CCL5 Antibody
- Known as:
- CCL5 Antibody
- Catalog number:
- XW-7512
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CCL5 Antibody
Ask about this productRelated genes to: CCL5 Antibody
- Gene:
- CCL5 NIH gene
- Name:
- C-C motif chemokine ligand 5
- Previous symbol:
- D17S136E, SCYA5
- Synonyms:
- RANTES, SISd, TCP228, MGC17164
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-05
- Date modifiied:
- 2016-03-01
Related products to: CCL5 Antibody
Related articles to: CCL5 Antibody
- Oligoarticular juvenile idiopathic arthritis (oligo JIA) is the most common JIA subtype and is often complicated by uveitis, a potentially sight-threatening comorbidity. Despite its prevalence, the immunopathogenic mechanisms underlying oligo JIA and its extra-articular manifestations remain poorly understood. The objective was to characterize the immune landscape of oligo JIA and identify pathogenic cell populations and regulatory mechanisms associated with the disease and uveitis. - Source: PubMed
Publication date: 2026/04/27
Lopez-Corbeto MireiaGuillén YolandaJiménez-Gracia LauraMoreno-Ruzafa EstefaníaAlvarez-Errico DamianaPalau NúriaMartín-Begué NievesHeyn HolgerJulià AntonioMarsal Sara - Skin diseases frequently coexist with other disorders, such as metabolic syndrome, diabetes mellitus, depression, psoriatic arthritis, and cardiovascular disease. Altered levels of distinct chemokines, like CCL5/RANTES, CXCL12/SDF-1a, CCL7/MCP-3, CCL2/MCP-1, CXCL1/GROa, and the eotaxin family, contribute to the development and/or exacerbation of inflammation, which is a common feature of numerous skin diseases as well as metabolic syndrome. The pathological and molecular connections between chronic inflammatory skin diseases and metabolic syndrome are increasingly recognized as being driven by shared inflammatory pathways, oxidative stress, and adipokine dysregulation. While systemic inflammation acts as a common thread, the precise mechanisms for some conditions remain partially understood. Nevertheless, the exact pathological and molecular connections between skin diseases (i.e., psoriasis, atopic dermatitis, pemphigus vulgaris, acute and chronic spontaneous urticaria, bullous pemphigoid, squamous cell carcinoma, alopecia areata, systemic sclerosis, discoid lupus erythematosus, diffuse large B-cell lymphoma) and metabolic syndrome are not yet fully understood. This narrative review summarizes the robust association between various chronic inflammatory skin diseases and metabolic syndrome in the context of pro-inflammatory chemokines. - Source: PubMed
Publication date: 2026/04/10
Matwiejuk MateuszMyśliwiec HannaMikłosz AgnieszkaChabowski AdrianFlisiak Iwona - Allogeneic hematopoietic stem cell microtransplantation (MST) has been shown in prior studies to improve outcomes compared to chemotherapy alone in acute myeloid leukemia, but its mechanism requires further investigation. In MST, donor peripheral blood mononuclear cells (GPBMCs) mobilized by granulocyte colony-stimulating factor (G-CSF), which contain a large number of NK cells, are infused after each chemotherapy cycle (typically 3-5 infusions total). - Source: PubMed
Publication date: 2026/04/24
Zhang Tian-YaoLiu Ru-YuLei Yang-YangCai BoYu Chang-LinGuo MeiAi Hui-ShengWang YiHu Kai-Xun - Avian influenza virus primarily invades the respiratory mucosa, necessitating the establishment of a robust mucosal secretory IgA (sIgA) barrier. However, the efficacy of avian mucosal vaccines is often hindered by inefficient antigen uptake and immune tolerance. Consequently, modern vaccine strategies focus on active targeting delivery, immune microenvironment remodeling, and activation of multifaceted immune responses. The immunogenicity and molecular mechanisms of a novel Salmonella-delivered self-amplifying RNA (saRNA) vector platform were evaluated in this study. This platform integrates bacterial surface display of a dendritic cell (DC)-targeting nanobody (Nb-phage54 via LppOmpA) with co-expression of molecular adjuvants against H9N2 influenza. The expression of HA1 and NA antigens from recombinant plasmids (pYL673, pYL679, and pYL681) was confirmed using confocal microscopy and Western blot analysis. In vitro assays revealed that the Nb-mediated targeting strain (S673) significantly increased invasion efficiency into bone marrow-derived dendritic cells and up-regulated the transcription of CCL5, CCR7, CD83, and CD86, effectively promoting DC maturation. Transcriptomic analysis (RNA-seq) revealed divergent mechanisms among vaccine candidates. The non-targeting group (S615) primarily activated antiviral innate pathways, such as JAK-STAT, whereas the targeting group (S673) significantly improved antigen processing, presentation, and natural killer cell-mediated cytotoxicity. Moreover, the adjuvant-integrated groups, S679 (CpG) and S681 (FliC), specifically triggered Toll-like receptor-21 (TLR21) and TLR5 signaling cascades by increasing cell adhesion, phagocytosis, and transmembrane signal transduction. Animal trials revealed that the targeted adjuvant vectors (S679 and S681) significantly elevated serum IgG and intestinal mucosal sIgA titers in chickens. The S679 group excelled in stimulating lymphocyte proliferation and secreting interferon-gamma and interleukin-4, indicating a potent Th1/Th2 balanced response. Challenge experiments with H9N2 virus confirmed that S679 and S681 effectively mitigated weight loss, shortened the viral shedding window, reduced viral loads in the lungs and trachea, and significantly alleviated respiratory pathological damage and inflammation. The DC-targeting saRNA-Salmonella vector developed in this study, particularly when synergized with CpG or FliC adjuvants, induced robust systemic, mucosal, and cellular immunity by activating specific intracellular signaling cascades. These findings demonstrate that this platform is a highly effective and promising candidate strategy for preventing and controlling H9N2 avian influenza. - Source: PubMed
Publication date: 2026/04/24
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