MDC CCL22, Rat
- Known as:
- MDC CCL22, Rat
- Catalog number:
- Z02959-5
- Product Quantity:
- 5,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- MDC CCL22 Rat
Related genes to: MDC CCL22, Rat
- 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, Rat
α - Calcitonin Gene Related Peptide, α - CGRP, rat'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala13)-Apelin-13 (human, bovine, mouse, rat) 98% C63H107N23O16S CAS: 568565-11-7(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala96)-Myelin Basic Protein (87-99) (human, bovine, rat) 98% C70H110N20O17 CAS:(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2 Related articles to: MDC CCL22, Rat
- Immune checkpoint inhibitors, notably PD-1/PD-L1 monoclonal antibodies, are now used as first-line treatments for hepatocellular carcinoma (HCC) and have improved outcomes for some patients. Nevertheless, their response rate remains below 30%, largely due to HCC's immunosuppressive microenvironment and insufficient T-cell infiltration. Strategies to address these limitations are urgently needed. Ion homeostasis has been recognized as a pivotal factor in modulating the tumor immune microenvironment. This study found that the expression and functionality of CFTR, a chloride channel, in human HCC tissues and cells were negatively correlated with HCC progression. Furthermore, it was utilized human/murine HCC cell lines, mouse models, and human HCC organoids to investigate how CFTR activation (genetic/pharmacological) impacts HCC biology. Key assessments included: (1) tumor cell ion homeostasis, (2) downstream signaling proteins, (3) tumor microenvironment cytokine levels, and (4) functional changes in TAMs, CD8 + T cells, and Tregs. We further assessed combined effects with PD-L1 antibodies to explore CFTR-immune checkpoint interplay, providing multidimensional insights into CFTR-mediated HCC pathogenesis and immunomodulation. The results showed that upregulation of CFTR expression and channel activity reduced intracellular Cl⁻ and Ca²⁺ concentrations in HCC cells, thereby suppressing the expression of chloride-associated transcription factor RUNX1 and calcium pathway transcription factor NF-κB. This regulatory mechanism orchestrates the synthesis and secretion of cytokines/chemokines (CSF-1, TGF-β, CCL20, CCL22), driving macrophage polarization toward M1 phenotype while promoting M1 macrophage and CD8 + T lymphocyte infiltration. Concurrently, it suppressed Treg proliferation and tumor infiltration. These immunomodulatory effects synergistically enhanced PD-1/PD-L1 immune checkpoint blockade efficacy, ultimately augmenting therapeutic outcomes in HCC. Therefore, this study establishes CFTR potentiation as a novel immunomodulatory axis, proposing biomarker-driven combination regimens to enhance therapeutic efficacy while mitigating immune-related adverse events, thereby addressing an urgent unmet need in translational hepatology. - Source: PubMed
Publication date: 2026/06/10
Xu YijiaSun JianfangHe ChongyangXie YipinLu YuyingFan YujieYang LiyingZhang MengyingLiu XinKong LijuanLiu YanfengZhang JinghaiSu YangZhao Mingyi - The tumor microenvironment (TME) in hematologic malignancies constitutes a dynamic ecosystem supporting leukemogenesis, therapeutic resistance, and immune evasion. Key drivers of this immunosuppressive network are regulatory T cells (Tregs), a CD4+ subset conventionally defined by FoxP3 and CD25 expression. While physiological Tregs are essential for self-tolerance, leukemic blasts frequently co-opt these cells to dampen anti-tumor immunity. Here, we review the distinct roles of Tregs across the spectrum of leukemias, including Acute Myeloid Leukemia (AML), Acute Lymphoblastic Leukemia (ALL), Chronic Myeloid Leukemia (CML), and Chronic Lymphocytic Leukemia (CLL). We dissect the molecular machinery governing Treg recruitment and suppression within the bone marrow niche, highlighting the CCL22/CCR4 axis, metabolic reprogramming via the CD39/CD73 adenosine pathway, and indoleamine 2,3-dioxygenase (IDO)-mediated tryptophan catabolism. Additionally, we critically evaluate the nuanced and often discordant prognostic impact of Treg infiltration across different subtypes. A significant portion of this review examines the evolving therapeutic landscape, scrutinizing Treg-depleting antibodies (e.g., mogamulizumab, RG6292), immunomodulatory small molecules (venetoclax, hypomethylating agents, TKIs), and the challenges Tregs pose to cellular therapies. Finally, we discuss novel strategies to circumvent Treg-mediated resistance, offering a perspective on restoring anti-leukemic immunity. - Source: PubMed
Publication date: 2026/05/20
Xu HuiliZhang XiaoliZhang Jun - This study explores the role of immunological and molecular monitoring in evaluating the efficacy of skin allergy therapies. The analysis focused on Th2-associated cytokines (IL-4, IL-5, IL-13), systemic markers (IgE, CD25), and chemokines (CCL17, CCL22, CCL26) as indicators of inflammatory activity. Structural proteins of the epidermal barrier (filaggrin, claudin-1, loricrin) and regulatory microRNAs (miRNA-155, miRNA-146a) were also assessed for their contribution to skin integrity and immune regulation. The findings demonstrated that elevated IL-4 and IL-13 levels, along with an imbalance between Th2 and Treg cells, correlated with disease severity. Successful therapy was associated with decreased cytokine levels, improved expression of barrier proteins, and modulation of microRNAs, indicating restored immune balance and reduced inflammation. These results highlight the value of integrated immunological and molecular monitoring for personalised assessment of therapy efficacy and the development of combined strategies targeting both immune dysfunction and barrier restoration. - Source: PubMed
Publication date: 2026/04/15
Lisiecka Maria Zofia - Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, necessitating the identification of novel therapeutic targets. The transmembrane protein MAL2 has been implicated in various cancers, but its functional role and mechanistic underpinnings in HCC are not fully understood. To comprehensively understand its role in HCC, we analyze public single-cell RNA sequencing (scRNA-seq) data and find that MAL2 is significantly enriched in malignant HCC cells. , is stably knocked down by shRNA in Hep-3B and HCC-LM3 cell lines, and functional experiments including colony formation, EdU, transwell, and wound healing assays demonstrate that depletion markedly suppresses proliferation, invasion, and migration of HCC cell lines. , a subcutaneous tumor model using H22 cells reveals that knockdown inhibits tumor growth, accompanied by reduced Ki-67 level and increased apoptosis. Further analysis via mass cytometry indicates that MAL2 downregulation reshapes the immune microenvironment, notably reducing CD4 T cells, Tregs, CD8 T cells, and exhaustion markers (PD-L1, PD1, and TIGIT) while increasing B cells and myeloid-derived suppressor cells (MDSCs). Mechanistically, ELISA and immunofluorescence staining validate that knockdown impairs the secretion of CCL22, a chemokine known for recruiting Tregs, leading to reduced Treg recruitment and decreased production of the immunosuppressive cytokines IL-10 and TGF-β. In conclusion, MAL2 drives HCC progression by promoting tumor cell proliferation, invasion, and immunosuppression through CCL22-mediated Treg recruitment, positioning MAL2 as a promising therapeutic target to counteract tumor growth and remodel the immunosuppressive microenvironment in HCC. - Source: PubMed
Zhang QianSun XiaoweiZhang LantianNi TianyiWang YingyingTu LiyingYan WeiTang WeiweiWang Xuehao - Haemophilia A (HA) is an X-linked bleeding disorder caused by factor VIII (FVIII) deficiency, treated with FVIII infusions or, more recently, Emicizumab subcutaneously. Although Emicizumab is safe and effective, FVIII is still required for severe bleeding, trauma, or surgery, and few studies have compared these prophylactic options in paediatric patients. This study explores the immunological and haematological profiles of paediatric HA patients receiving FVIII or Emicizumab, using haemophilia B patients and healthy controls. Clinical parameters and immune cell populations showed no major differences aside from age-related variations. However, HA patients displayed higher HLA-DR expression on CD14 cells than healthy controls, and Emicizumab-treated patients showed increased HLA-DR expression on CD11c cells compared with FVIII-treated patients. Plasma cytokines including IL-12p40, TNF-α, CCL-22, IL-18, and CCL-4 were elevated in HA, suggesting a dysregulated myeloid compartment in HA. Patient-derived macrophages exhibited a stronger pro-inflammatory (M1-like) polarization after in vitro FVIII stimulation, with increased TNF-α and reduced TGF-β gene expression. Stratification by prophylaxis showed that macrophages from FVIII-treated patients maintained the M1 phenotype, whereas those from Emicizumab-treated patients showed no clear shift and tended toward an immune-regulatory profile. These findings highlight distinct myeloid and cytokine signatures associated with different prophylaxis, emphasizing the need for optimized therapeutic strategies. - Source: PubMed
Cottonaro AlessiaAkula SaicharanPollio BerardinoRicca IreneMartini TizianoAlbiani RobertoGiacchello Jacopo AgnelliSciancalepore PatriziaSanti RobertoFollenzi AntoniaMerlin Simone