CCL22 siRNA_Lentivectors
- Known as:
- CCL22 siRNA_Lentivectors
- Catalog number:
- i004016d
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CCL22 siRNA_Lentivectors
Related genes to: CCL22 siRNA_Lentivectors
- 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 siRNA_Lentivectors
Related articles to: CCL22 siRNA_Lentivectors
- Radiotherapy (RT) is increasingly recognized as a system‑level immunomodulator capable of reshaping cytokine networks across spatial, temporal and dosimetric dimensions. This review synthesizes existing evidence on RT parameters, key signaling axes, major effector cells, organ‑specific contexts and clinical translation. It describes how the cyclic GMP‑AMP synthase/stimulator of interferon genes (STING)/IFN‑I, NF‑κB and TGF‑β pathways coordinate immune activation and immune suppression after irradiation. It then summarizes macrophage‑centered regulatory circuits and chemokine axes, including C‑C motif chemokine ligand (CCL)2/CCR2 and CCL22/CCR4 that govern T‑cell trafficking and functional states. A map of organ‑specific cytokine programs that link therapeutic benefit and toxicity in the brain, lung, gastrointestinal tract, oral mucosa and liver is then provided, and actionable targets within inflammasome‑associated pyroptosis and fibrogenic cascades are highlighted. RT technical parameters, including fractionation, treatment volume, stereotactic body RT, Fast Linear Accelerator‑based Scanning Hybrid ultra‑high dose-rate delivery and proton therapy can differentially shape cytokine dynamics and modify the therapeutic window. The DNA damage response network with poly (ADP‑ribose) polymerase (PARP)1 as a central node represents a second hub that interfaces with antigen presentation and IFN signaling, supporting rational combinations with PARP inhibitors and immune checkpoint blockade. Finally, a translational algorithm with three pillars is proposed. The first pillar uses IFN‑related gene signatures and circulating cytokine profiles to stratify tumors by baseline IFN activity. The second pillar aligns RT timing with endogenous STING or IFN pulses and incorporates CCR2, CCR4 or colony stimulating factor 1 receptor blockade to counter myeloid cell‑mediated immunosuppression. The third pillar co‑manages treatment‑related toxicities by targeting the NLR family pyrin domain containing 3/gasdermin D axis or by using fibrosis‑modulating interventions. Furthermore, ongoing clinical trials of cytokine-directed agents combined with RT are summarized. This framework positions cytokines as measurable and modifiable variables for individualizing combined RT and immunotherapy. - Source: PubMed
Publication date: 2026/05/08
Zhou SiyuanJiang YurongFan JixuGuo MinjieWen YiDai Chunhua - Differentiating between infectious and non-infectious etiologies in systemic inflammatory disorders may be challenging due to overlapping clinical presentations and the lack of reliable discriminating biomarkers. Regulatory T-cells (Tregs) modulate immune responses. Their functionality is governed by specific chemokines, including CCL1 and CCL22. We investigated whether these Treg-attracting chemokines are differentially regulated in infectious versus sterile inflammation. This prospective, single-center biomarker study enrolled patients with sepsis, acute pancreatitis, and hospitalized controls without infectious diseases. Serum samples were collected on days 1, 3, 5, and 7, measuring CRP, IL-6, PCT, CCL1, and CCL22. Between March 2019 and October 2022, 159 patients were enrolled, comprising 45 patients suffering from acute pancreatitis, 15 patients with confirmed sepsis as well as 99 hospitalized controls. Established inflammatory parameters CRP, IL-6 and PCT showed typical kinetics. Decreased CCL1 levels, but not CCL22, distinguished acute pancreatitis from sepsis at all time points. Additionally, CCL1 levels inversely correlated with organ failure severity in sepsis patients. CCL1 shows potential to serve as a biomarker to differentiate sterile and non-sterile inflammation in sepsis and acute pancreatitis. This may support clinical decision-making and allow a more precise use of antibiotics in these patient cohorts. - Source: PubMed
Publication date: 2026/05/06
Vornhülz MarliesMüller JenniferTakken Lara LouisaLayritz PatrickPerleberg CarolinGärtig JanBeimert AntoniaWeber PatrickEndres StefanMayerle JuliaHoldt LescaPiseddu IgnazioAnz David - Cutaneous gene therapy has the potential to treat a wide range of skin disorders, but effective delivery remains limited by the skin's barrier properties and immune surveillance. Here, we identify AAVrh32.33 as a potent vector for targeting dermal stromal compartments. Following systemic administration in mice, AAVrh32.33 mediated robust and durable transgene expression, with preferential targeting of dermal fibroblasts and hair follicle bulge cells. Expression peaked at one month and persisted for up to two years, highlighting its suitability for chronic conditions. To reduce immunogenicity, a dominant CD8 T cell epitope was disrupted, generating the IDPΔ variant. This modification attenuated peptide-specific T cell responses while preserving stromal transduction. In human skin explants, IDPΔ achieved high levels of gene expression, primarily in dermal fibroblasts and precursors, confirming translational relevance. Finally, vectors encoding CCL17, CCL20, and CCL22 demonstrated localized targeted therapeutic gene delivery in both healthy and inflamed skin, underscoring the feasibility of using this platform to reshape local immune responses. Together, these findings establish AAVrh32.33 and IDPΔ as promising platforms for durable cutaneous gene therapy, with direct applications in diseases such as vitiligo where long-term modulation of the dermal microenvironment is essential. - Source: PubMed
Publication date: 2026/05/01
Arjomandnejad MotaharehEssien KingsleySylvia KatelynBlackwood MeghanTutto AmandaKatz EricaTang QiushiHarris John EKeeler Allison M - This study explored the effect and dual-targeting mechanism of total lignans from flower buds of Magnolia biondii Pamp. (TLFM) against AD. - Source: PubMed
Publication date: 2026/04/22
Yan MengdanYu WenchaoCheng MeiyuWu LonglongHan LinhangChen KaixianLi YimingZhang QingguangZhang LiuqiangQian Fei - Extranodal natural killer/T-cell lymphoma (ENKTL) is clinically characterized by destructive lesions that first appear in the nasal cavity and progress along the midline of the face. It was historically described as "rhinitis gangrenosa progressiva" or "lethal midline granuloma" due to its destructive clinical nature and had significant diagnostic and therapeutic challenges. This review synthesizes about 40 years of research, beginning with the 1980s and 1990s, when the disease was identified as a T-cell- or NK-cell-derived lymphoma, and the authors' discovery that clearly linked it to Epstein-Barr virus (EBV). ENKTL is highly prevalent in East Asia and characterized by a type II EBV latency pattern, in which the oncoprotein latent membrane protein 1 (LMP1) acts as a central driver of pathogenesis, activating critical signaling pathways including JAK/STAT, NF-κB, PI3K/Akt, and RAS/MAPK. These pathways, often bolstered by mutations in genes, trigger an oncogenic cascade involving epigenetic modifiers-enhancer of zeste homolog 2 (EZH2), histone deacetylase (HDAC). The deletion of chromosome 6q, leading to loss of function of tumor suppressor PR domain zinc finger protein 1 (PRDM1) and forkhead box O3 (FOXO3), as well as transcription of TNF α-induced protein 3 (TNFAIP3) and protein tyrosine phosphatase receptor type kappa (PTPRK), also contributes to pathogenesis. In vitro studies by the author's group demonstrated that autocrine/paracrine positive feedback loops involving several pro-proliferative molecules/cytokine/chemokine-CD27, ICAM1, hepatocyte growth factor (HGF), IL-9, IL-10, IL-15, CCL17, CCL22, CXCL10- further amplify ENKTL proliferation. Diagnostic precision has improved through the use of serum EBV DNA copy numbers and viral microRNAs (miRs), specifically miR-BART2-5p, alongside the emergence of soluble CD27 as a novel biomarker. While early anthracycline-based regimens failed due to multidrug resistance (MDR), modern concurrent chemoradiotherapy composed of MDR-independent drugs has significantly improved 5-year overall survival (OS) rates for localized disease to over 80%. For advanced or relapsed/refractory cases, L-asparaginase-based regimens are standard, though outcomes remain unsatisfactory. The therapeutic paradigm is currently shifting toward chemoradiotherapy combined with either immune checkpoint inhibitors or small-molecule drugs. Future research should focus on novel molecular-targeted therapies, immunotherapies, or combination strategies targeting proliferation-related molecules or LMP1. - Source: PubMed
Publication date: 2026/04/17
Harabuchi Yasuaki