Exodus-2 CCL21, Mouse
- Known as:
- Exodus-2 CCL21, Mouse
- Catalog number:
- Z02855-20
- Product Quantity:
- 20,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- Exodus-2 CCL21 Mouse
Related genes to: Exodus-2 CCL21, Mouse
- Gene:
- CCL21 NIH gene
- Name:
- C-C motif chemokine ligand 21
- Previous symbol:
- SCYA21
- Synonyms:
- SLC, exodus-2, TCA4, CKb9, 6Ckine, ECL
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-10
- Date modifiied:
- 2016-10-05
Related products to: Exodus-2 CCL21, Mouse
Related articles to: Exodus-2 CCL21, Mouse
- Exclusive Liquid Repellency Isolation (ELRi) is a novel, chip-free platform designed for efficient microscale immune cell isolation. Leveraging the inherent exclusive liquid repellency (ELR) properties of polypropylene tubes with an oil overlay, ELRi ensures that small sample volumes, as low as 8 μL, have no contact with container walls, preventing cell loss. Here we describe ELRi and demonstrate magnetic bead-based isolation of diverse immune cells, including T cells, and monocytes, from whole blood. The platform's utility is highlighted in its application to pediatric asthma research, where sample volume is highly restricted. It has been reported that the T cell homing receptor CCR7 is downregulated in cells from asthmatic patients, but a direct functional link to impaired cell migration remains unconfirmed (1, 2). Using ELRi-isolated cells, we provide the first functional evidence that T cells from asthmatic children exhibit significantly impaired chemotaxis toward the CCR7 ligand, CCL21. By simplifying RBC depletion and enabling such functional assays alongside RNA sequencing from the same tiny sample, ELRi overcomes the limitations of large-volume flow cytometry or cell-specific sorting methods. Easily integrated into lab workflows and scalable for various needs, ELRi facilitates more frequent, minimally invasive, and functionally informative immune profiling of restricted volume samples. - Source: PubMed
Publication date: 2026/07/15
Juang Terry DJoyce Brendan MPrasad NehaLi YuanshanAhmed FauzanCrisafi Gina MSeroogy Christine MGern James EOng Irene MBeebe David JKerr Sheena C - Magnesium-containing intramedullary nails (Mg-IMN) have been shown to promote fracture healing across various types of fractures, including osteoporotic and atypical femoral fractures. However, their role in the challenging chronic inflammatory type 2 diabetes (T2D) fracture healing remains unclear. In this study, we investigated the effect of Mg-IMN on fracture healing in a T2D mouse model and explored the involvement of regulatory T cells (Tregs) in this process. Our results demonstrated that Mg-IMN promotes fracture healing in Lepr T2D mice. At 5 days post-fracture, flow cytometry showed an increased number of Tregs in the fracture callus. Notably, depletion of Tregs via injection of PC61 neutralizing antibody abolished the promotive effect of Mg-IMN, indicating the critical role of Tregs in this process. Bulk RNA sequencing of the bone callus at 5 days post-fracture revealed significant enrichment of pathways related to chemokine signaling and CCR chemokine receptor interactions, suggesting a mechanism of Treg recruitment. Transwell migration assays preliminarily indicated the chemotactic effect of CCL19 and CCL21 in recruiting Tregs. Furthermore, Mg treatment enhanced the mRNA expression levels of amphiregulin () and granulin () in Tregs, as indicated by qRT-PCR analysis. These findings may pave the way for new applications of Mg-IMN in fracture repair and provide unique insights into osteoimmunology during the complex process of T2D fracture healing. - Source: PubMed
Publication date: 2026/07/14
Zhang Shi'anDai BingyangAn YuanmingJin ZheyuLiu WeiyangXiong NapingShao HongweiShan ZhengmingZheng LizhenLi XuZhu YanbinXu JiankunChow Dick Ho KiuWong Ronald Man YeungQin LingTong Wenxue - Gallbladder cancer (GBC), the most common malignancy of the biliary tract, exhibits a high propensity for lymphatic system invasion. However, the mechanisms underlying lymphatic metastasis in GBC remain poorly understood. Here, we demonstrate that C-C motif chemokine ligand 21 (CCL21) is significantly upregulated in GBC and positively correlates with lymphatic vessel density and lymph node metastasis. Both in vivo and in vitro experiments confirm that CCL21/CCR7 axis promotes lymphangiogenesis and lymphatic metastasis in GBC. Mechanistically, CCL21/CCR7 modulates Vascular Endothelial Growth Factor-D (VEGF-D) mRNA N6-Methyladenosine (mA) modification in an AlkB homolog 5 (ALKBH5)-dependent manner, thereby regulating VEGF-D protein expression. Site-directed mutagenesis experiments reveal that mA modification sites in the coding sequence (CDS) region of VEGF-D mRNA are critical for VEGF-D protein regulation. Collectively, our findings highlight that CCL21/CCR7 regulates VEGF-D expression via mA modification, driving lymphatic metastasis in GBC. - Source: PubMed
Publication date: 2026/07/24
Wu ZhenhengCai XinranJiang LeiLin BinPan WeiLin ShengzheChen YanlingHong Haijie - Current adoptive cell-based immunotherapies show limited efficacy against solid tumors, largely due to dynamic cellular phenotypic shifts and the immunosuppressive tumor microenvironment (TME). To address these challenges, we engineer therapeutic bacteria controlled by a temperature-actuated genetic switch. Brief exposure to focused ultrasound (US) hyperthermia activates this switch, driving sustained CCL21 release to recruit immune cells. These bacteria are surface-modified for bromelain conjugation and bacterial "backpack" formation on macrophages. Following in vitro co-incubation, bacteria-loaded macrophages are intravenously administered for tumor-targeted delivery. In vivo experiments confirm that system activation promotes macrophage repolarization toward a CD86-expressing phenotype within the TME and enhances immune cell infiltration. Moreover, treatment reduces collagen I deposition, weakens the mechanobiological properties of tumor cells, and mitigates tumor-mediated immune evasion. Collectively, this system remodels the immunosuppressive TME through macrophage-mediated bacterial delivery and US-triggered CCL21 release, facilitating dendritic cell and CD4/CD8 T cell infiltration and improving antitumor immunotherapy. - Source: PubMed
Publication date: 2026/07/17
Fan ZheChen PengfeiZuo ShuangmeiCai KehanLi SitianQin HaoyangLi RuiLee KyubaeChen TaoJin ChenwangLi JingchaoChen Yazhou - Tumor-draining lymph nodes (DLNs) are crucial for the development of anti-tumor immunity upon irradiation. However, in radiotherapy, DLNs are frequently co-irradiated, which impairs their function. Here, we examine the consequences of DLN irradiation on anti-tumor immunity, focusing on the recently described radiotherapy-induced disruption of the CCR7-CCL19/CCL21 axis, which governs tumor-to-DLN trafficking. We use in vivo irradiated murine LNs and in vitro assays to assess irradiation-induced structural and functional changes in the DLNs. DLN-infiltrating lymphocytes and CCL19/CCL21 chemokines were depleted early after irradiation in a dose-dependent manner. Lymphocyte numbers recovered only in DLNs irradiated with 5 Gy or less. Lymphopenia persisted in DLNs irradiated with 15 Gy, with few surviving lymphocytes showing a compensatory increase in proliferation. Irradiation-deregulated secretion of CCL19 could be related to lymphodepletion and/or direct irradiation-induced processes in stromal cells. In conclusion, radiotherapy depletes DLNs, and impairs stromal function and chemokine signaling, thereby compromising anti-tumor immunity. - Source: PubMed
Publication date: 2026/07/11
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