MDC _ CCL22 Rabbit antibody Ab Biotin
- Known as:
- MDC _ CCL22 Rabbit (anti-) Antibody Biotin
- Catalog number:
- PP1049B2
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- ACR
- Gene target:
- MDC _ CCL22 Rabbit antibody Biotin
Related genes to: MDC _ CCL22 Rabbit antibody Ab Biotin
- 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 Rabbit antibody Ab Biotin
Related articles to: MDC _ CCL22 Rabbit antibody Ab Biotin
- Diffuse large B-cell lymphoma (DLBCL) frequently relapses following therapy, partly due to microenvironment-mediated drug resistance. Bone marrow involvement is associated with poor prognosis, yet preclinical models that faithfully recapitulate its extracellular matrix (ECM) remain limited. We used a decellularized human bone-derived 3D scaffold to evaluate the impact of extracellular matrix (ECM) interactions on proliferation, cytokine secretion, and ibrutinib sensitivity in four DLBCL cell lines (OCI-LY1, OCI-LY18, RIVA, NU-DUL-1). Functional assays and cytokine profiling were performed under 2D and 3D culture conditions. Compared with 2D cultures, the 3D ECM model induced a profound remodeling of the DLBCL secretome, with upregulation of a coordinated network of pro-migratory chemokines, particularly CXCL9, CCL22, CCL17, CCL4 and CXCL1/2/3. ECM engagement enhanced DLBCL migration and promoted scaffold colonization, indicating a positive feedback loop between tumor cells and the microenvironment. While all DLBCL cell lines were sensitive to ibrutinib in 2D, ECM-adherent OCI-LY18 and RIVA cells showed reduced drug-induced apoptosis in 3D. This effect was dependent on direct ECM contact, was not reproduced by inert 3D scaffold, and was fully reversible upon disruption of cell-ECM interaction. Mechanistically, ECM adhesion was associated with activation of the AKT/mTOR pathway. The human bone-derived 3D ECM model reveals that direct tumor-matrix interactions induce reversible ibrutinib resistance and reshape the cytokine milieu in DLBCL. These findings highlight the role of ECM as a dynamic regulator of drug response and support the use of physiologically relevant 3D models to investigate microenvironment-driven resistance and guide therapeutic strategies. - Source: PubMed
Publication date: 2026/07/15
Ceccato JessicaPiazza MariaGualtiero GiuliaCarraro SamuelaCinetto FrancescoBiz CarloManni SabrinaPizzi MarcoPianalto SabrinaZoletto SimoneCarabotta ValeriaDanesin Nicolo'Ruggieri PietroDei Tos Angelo PaoloPiazza FrancescoTrentin LivioVianello Fabrizio - The recruitment of immunosuppressive regulatory T cells (Treg) into the tumor microenvironment (TME) dampens the antitumor immune response and is thought to be a key driver in tumor immune evasion. Treg express the CC chemokine receptor 4 (CCR4) broadly and are recruited to the TME through interactions with its specific chemokines CCL17 and CCL22 that are elevated in many cancer types. The selective blocking of Treg migration to the TME has the potential to restore antitumor immunity and potentiate the efficacy of a variety of conventional and immuno-therapies. We have developed novel CCR4 antagonist small molecules that selectively and potently inhibit the migration of Treg to the TME (hTreg CTX IC: 27 nM) and have culminated in our clinical candidate (, FLX475, Tivumecirnon). The discovery of this potent, selective, and orally bioavailable CCR4 antagonist and its characterization in several preclinical models is described herein. - Source: PubMed
Publication date: 2026/07/13
Robles OmarBrockstedt Dirk GAponte-Guzman JoelBradford DeliaChian DavidColas ChristophGrandcolas MollyHu Dennis XJackson JeffreyJacobson ScottKarbarz EmilyKassner Paul DKatibah George EKetcham John MMarshall LisaMcKinnell JennyMeleza CesarMilestone HeatherOkano AkinoriQiu JingtaoReilly Maureen KRiegler ErinShunatona Hunter PTalay OezcanYounai AshkaanZiari NiloufarZibinsky MikhailWustrow David J - Atopic dermatitis (AD) is a chronic inflammatory skin disorder involving complex interactions among multiple cell types. The cellular heterogeneity and intercellular communication networks driving AD pathogenesis remain to be fully elucidated. - Source: PubMed
Publication date: 2026/07/06
Wei YanBai Rui-MinGuo Hao-RanShan JinWang Li-JuanZhou YanMou Kuan-HouZheng YanZhang Ya-Guang - Acute appendicitis is one of the leading causes of surgical emergency hospitalizations. However, the mechanisms leading to the development of appendicitis are poorly understood. Current knowledge suggests an interplay probably led by dietary habits with impact on the microbiome which elicits responses in genetically predisposed individuals. The aim of this review is to assess the nutrition-microbiome-genetic axis associated with acute appendicitis development. The main dietary and nutritional patterns associated to acute appendicitis were low consumption of fiber, water and fish oil, and high levels of saturated fat, salt, processed meat and ultra-processed foods. Collectively, these westernised dietary patterns (WDP) may increase more than 40% the risk of developing acute appendicitis. The WDP are associated to shifts in the microbiome observed in inflamed appendices such as an increased abundance of Fusobacteria together with a lower level of Proteobacteria. While dietary patterns and associated changes in the microbiome may affect a large proportion of the population, only a relatively small percentage develop acute appendicitis suggesting the existence of predisposing genetic factors. Several single nucleotide polymorphisms (SNP) have been identified linking nutrition and microbiome to the genetic background in acute appendicitis. These include the HLA-C SNP rs2524046, associated with coeliac disease, and the variant rs9953918 of NEDD4L (involved in fluid/water mobilisation). A hypothetical allergy model for appendicitis has been recently proposed providing a preliminary groundwork that identifies SNPs in or near and and involved in the pathogenesis of both inflammatory diseases. - Source: PubMed
Publication date: 2026/07/03
Ryoo MichaelHwang Liang-DarRoura Eugeni - Peritoneal metastasis is a major contributor to progression, recurrence, and treatment failure in epithelial ovarian cancer (EOC) and is closely associated with dynamic remodeling of the peritoneal tumor microenvironment (TME). Interactions among tumor cells, ascites, the omental niche, stromal components, and immune cells collectively shape metastatic dissemination and therapeutic response. CC chemokines are important regulators of these processes, linking immune-cell trafficking with tumor-cell plasticity, metabolic adaptation, angiogenesis, and therapy resistance. This review summarizes the roles of CC chemokines in EOC progression within a chemokine-driven peritoneal niche remodeling framework encompassing four key stages: early dissemination, survival in ascites, omental colonization, and therapy resistance. Among the major signaling axes, CCL2-CCR2 is primarily associated with monocyte recruitment and myeloid-dominant immunosuppression, whereas CCL5-CCR5 is linked to stromal immune regulation and cancer stem-like phenotypes. Additional pathways, including CCL18, CCL20-CCR6, CCL22-CCR4, and CCL1-CCR8, contribute to T-regulatory cell recruitment, immune suppression, and hypoxia-associated responses. The review further discusses the limited efficacy of chemokine-targeted monotherapy, highlighting challenges posed by signaling redundancy, compensatory pathways, spatial heterogeneity, and insufficient biomarker-guided patient selection. Recent advances in single-cell and spatial transcriptomic technologies have improved the characterization of compartment-specific chemokine programs within the EOC microenvironment. Finally, emerging combination strategies involving chemokine blockade together with immune checkpoint inhibitors, metabolic interventions, PARP inhibitors, and ferroptosis-related approaches are evaluated. However, successful clinical translation will require precise patient stratification, effective toxicity management, and validation in clinically annotated cohorts. - Source: PubMed
Publication date: 2026/06/30
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