Ask about this productRelated genes to: CCL8 Blocking Peptide
- Gene:
- CCL8 NIH gene
- Name:
- C-C motif chemokine ligand 8
- Previous symbol:
- SCYA8
- Synonyms:
- MCP-2, HC14
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-14
- Date modifiied:
- 2016-10-05
Related products to: CCL8 Blocking Peptide
Related articles to: CCL8 Blocking Peptide
- The hydroxycarboxylic acid receptor HCA2 is expressed in keratinocytes and immune cells. In mice, the anti-inflammatory potential of HCA2 receptor signalling in the skin was first described in experimental models of psoriasis-like inflammation and bullous pemphigoid-like epidermolysis bullosa acquisita. We examined contact allergic immune responses to the obligate contact sensitiser DNFB in Hcar2 and wild-type C57BL/6 mice. Basal mRNA levels of pro-inflammatory mediators like IFNγ were already increased in the ear tissue of naïve Hcar2 animals. After sensitisation and challenge with DNFB, contact allergic ear swelling and infiltration of neutrophils and CD3+ T cells were increased in Hcar2 mice. To investigate the impact of HCA2 receptors on T cells, we performed in vitro co-stimulation assays with allergen-loaded dendritic cells and antigen-specific T cells, showing increased proliferation and IFNγ production of Hcar2 T lymphocytes. Adoptive transfer of sensitised lymphocytes and experiments with bone marrow chimeric mice indicated that HCAR2 exerts its anti-inflammatory effect in part through radio-resistant, skin-resident cells in the challenge phase. As a potential mechanism, we found that Hcar2 keratinocytes produced higher levels of the neutrophil-attracting chemokine CCL8. In summary, we show that HCA2 receptors are functionally expressed in lymphocytes and keratinocytes and participate in the attenuation of contact allergic immune responses. Our data indicate that the dominant anti-inflammatory effect of HCA2 signalling during the elicitation phase resides in radio-resistant, skin-resident cells, whereas effects on lymphocyte activation are likely to be modulatory. The precise contribution of distinct skin-resident cell populations and the role of endogenous ligands driving HCA2 signalling in this context remain unresolved. - Source: PubMed
Polkownik SinaMeens JuliaLange HagenWeil JohannesKruse BastianBuzzai AnthonyWulff KatharinaBraun Andreas DBonfiatius SusanneTüting ThomasGaffal Evelyn - Photosensitivity is central to cutaneous lupus erythematosus and dermatomyositis (DM), but the mechanisms linking UVB exposure to tissue-specific autoimmunity are poorly defined. Using single-cell RNA sequencing, spatial transcriptomics, proteomics, UVB provocation and in vitro modeling, we identify MMP9⁺CD14⁺ myeloid cells as critical mediators of photosensitivity. These cells expand significantly in lesional skin, produce interferon-β (IFNβ) and colocalize with cytotoxic CD4⁺ T cells at the dermal-epidermal junction. Keratinocytes activate fibroblasts in the superficial dermis, prompting them to release chemokines (CCL2, CCL19, CCL7, CCL8) that recruit MMP9⁺CD14⁺ cells. In vitro, type I interferon-primed keratinocytes exposed to UVB release cytokines activating dendritic cells, mirroring in vivo responses. UVB irradiation of non-lesional skin of patients with DM rapidly recruits these myeloid cells. In a clinical proof-of-concept study, anti-type I interferon treatment with anifrolumab prevented UVB-induced myeloid infiltration and reduced photosensitivity. Therefore, targeting MMP9⁺CD14⁺ cells may offer therapeutic potential for managing photosensitive autoimmune skin conditions. - Source: PubMed
Publication date: 2026/04/24
Wang YuqingAfshari KhashayarHaddadi Nazgol-SadatLopes Carolina SalomãoEng Chee-Huat LinusWhiteman Leah MMartinez NuriaKyawe Pyae PAnufrieva Ksenia SWei KevinFrieda KirstenRosenbach MishaVleugels Ruth AnnGallucci StefaniaHarris John ERashighi MehdiGarber Manuel - To investigate the effects of a matrikine, fibronectin fragment (FN7-10), on human osteoarthritic (OA) synovial fibroblasts and implications for inflammation and cartilage degradation. - Source: PubMed
Publication date: 2026/04/20
Fernandez Davila Jorge GAlberto Ralph AByun SeyounD'Costa SusanShine JacquelineAlvarez CarolinaYanke Adam BOlcott Christopher WDiekman Brian OPhanstiel Douglas HLoeser Richard F - - Source: PubMed
Publication date: 2026/04/20
Li YaoWu JiaweiXing BoWan MingzhiWang YiwenQin NanaZhou ZijunLi JiahuiYu LimingWang Huishan - With the intensification of global warming and environmental pollution, hypoxia is an unavoidable environmental factor in aquatic ecosystems and has multiple adverse effects on fish. Gymnocypris eckloni, a representative species of the Qinghai-Tibetan Plateau, exhibits excellent adaptability to hypoxic environments, however, little is known about the hypoxic adaptation mechanisms of G. eckloni. Herein, effects of acute hypoxia for 12 h (H12S) and chronic hypoxia for different durations (H24S, H96S and H168S) on biochemical parameters and transcriptome of G. eckloni gills were investigated. We found that the gills suffered severe oxidative damage and increased anaerobic glycolysis was observed across all groups, and aerobic glycolysis was elevated in H12S. Inflammatory response, apoptosis and translation process were markedly suppressed, and signal transmission and protein synthesis process were strengthened under acute hypoxia stress. Through STEM and WGCNA, we identified several key hub genes (egln, akt, pdk1, foxo1, pfk, gapdh, gk, bax, casp8, il-8 and il-1β) related to hypoxia from 3608 DEGs, and expression of akt, gk, sdh, gapdh and ldh was significantly upregulated under hypoxia stress, and sod1, cat, bax, casp8 and ccl8 showed an opposite trend. Enrichment analysis revealed that most DEGs were significantly enriched in MAPK signaling pathway, cytokine-cytokine receptor interaction, FoxO signaling pathway, mTOR signaling pathway, glycolysis/gluconeogenesis and apoptosis. The study revealed the differences in the molecular mechanisms of G. eckloni in responding to acute and chronic hypoxia stress, and provided valuable genetic resources for breeding hypoxic-tolerant fish. - Source: PubMed
Publication date: 2026/04/12
Wu ShenjiXia MingzheWang ZiyiLiu DanWang WeiZhang CunfangJia JunmeiTian FeiQi Delin