Sheep Skin Tissue, Individual Donor
- Known as:
- Sheep Skin Tissue, Individual Donor
- Catalog number:
- Tissues-303-SKIN
- Product Quantity:
- 1unit
- Category:
- -
- Supplier:
- SeraLab
- Gene target:
- Sheep Skin Tissue Individual Donor
Related genes to: Sheep Skin Tissue, Individual Donor
- Gene:
- CCL27 NIH gene
- Name:
- C-C motif chemokine ligand 27
- Previous symbol:
- SCYA27
- Synonyms:
- ALP, ILC, CTACK, skinkine, ESkine, PESKY, CTAK
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-30
- Date modifiied:
- 2016-10-05
Related products to: Sheep Skin Tissue, Individual Donor
Related articles to: Sheep Skin Tissue, Individual Donor
- Cutaneous T-cell lymphoma (CTCL) is a heterogeneous malignancy characterized by the proliferation of skin-homing CD4 T cells and profound immune dysregulation within the tumor microenvironment (TME). This review synthesizes evidence on chemokine-receptor networks that govern malignant T-cell trafficking among blood, skin, and lymph nodes, the formation of immunosuppressive niches, and clinically actionable biomarker candidates. Among the best-supported axes, CCL17/CCL22-CCR4 and CCL27/CCL28-CCR10 mediate skin tropism, CCL19/CCL21-CCR7 contributes to lymph node homing, and CXCL12-CXCR4 supports skin trafficking and is associated with disease progression. In contrast, CCR2/CCR5/CCR6/CCR8-centered circuits and CXCR3/CXCR5 pathways are emerging regulators of myeloid recruitment, regulatory T-cell accumulation, and context-dependent immune activation. Therapeutically, agents targeting chemokine pathways, most notably the CCR4 monoclonal antibody Mogamulizumab, have demonstrated clinical efficacy, while emerging inhibitors of CCR6, CCR5, and CXCR4 offer promising avenues for intervention. We further highlight how recent single-cell and other high-dimensional omics studies refine cell-type-specific chemokine sources and receptor expression, enabling more precise mapping of chemokine-driven intercellular communication programs in CTCL TME remodeling and better prioritization of therapeutic targets and biomarkers. - Source: PubMed
Publication date: 2026/01/13
Yu ZihaoLi FeiQuan YingHu WeijianZhang PingXie Xin - Major depressive disorder (MDD) is accompanied by activation of the immune-inflammatory response system (IRS) and the compensatory immunoregulatory system (CIRS). Fluoxetine, the most commonly used selective serotonin reuptake inhibitor (SSRI), shows anti-inflammatory effects in both MDD patients and depressive-like behaviors in rodents. The present study examines the effects of fluoxetine on immune profiles, such as M1 and M2 macrophages, T helper (Th)1, Th2, Th17, IRS, and CIRS in MDD and healthy controls (HC). Culture supernatant of immunogen-stimulated whole blood of 18 MDD and 18 HC was measured for 48 cytokines using a multiplex assay. The effects of three fluoxetine concentrations (0.1 mM, 0.01 mM, and 0.001 mM) were examined. MDD was characterized by significantly increased M1, M2, Th1, Th2, Th17, IRS, and CIRS profiles under the stimulation of phytohemagglutinin (PHA) and lipopolysaccharide (LPS). Fluoxetine exhibited different effects on immune functions when comparing culture supernatant from MDD to HC. In HC samples, the administration of fluoxetine did not impact the immune system. In MDD samples, fluoxetine administration significantly reduces the stimulated production of Th1, Th17, M2, IRS, Th2, as well as IL-1 and TNF signaling pathways. Fluoxetine significantly attenuated the production of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor-α, IL-12, interferon-γ, chemokines (CCL27, CXCL10), growth factors, and colony-stimulating factors. However, this suppressant effect is merely partial, insufficient to normalize the immune sensitization in the culture supernatant from MDD patients. In summary, fluoxetine has highly significant immunoregulatory effects in patients with MDD and not in controls. Unfortunately, these effects only partly attenuate the immune sensitization in MDD. - Source: PubMed
Publication date: 2026/01/11
Zhang YingqianLai QiChen TangcongLuo YueyangLi MengdieNiu MengqiLi JingMaes Michael - The reasons for the aggressive clinical phenotype of signet ring cell carcinoma (SRCC) have not been fully elucidated. Previous studies suggest similarities in the genotype of colorectal and gastric SRCC and a clear distinction from non-SRCC. The immune microenvironments of gastric and colorectal SRCC have not been comprehensively examined. We isolated RNA from formalin-fixed, paraffin-embedded (FFPE) sections of 34 tumor specimens, 10 colorectal SRCC, 24 gastric SRCC, 4 non-SRCC colorectal (CCC), and 3 gastric adenocarcinoma (GCC) samples. The PanCancer Immune Profiling Panel was used to evaluate the expression of 770 immune-related genes. We compared the expression profiles of colorectal and gastric SRCC and non-SRCC adenocarcinoma. We found that the immune-related gene expression profiles (GEPs) of colorectal SRCC (CR-SRCC) and gastric SRCC (G-SRCC) were distinct from the non-SRCC. A total of 127 genes were upregulated and 32 downregulated in CR-SRCC compared to CCC. Only two genes (CCL27 and LAIR2 reached statistical significance (-adj < 0.05)) among the differentially expressed genes in G-SRCC compared to GCC. None of the clinically relevant immune checkpoints were significantly differentially expressed in SRCC vs. non-SRCC. Overall, we noted a relative abundance of CD8+ cells in CR-SRCC and G-SRCC and relative overexpression of genes involved in innate immune response including the complement pathway. Finally, we identified IL13RA2 as a potential biomarker and therapeutic target candidate for CR-SRCC. The immune microenvironments of CR-SRCC and G-SRCC are distinct from non-SRCC. Broadly, both CR-SRCC and G-SRCC are characterized by a complex immune microenvironment that features cytotoxic cells and innate immune activity that may facilitate immune evasion. - Source: PubMed
Publication date: 2025/12/23
Zhang JianqingCollingwood RobinAl Diffalha SameerManna Deborah DellaPaluri Ravi KumarMejbel Haider AGbolahan Olumide - Cendakimab is a recombinant, humanized, high-affinity, neutralizing monoclonal antibody that targets IL-13, a cytokine implicated in the pathogenesis of atopic dermatitis (AD). - Source: PubMed
Publication date: 2025/11/19
Li JieGilvary CoryandarGao LuDellon Evan SCharriez Christina Mde Oliveira Claudia H M CLinaberry Misti JHarris SarahSilverberg Jonathan I - Atopic dermatitis (AD) is an inflammatory skin disease that is heterogeneous in clinical presentation and biological mechanisms. Several studies have suggested biomarker-defined molecular endotypes in AD. This study aimed to characterize potential endotypes in Japanese patients with moderate-to-severe AD and comprehensively evaluate their circulating protein profiles to better understand disease etiology. - Source: PubMed
Publication date: 2025/11/20
Serelli-Lee VictoriaOzeki AkichikaPreuss ChristophBenschop Robert JTorisu-Itakura HitoeMatsuo TakashiSims Jonathan T