This recombinant human CCL17 is produced in E.coli. It boasts over 97% purity by SDS-PAGE and below 1.0 EU/μg endotoxin levels by the LAL method. It has been validated as an active protein by a chemotaxis bioassay using human T-lymphocytes, shows a concentration range of 1.0-10 ng/ml. Provided as lyophilized powder, it is ideal for immunology research, particularly in investigating MET's role in tumor progression and therapy resistance.
Human CCL17, also called TARC, is a pivotal chemokine that orchestrates immune responses through its interactions with CCR4, particularly in the context of T cell recruitment and inflammation [1][2]. CCL17 is primarily produced by dendritic cells (DCs) and macrophages. The CCL17-CCR4 interaction is crucial for the trafficking of these cells to sites of inflammation, thereby influencing various immune responses, including those associated with allergic reactions and autoimmune diseases [3][4].
In inflammatory conditions, CCL17 has been shown to facilitate the migration of Tregs and other immune cells, contributing to the maintenance of immune homeostasis and the modulation of inflammatory responses [5][6]. Additionally, CCL17's involvement in fibrotic processes indicates its pro-fibrotic properties, particularly in organs such as the lung and kidney [7][8].
References:
[1] G. Feng, C. Zhu, C. Lin, A. Bredemeyer, I. Förster, D. Kreiselet al., Ccl17 protects against viral myocarditis by suppressing the recruitment of regulatory t cells, Journal of the American Heart Association, vol. 12, no. 4, 2023. https://doi.org/10.1161/jaha.122.028442
[2] A. Iellem, M. Mariani, R. Lang, H. Recalde, P. Panina-Bordignon, F. Sinigagliaet al., Unique chemotactic response profile and specific expression of chemokine receptors ccr4 and ccr8 by cd4+cd25+ regulatory t cells, The Journal of Experimental Medicine, vol. 194, no. 6, p. 847-854, 2001. https://doi.org/10.1084/jem.194.6.847
[3] H. Hirata, T. Yukawa, A. Tanaka, T. Miyao, T. Fukuda, Y. Fukushimaet al., Th2 cell differentiation from naive cd4+ t cells is enhanced by autocrine cc chemokines in atopic diseases, Clinical & Experimental Allergy, vol. 49, no. 4, p. 474-483, 2018. https://doi.org/10.1111/cea.13313
[4] R. Solari and J. Pease, Targeting chemokine receptors in disease – a case study of ccr4, European Journal of Pharmacology, vol. 763, p. 169-177, 2015. https://doi.org/10.1016/j.ejphar.2015.05.018
[5] K. Lee, A. Jarnicki, A. Achuthan, A. Fleetwood, G. Anderson, C. Ellsonet al., Ccl17 in inflammation and pain, The Journal of Immunology, vol. 205, no. 1, p. 213-222, 2020. https://doi.org/10.4049/jimmunol.2000315
[6] C. Weber, S. Meiler, Y. Döring, M. Koch, M. Drechsler, R. Megenset al., Ccl17-expressing dendritic cells drive atherosclerosis by restraining regulatory t cell homeostasis in mice, Journal of Clinical Investigation, vol. 121, no. 7, p. 2898-2910, 2011. https://doi.org/10.1172/jci44925
[7] Y. Chen, H. Hsu, C. Lin, S. Pan, S. Liu, C. Wuet al., Inflammatory macrophages switch to ccl17‐expressing phenotype and promote peritoneal fibrosis, The Journal of Pathology, vol. 250, no. 1, p. 55-66, 2019. https://doi.org/10.1002/path.5350
[8] T. Inoue, S. Fujishima, E. Ikeda, O. Yoshie, N. Tsukamoto, S. Aisoet al., Ccl22 and ccl17 in rat radiation pneumonitis and in human idiopathic pulmonary fibrosis, European Respiratory Journal, vol. 24, no. 1, p. 49-56, 2004. https://doi.org/10.1183/09031936.04.00110203
