MIP-3 beta/CCL19 Protein, Mouse

CCL19, also known as MIP-3 beta, is an immunostable chemokine that is located on chromosome 9 in the human genome. CCL19 is abundantly expressed in the thymus and lymph nodes, moderately expressed in the trachea and colon, and less expressed in the stomach, small intestine, lung, kidney, and spleen. CCL19 binds to and functions as a chemokine receptor, CCR7. CCR7 is the first CCR7 is the first lymphocyte-specific G protein-coupled receptor (GPCR) identified with seven transmembrane alpha helices. CCR7 is expressed on both double-negative and single-positive thymocytes, including naive T cells, central memory T cells, regulatory T cells, naive B cells, semimature/mature DCs and NK cells, as well as a few tumor cells, where it serves as a key regulator for directing steady-state lymphocytes to secondary lymphoid organs. In contrast, CCL19 is the only chemokine known to effectively stimulate β-arrestin-mediated phosphorylation and internalization of CCR7, leading to receptor desensitization and migration of antigen (Ag)-presenting DCs, thereby affecting T cell responses. The CCL19-CCR7-based signaling pathway plays an important role in tissue immunity and inflammatory response memory. In addition, it also plays a role in vaccine-based protection against a variety of viruses, such as HIV-1 infection, hepatitis C virus (HCV), and herpes simplex virus 1 (HSV-1), etc. The interaction of CCL19 and CCR7 also contributes to the release of antiviral-associated cytokines (e.g., IFN-γ and IL-4) by immune cells, thereby promoting T cell proliferation and DC uptake of antigens^[1][2].

CCL19 (1 μg/mL, 6 h) induces T cell proliferation in immature mouse dendritic cells (DC)-T cell co-culture systems, induces upregulation of costimulatory molecules and cytokine production in DCs, and maturation of DC to induce the Th1 response in DC isolated from spleens and mesenteric lymph nodes of naïve BALB/c mice^[3].

CCL19 (5 mg/mouse by osmotic pump) significantly increases IL-10 production in plt (plt) mice，and after treatment with 100 mg acetylcholine, the number of lymphocytes at bronchoalveolar lavage fluid (BALF) and enhanced pause (Penh) levels is significantly lower in CCL19-treated mice than in untreated mice^[2].
CCL19 can lead to rapid clearance of intrahepatic HBV likely through increased intrahepatic CD8+ T-cell proportion, decreased frequency of PD-1⁺ CD⁸⁺ T cells in blood and compromised suppression of hepatic APCs, with lymphocytes producing a significantly high level of Ag-responsive TNF-α and IFN-γ from CD⁸⁺ T cells in C57BL/6 mice transfected with the mouse CCL19-encoding plasmid^[4].