Cytokines
Product List
Recombinant Human C-C motif chemokine 20 protein (CCL20) (Active)
Recombinant human CCL20 protein is expressed in *E. coli* and encompasses the full length of the mature 27-96 amino acid sequence. This tag-free protein is supplied as a lyophilized powder, facilitating convenient reconstitution with sterile water or buffer. Achieving a purity exceeding 97%, as determined by SDS-PAGE and HPLC, our recombinant CCL20 also maintains a low endotoxin level of less than 1.0 EU/µg, measured using the LAL method. The protein retains full biological activity, demonstrated by its efficacy in a chemotaxis bioassay utilizing human T-lymphocytes, with an activity concentration range of 10-50 ng/ml.
C-C motif chemokine 20 (CCL20) is a member of the CC chemokine family and plays a crucial role in immune cell trafficking and function. Consequently, understanding the functions and mechanisms of CCL20 is paramount in elucidating its roles within the immune system and developing potential therapeutic interventions for immune-related diseases.
Recombinant Human C-C motif chemokine 17 protein (CCL17) (Active)
This recombinant human CCL17, produced in E. coli, exhibits >97% purity (SDS-PAGE) and <1.0 EU/μg endotoxin levels (LAL method). Its biological activity has been confirmed via a chemotaxis bioassay using human T-lymphocytes, demonstrating a concentration range of 1.0-10 ng/ml. Supplied as a lyophilized powder, it is ideally suited for immunology research, particularly studies investigating the role of MET in tumor progression and therapeutic resistance.
Human CCL17 (TARC) is a crucial chemokine mediating immune responses through its interaction with CCR4, significantly influencing T cell recruitment and inflammation [1, 2]. Primarily secreted by dendritic cells (DCs) and macrophages, CCL17's interaction with CCR4 is essential for the migration of these cells to inflammatory sites, thus impacting various immune responses, including those in allergic reactions and autoimmune diseases [3, 4].
In inflammatory contexts, CCL17 facilitates the migration of Tregs and other immune cells, contributing to immune homeostasis and inflammatory response modulation [5, 6]. Furthermore, its involvement in fibrotic processes, particularly in the lung and kidney, highlights its pro-fibrotic properties [7, 8].
References:
[1] Feng, G., Zhu, C., Lin, C., Bredemeyer, A., Förster, I., Kreise et al. (2023). Ccl17 protects against viral myocarditis by suppressing the recruitment of regulatory t cells. Journal of the American Heart Association, 12(4). https://doi.org/10.1161/jaha.122.028442
[2] Iellem, A., Mariani, M., Lang, R., Recalde, H., Panina-Bordignon, P., Sinigaglia et al. (2001). Unique chemotactic response profile and specific expression of chemokine receptors ccr4 and ccr8 by cd4+cd25+ regulatory t cells. The Journal of Experimental Medicine, 194(6), 847-854. https://doi.org/10.1084/jem.194.6.847
[3] Hirata, H., Yukawa, T., Tanaka, A., Miyao, T., Fukuda, T., Fukushima et al. (2018). Th2 cell differentiation from naive cd4+ t cells is enhanced by autocrine cc chemokines in atopic diseases. Clinical & Experimental Allergy, 49(4), 474-483. https://doi.org/10.1111/cea.13313
[4] Solari, R., & Pease, J. (2015). Targeting chemokine receptors in disease – a case study of ccr4. European Journal of Pharmacology, 763, 169-177. https://doi.org/10.1016/j.ejphar.2015.05.018
[5] Lee, K., Jarnicki, A., Achuthan, A., Fleetwood, A., Anderson, G., Ellson et al. (2020). Ccl17 in inflammation and pain. The Journal of Immunology, 205(1), 213-222. https://doi.org/10.4049/jimmunol.2000315
[6] Weber, C., Meiler, S., Döring, Y., Koch, M., Drechsler, M., Megen et al. (2011). Ccl17-expressing dendritic cells drive atherosclerosis by restraining regulatory t cell homeostasis in mice. Journal of Clinical Investigation, 121(7), 2898-2910. https://doi.org/10.1172/jci44925
[7] Chen, Y., Hsu, H., Lin, C., Pan, S., Liu, S., Wu et al. (2019). Inflammatory macrophages switch to ccl17‐expressing phenotype and promote peritoneal fibrosis. The Journal of Pathology, 250(1), 55-66. https://doi.org/10.1002/path.5350
[8] Inoue, T., Fujishima, S., Ikeda, E., Yoshie, O., Tsukamoto, N., Aiso et al. (2004). Ccl22 and ccl17 in rat radiation pneumonitis and in human idiopathic pulmonary fibrosis. European Respiratory Journal, 24(1), 49-56. https://doi.org/10.1183/09031936.04.00110203
Recombinant Human C-C motif chemokine 18 (CCL18) (Active)
Recombinant Human CCL18 is a key protein involved in immune responses, playing a crucial role in various immune-related processes, including chemotaxis of T-lymphocytes[1]. Our Recombinant Human CCL18 is a full-length mature protein comprising amino acids 21-89 and is expressed in E. coli. It is presented as a lyophilized powder and is tag-free, making it suitable for a wide range of research applications.
Our recombinant human CCL18 protein exhibits a purity exceeding 97%, as determined by SDS-PAGE and HPLC. The endotoxin level is less than 1.0 EU/ug, as confirmed by the LAL method. The biological activity of our product has been validated through a chemotaxis bioassay employing human T-lymphocytes, demonstrating activity within a concentration range of 1.0-10 ng/ml.
Research has demonstrated that CCL18 plays a critical role in the regulation of immune responses and has been implicated in various immune-mediated disorders, such as asthma, allergy, and inflammatory diseases[2]. Furthermore, elevated levels of CCL18 have been associated with tumor progression in specific cancers[3].
References:
1. Adema GJ, et al. A dendritic-cell-derived C-C chemokine that preferentially attracts naive T cells. Nature. 1997;387(6634): 713-7.
2. Kodelja V, et al. Alternative macrophage activation-associated CC-chemokine-1, a novel structural homologue of macrophage inflammatory protein-1 alpha with a Th2-associated expression pattern. J Immunol. 1998;160(3): 1411-8.
3. Schutyser E, et al. Identification of biologically active chemokine isoforms from ascitic fluid and elevated levels of CCL18/pulmonary and activation-regulated chemokine in ovarian carcinoma. J Biol Chem. 2002;277(27): 24584-93.
