, inflammatory control, and matrix remodeling during cutaneous repair. Although betanin has reported cytoprotective and antioxidant properties, its wound-relevant transcriptional program in keratinocytes remains incompletely defined. This study therefore asked whether betanin engages barrier, inflammatory, and remodeling-related keratinocyte programs under inflammatory conditions, and whether existing wound-healing databases can account for the resulting transcriptional pattern. Scratch closure was quantified by ImageJ measurement and by an independent rule-based automated image-analysis pipeline with first-order kinetic modeling; transcriptional responses in IFN-γ/TNF-α-stimulated HaCaT cells were interpreted through database-weighted evidence scoring and machine learning-based stress testing. Betanin (20 μg/mL) significantly reduced residual wound area at 24 h (p = 0.020) and 48 h (p = 0.035) by ImageJ quantification, and automated image analysis with kinetic modeling yielded an approximately 1.5-fold higher first-order closure rate constant relative to the vehicle-treated wounded control. Betanin partially restored FLG, reduced KRT14, and selectively attenuated inflammatory mediators including IL1B, ICAM1, CCL22, and CXCL8. Among remodeling-associated genes, TGFB1, COL1A1, and VEGFA were suppressed while COL3A1 was partially restored. NFE2L2 and HMOX1 were only modestly affected, indicating a dominant anti-inflammatory and barrier-modulating response rather than canonical antioxidant axis activation. Database-weighted evidence scoring stably prioritized FLG, COL3A1, COL1A1, and ICAM1, corroborated by betanin-specific experimental responses. Three architecturally distinct machine learning models showed no evidence that database-derived wound-healing features predict betanin-induced transcriptional responses, indicating that the selected prior-knowledge annotations were insufficient to account for the observed pattern in this 15-gene, single-context dataset. - Source: PubMed
Park Sun YoungKim Youjin