TECK (CCL25), human recombinant
- Known as:
- TECK (CCL25), H. sapiens Rec.
- Catalog number:
- 7214-10
- Product Quantity:
- 10 μg
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- TECK (CCL25) human recombinant
Related genes to: TECK (CCL25), human recombinant
- Gene:
- CCL25 NIH gene
- Name:
- C-C motif chemokine ligand 25
- Previous symbol:
- SCYA25
- Synonyms:
- TECK, Ckb15
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-14
- Date modifiied:
- 2016-03-01
Related products to: TECK (CCL25), human recombinant
Related articles to: TECK (CCL25), human recombinant
- Conventional dendritic cells (cDCs) in the gut express the vitamin A (VA)-converting enzyme retinal dehydrogenase 2 (RALDH2) and produce significant amounts of retinoic acid (RA). RA derived from gut cDCs contributes to the generation of tolerogenic responses by promoting Treg differentiation while inhibiting Th1 and Th17 cell differentiation. In this study, we investigated whether similar RA-mediated immunoregulatory mechanisms operate in the pancreas using an experimental autoimmune pancreatitis (AIP) model. Our previous studies have shown that activated cDCs and plasmacytoid DCs (pDCs) play crucial roles in the induction and maturation phases of experimental AIP, respectively. - Source: PubMed
Publication date: 2025/09/02
Kurimoto MasayukiWatanabe TomohiroOtsuka YasuoHara AkaneOmaru NaoyaSekai IkueMasuta YasuhiroMasaki ShoKamata KenMinaga KosukeHonjo HajimeArai YasuyukiYamashita KouheiKudo Masatoshi - Breast cancer remains the most frequently diagnosed malignancy and a leading cause of cancer-related mortality among women worldwide. Increasing evidence underscores the pivotal yet paradoxical roles of innate immune cells and their associated cytokines in orchestrating the dynamic landscape of the breast tumor immune microenvironment (TIME). Innate immune effectors, including tumor-associated macrophages (TAMs) and natural killer (NK) cells, exert dual functions by either initiating robust antitumor responses or facilitating immune evasion, metastatic dissemination, and therapeutic resistance. For instance, MDSCs suppress T and NK cell activity via STAT3/NF-κB signaling and modulate the cytokine milieu through IL-10 and TGF-β. Similarly, M2-polarized TAMs promote angiogenesis, epithelial-mesenchymal transition, and chemoresistance via IL-10/STAT3/Bcl-2 pathways. In contrast, NK cells and CD103 DCs mediate tumor cell cytolysis and prime antigen-specific immunity, though their activity is frequently compromised in advanced disease. Moreover, key cytokines and chemokines, including IL-6, IL-10, IL-8, TNF-α, TGF-β, and CCL2/5, demonstrate subtype-specific and context-dependent effects, acting as both tumor-promoting and tumor-suppressing agents through complex signaling networks. This review highlights the dualistic nature of innate immune components in breast cancer, discusses their prognostic and therapeutic implications, and proposes novel intervention strategies, such as TAM repolarization, and cytokine modulation, to reprogram the TIME and restore effective immune surveillance, particularly in aggressive subtypes like triple-negative breast cancer. - Source: PubMed
Publication date: 2025/08/20
Zhang ChenLiu WeiYang PingLin RubingPu LulanZhang Hongying - In 2021, the rapid rollout of two doses of SARS-CoV-2 vaccines reduced COVID-19 severity and mortality. However, further vaccine doses as a prime-boost schedule were limited, and lifting of public health restrictions by late 2021 frequently led to infection, rather than vaccine, as a third exposure. - Source: PubMed
Publication date: 2025/08/21
Ahimbisibwe GiftGreenwood DavidWilkinson Katalin AndreaGahir JoshuaTownsley HermaleighMiah MuradBawumia PhilipChaloner CharlotteLevi DinaHobson PhilipRiddell AndyHobbs AgnieszkaDowgier GiuliaPenn RebeccaSanderson TheoStevenson-Leggett PhoebeDaley OdiesiaBazire JamesHarvey RuthFowler Ashley SSmith CallieMiranda MauroO'Reilly NicolaWarchal ScottAmbrose KarenStrange AmyKelly GavinKjar Svend Williams BryanLibri VincenzoGamblin SteveGandhi SoniaSwanton CharlesBauer David LvWilkinson Robert JohnCarr Edward JWall Emma C - Sepsis-induced myocardial injury (SIMI) significantly contributes to sepsis-related mortality, yet effective therapies remain limited. This study investigated the cardioprotective potential of isopropyl 3-(3,4-dihydroxyphenyl)-2-hydroxypropanoate (IDHP), a bioactive metabolite from , focusing on its mechanism via the GAS6/Axl signaling axis in lipopolysaccharide (LPS)-induced myocardial injury. Using an in vitro HL-1 cardiomyocyte model, IDHP's cytotoxicity was assessed (0-20 μM). Cells were pretreated with IDHP (10 μM, optimal concentration) before LPS exposure. Inflammatory cytokines (IL-6/TNF-α/IL-1β/IL-18), chemokines (CCL2/CCR2, CCL25/CCR9), ROS levels (Nrf2 pathway), and apoptosis markers (Bax) were quantified. GAS6/Axl-AMPK signaling was evaluated via GAS6 knockout experiments. IDHP (≤20 μM) showed no cytotoxicity. At 10 μM, it exhibited anti-inflammatory effects by reducing LPS-induced cytokine/chemokine release, demonstrated antioxidant activity through lowering ROS via Nrf2 activation, and exerted anti-apoptotic action by downregulating Bax. Mechanistically, IDHP restored GAS6/Axl-AMPK phosphorylation, an effect abolished in GAS6-knockout cells. IDHP mitigates LPS-induced cardiomyocyte injury by concurrently targeting inflammation, oxidative stress, and apoptosis via GAS6/Axl-AMPK signaling, proposing a novel therapeutic avenue for SIMI. - Source: PubMed
Publication date: 2025/08/12
Chen JunminWang YijieLi XinggeGuo XiaoqingTian JiayinZheng XiaohuiYang YangCao Yanting - Tumor-antigen-specific CD8 T cells (CTLs) are the main effector immunocytes in anti-tumor immunity, but their systemic deployment against cancer metastasis remains uncharacterized. Here, we found that the abundance of tumor-specific CD103CD8 T cells in the tumor-draining lymph nodes (TDLNs) was associated with improved lung-metastasis-free survival in breast cancer patients. In mouse cancer models, CD103CD8 T cells were primed in TDLNs and recruited to the lungs via C-C motif chemokine ligand 5/receptor 9 (CCL25/CCR9) signaling to inhibit metastasis through antigen-specific immunity. Furthermore, extracellular vesicles (EVs) from early- and late-stage tumors differentially polarized alveolar macrophages to release CCL25 and IDO1, respectively, and the latter impaired pulmonary CD103CD8 T cell deployment, facilitating lung metastasis. Depleting IDO1 effectively rescued CD103CD8 T cell-mediated protection against lung metastasis. These findings exemplified long-range deployment of adaptive immunity to protect distant organs from metastasis, highlighting the therapeutic potential of reconstituting effector immune cell deployment (EICD) for cancer treatment. - Source: PubMed
Publication date: 2025/08/22
Xing YueZhou YanWang RuxinChen JianingYang LinbinMeng XiangyuWang JiawenOuyang QianZhao JinghuaChen FeiSaw Phei ErFan JiaHuang Jian-DongWu WeiLiu QiangSong ErweiHuang Di