Ask about this productRelated genes to: CCL22 antibody (HRP)
- 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
- Gene:
- CDC73 NIH gene
- Name:
- cell division cycle 73
- Previous symbol:
- C1orf28, HRPT2, HRPT1
- Synonyms:
- parafibromin, FIHP
- Chromosome:
- 1q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-08
- Date modifiied:
- 2019-04-23
- Gene:
- CYHR1 NIH gene
- Name:
- cysteine and histidine rich 1
- Previous symbol:
- -
- Synonyms:
- CHRP, KIAA0496, MGC13010
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-17
- Date modifiied:
- 2016-10-05
- Gene:
- FOXO1B NIH gene
- Name:
- forkhead box O1B (pseudogene)
- Previous symbol:
- FKHRP1
- Synonyms:
- -
- Chromosome:
- 5q35.3
- Locus Type:
- pseudogene
- Date approved:
- 1998-03-23
- Date modifiied:
- 2018-10-24
- Gene:
- HDGFL1 NIH gene
- Name:
- HDGF like 1
- Previous symbol:
- PWWP1
- Synonyms:
- dJ309H15.1, Hdgfrp1, HRP-1
- Chromosome:
- 6p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-20
- Date modifiied:
- 2017-03-24
Related products to: CCL22 antibody (HRP)
Related articles to: CCL22 antibody (HRP)
- The persistent HIV reservoir constitutes the main obstacle to curing HIV/AIDS disease. Our understanding of how non-productive HIV infections are established in primary human CD4 T cells during the first round of infection is still incomplete. In this study, we leverage the HIV reporter virus pMorpheus-V5 to delineate cellular expression patterns upregulated in non-productively infected stem cell memory (T) CD4 T cells. We find that CD4 T harboring non-productive proviruses display a distinct transcriptomic signature comprising 118 upregulated genes, distinct from that of productively infected cells as well as from negative-exposed and mock-infected cells. Among the cellular genes most upregulated in CD4 T cells harboring non-productive proviruses are CCR4-binding migratory chemokines (CCL22, CCL17), tryptophan catabolic enzymes (IDO1, KYNU), and genes encoding cytoskeletal rearrangement proteins (BASP1, TNFAIP2). Flow cytometry-based analyses confirm that non-productively infected CD4 T cells are enriched for CCL22 and IDO1 co-expression compared to other CD4 T memory subsets, underscoring a CD4 T cell subset specificity for the upregulation of these two immune gene sets associated with non-productive infections. These findings suggest that primary human CD4 T harboring non-productive proviruses display a distinct immunoregulatory phenotype which may facilitate immune evasion and contribute to the persistence of the HIV reservoir. - Source: PubMed
Publication date: 2026/06/25
Butta Giacomo MAlburquerque BremyKearns CharlotteHadas YoavVanDyck Max WScaglioni SusannaPeña NoahWong Hoi TongLevendosky ElizabethGleason CharlesLin XiaoManganaro LaraPinto DalilaMulder Lubbertus C FSimon Viviana - Atopic dermatitis (AD) is a chronic inflammatory skin disorder driven by Th2-related cytokines, including interleukin-4 (IL-4) and IL-13. Recent single-cell sequencing and proteomic studies have demonstrated that sustained immune activity can persist even after treatment with the anti-IL-4 receptor alpha antibody dupilumab. Thus, targeting C-C chemokine receptor 4 (CCR4), which is highly expressed by Th2 cells and drives their migration into the inflamed tissues such as skin in response CCL17 (TARC) and CCL22 (MDC), could be a promising therapeutic approach for the treatment of AD. - Source: PubMed
Publication date: 2026/06/26
Dahabreh DantePatel DevDel Duca EsterCorriden RossBrockstedt Dirk GGuttman-Yassky Emma - 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