MIP-3 beta/CCL19 Protein, Mouse (sf9, His)

MIP-3 beta/CCL19 Protein, Mouse (sf9, His) is a CC chemokine that is strongly chemotactic for CD4 T cells and CD8 T cells and acts as a ligand that binds specifically to the chemokine receptor CCR7 to mediate tissue immunity, inflammatory responses, and antiviral infections. MIP-3 beta/CCL19 Protein, Mouse (sf9, His) is a recombinant mouse MIP-3 beta/CCL19 (G26-S108) protein expressed by Sf9 insect cells with a his tag at the C-terminus^[1][2].

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].

Mouse

Sf9 insect cells

C-His

O70460 (G26-S108)

24047  [NCBI]

MAPRVTPLLAFSLLVLWTFPAPTLGGANDAEDCCLSVTQRPIPGNIVKAFRYLLNEDGCRVPAVVFTTLRGYQLCAPPDQPWVDRIIRRLKKSSAKNKGNSTRRSPVS

Approximately 10.7 kDa

Greater than 95% as determined by reducing SDS-PAGE.

Lyophilized powder.

Lyophilized a 0.2 μm filtered solution of 20 mM Tris, 300 mM NaCl, 10 % glycerol, pH 8.0. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O.

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Yan Yan, et al. CCL19 and CCR7 Expression, Signaling Pathways, and Adjuvant Functions in Viral Infection and Prevention. Front Cell Dev Biol. 2019 Oct 1;7:212.  [Content Brief]

  [2]. Naomi Yamashita, et al. Role of CCL21 and CCL19 in allergic inflammation in the ovalbumin-specific murine asthmatic model. J Allergy Clin Immunol. 2006 May;117(5):1040-6  [Content Brief]

  [3]. Benjamin J Marsland, et al. CCL19 and CCL21 induce a potent proinflammatory differentiation program in licensed dendritic cells. Immunity. 2005 Apr;22(4):493-505.  [Content Brief]

  [4]. Yan Yan, et al. CCL19 enhances CD8+ T-cell responses and accelerates HBV clearance. J Gastroenterol. 2021 Aug;56(8):769-785.  [Content Brief]