MCP-3 CCL7, Human
- Known as:
- MCP-3 CCL7, Human
- Catalog number:
- Z02833-10
- Product Quantity:
- 10,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- MCP-3 CCL7 Human
Related genes to: MCP-3 CCL7, Human
- Gene:
- CCL7 NIH gene
- Name:
- C-C motif chemokine ligand 7
- Previous symbol:
- SCYA6, SCYA7
- Synonyms:
- MCP-3, NC28, FIC, MARC, MCP3
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-04
- Date modifiied:
- 2016-10-05
Related products to: MCP-3 CCL7, Human
Related articles to: MCP-3 CCL7, Human
- Psoriasis is a chronic immune-mediated inflammatory skin disease driven by persistent IL-23/Th17 axis activation. While biologics have improved disease control, their clinical use is constrained by immunotoxicity risks and long-term safety concerns. Plant-derived extracellular vesicle-like nanoparticles (EVLNs) are being investigated as a potential biocompatible nanotherapeutic platform, yet systematic safety profiling and network-level elucidation of their immunomodulatory mechanisms remain lacking. This study integrates Systems Pharmacology, computational transcriptomic profiling, and experimental validationto evaluate the preliminary safety profiles and therapeutic mechanisms of Panax notoginseng-derived EVLNs (PN-EVLNs) in Th17-driven psoriatic inflammation. - Source: PubMed
Publication date: 2026/07/16
Li LiLi ZhikangWang WeiTeng ZhaoweiLiu YuanjuZeng YongZhu Yun - "Trained immunity" describes long-term functional reprogramming of innate immune cells that enhances responses to secondary challenge. However, the extent to which diverse training stimuli converge on shared transcriptional programs remains unclear. Here, we systematically analyzed publicly available RNA-sequencing datasets from diverse human trained-immunity models to define both baseline and restimulated responses of trained cells. Cross-dataset comparisons identified shared transcriptional and functional programs, indicative of common baseline and trained immune states. By integrating gene-expression data across models, we derived a consensus signature of human trained-immunity, which was validated in independent bulk and single-cell datasets. Enrichment analyses showed activation of pro-inflammatory and metabolic programs, including modulation of cellular iron homeostasis and robust increases in chemokine CCL7 expression, alongside suppression of anti-inflammatory, resolution-associated genes. These findings indicate that diverse training stimuli converge on core, shared gene-expression programs and support a two-layer model in which durable baseline reprogramming precedes exaggerated inflammatory responses upon restimulation. - Source: PubMed
Publication date: 2026/07/15
Boden Katherine AKufazvinei Tafadzwa T JChai JasonAdhikari ShreyasJang InjungAkbar NaveedChoudhury Robin P - Dysregulated innate immunity contributes to clonal cytopenias and myeloid neoplasms, but its extent across disease stages and clinical relevance remain incompletely defined. We analyzed plasma ASC/NLRP3 double-positive (DP) specks, ASC single-positive (SP) specks, and 45 cytokines in 223 patients with idiopathic cytopenias of undetermined significance (ICUS)/clonal cytopenias of undetermined significance (CCUS), myelodysplastic syndromes (MDS), and chronic myelomonocytic leukemia (CMML) and 39 matched non-inflammatory controls using adjusted regression, survival modeling, and paired longitudinal analyses. Inflammasome activation and cytokine perturbations were evident across the disease spectrum. DP-ASC specks were elevated in MDS and CMML, whereas SP-ASC specks were increased across all groups, indicating activation of ASC-containing inflammasomes beyond NLRP3. Cytokines followed a graded ICUS → MDS → CMML pattern, with widespread upregulation of interleukins and chemokines (including IL-7, IL-8, IL-11/CXCL11, and CCL7) alongside suppression of stem and progenitor support factors such as CSF3, FLT3LG, TRAIL, and TWEAK. At baseline, elevated IL-15 and MMP1 predicted progression to acute myeloid Leukaemia, while higher IL-10, CXCL8, and IL-18 were associated with reduced survival; ASC specks were not independently prognostic. Longitudinal increases in selected cytokines distinguished progressors (area under the curve 0.82; 95% CI: 0.49-1.0). Cytokine patterns correlated with mutation categories, with the isolated SF3B1 mutation associated with higher DP-ASC specks. These findings define early and progressive inflammasome engagement and nominate dynamic cytokine panels and the inflammasome-IL-1 axis as actionable biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/07/07
Ibbotson AliceCrouch SimonFerrari JacquelineYoung ThomasMorgan Ann WGallì AnnaPozzi SaraSarchi MartinaCamilotto VirginiaBoldini MartinaElena ChiaraMalcovati LucaSavic Sinisa - Acute Respiratory Distress Syndrome (ARDS) is a life-threatening form of respiratory failure with widespread inflammation in the lungs. Based on decades of clinical practice by Professor Du Huaitang, the Yiqi Huayu Jiedu Formula (YQHYJDF) has been used to alleviate symptoms in ARDS patients. Although formal clinical trials are lacking, preliminary observations indicate its therapeutic potential, justifying further investigation. To elucidate its protective mechanisms, network pharmacology, single-cell RNA sequencing, and validation experiments both in vivo and in vitro were integrated. An ARDS rat model was established by tail vein injection of LPS, after pre-prepared intervention with YQHYJDF. Histopathological analysis was conducted to evaluate the pathological alterations. Single-cell RNA sequencing was performed to explore differentially expressed genes between groups. Network pharmacology analysis was executed for the prediction of the potential protective mechanism of YQHYJDF against ARDS. Following this prediction, the mechanism was further validated through both in vivo and in vitro experiments via quantitative real-time PCR (qPCR), enzyme-linked immunosorbent assay (ELISA), and Western blot. Hematoxylin-eosin (HE) staining demonstrated that YQHYJDF significantly ameliorated lung histopathological alterations, reduced inflammatory cell infiltration, and lowered lung injury scores. Single-cell RNA sequencing revealed that YQHYJDF effectively regulated macrophage chemotaxis and significantly attenuated neutrophil recruitment in ARDS lung tissues. Network pharmacology analysis illustrated that the efficacy of YQHYJDF on ARDS may be realized by inhibiting PI3K/AKT, MAPK, and NF-κB signaling pathways. In vivo experiments demonstrated that YQHYJDF markedly suppressed the mRNA expression of IL-6, IL-1ß, and TNF-α in lung tissues, and reduced aberrant activation of the PI3K/AKT, MAPK, and NF-κB signaling pathways. In vitro experiments showed that YQHYJDF effectively inhibited the synthesis and secretion of Ccl2, Ccl7, and Ccl12 in LPS-induced RAW264.7 cells. The protective effect of YQHYJDF on ARDS is likely associated with the suppression of macrophage chemotaxis and inflammatory responses in lung tissues. - Source: PubMed
Publication date: 2026/06/22
Wang Bo-YueLi YanWang Yi-FeiChen YuLi Yang-Min - Hyper-inflammation is common to multiple critical care syndromes, including acute respiratory distress syndrome (ARDS) and sepsis, and is associated with worse outcomes. A signature of hyper-inflammatory ARDS has been described in adults using IL-6, TNFR1, and bicarbonate, and has prognostic utility. We investigated the application of this traditional parsimonious signature to pediatric ARDS patients and tested whether we could improve prognostic enrichment using other cytokines. - Source: PubMed
Publication date: 2026/07/01
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