MDC _ CCL22
- Known as:
- MDC _ CCL22
- Catalog number:
- PP1049B2
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- MDC _ CCL22
Related genes to: MDC _ CCL22
- 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: MDC _ CCL22
AA,MDC, 1-122aa, Human, His tag, E.coliAA,MDC, 1-122aa, Human, His tag, E.coliAA,MDC, 1-122aa, Human, His tag, E.coliABCD1 / CCL22 antibody Isotype IgG Host RabbitABCD1 _ CCL22ABCD1 _ CCL22ABCD1 _ CCL22ABCD1 _ CCL22ABCD1 _ CCL22ABCD1 _ CCL22ABCD1 _ CCL22ABCD1 _ CCL22ABCD1 _ CCL22ABCD1 _ CCL22ABCD1 _ CCL22 Related articles to: MDC _ CCL22
- 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 - Breast cancer derived extracellular vesicles (EVs) mediate tumor progression through surface protein-dependent intercellular communication; however, their molecular heterogeneity remains poorly characterized. In this study, we employed a proximity-dependent barcoding assay (PBA) together with patient-derived organoid (PDO) models and identified CDCP1 as a key driver of EV-mediated oncogenesis. PBA-based surface proteomics revealed CDCP1 as the most upregulated protein in breast cancer-derived EVs compared with EVs from normal tissues. Clinical validation confirmed elevated CDCP1 expression in tumor tissues and matched EVs. PDOs generated from fresh clinical specimens recapitulated CDCP1 expression levels of the parental tumors and secreted CDCP1-enriched EVs. Functional experiments showed that CDCP1-knockdown EVs suppressed PDO proliferation and sensitized tumors to chemotherapy. Mechanistically, CDCP1-positive EVs promoted macrophage polarization toward an M2 phenotype, accompanied by upregulation of IL-10 and TGF-β and CCL22. Multiplex immunofluorescence confirmed that CDCP1-high tumors exhibited increased co-localization of CD68⁺ and CD163⁺ macrophages. These results establish CDCP1 as a master regulator of EV driven breast cancer progression, linking surface proteome remodeling to chemo-resistance and immunosuppressive microenvironment reprogramming. The integration of single-EV profiling and PDO modeling establishes a translational framework for targeting CDCP1 as a promising therapeutic target and a candidate biomarker for future liquid biopsy development in aggressive breast cancer subtypes. - Source: PubMed
Publication date: 2026/04/13
Liu YibingMa LiZhu TingWu DiLiu Yonglei - CCL22 (macrophage-derived chemokine, MDC) is an important member of the CC chemokine family. By binding to its receptor CCR4, it regulates immune cell trafficking, plays a dual role in maintaining immune homeostasis and promotes immune-mediated inflammation. The biological effects of CCL22-CCR4 signaling in autoimmune diseases are highly dependent on the tissue microenvironment. Under steady-state conditions, CCL22 secreted by dendritic cells and macrophages recruits regulatory T-cells (Tregs) to peripheral tissues, suppresses excessive immune responses, and maintains immune tolerance. When CCL22 expression is down-regulated, Treg recruitment becomes insufficient, leading to immune dysregulation and tissue injury. CCL22 plays a critical role in the pathogenesis of several autoimmune diseases including vitiligo, systemic lupus erythematosus, and type 1 diabetes, although its biological effects vary across different disease contexts. This review focuses on the central roles of the CCL22-CCR4 axis in immune tolerance and inflammatory responses and describes how its functions are finely regulated by cell type, tissue microenvironment, and signaling states in different disease contexts. - Source: PubMed
Publication date: 2026/04/11
Zhang ZiXianMao HanXiaoXia ZhangRongLv XinYiHe YuanMin