Quantitative Proteomics Reveals the Dynamic Protein Landscape during Initiation of Human Th17 Cell Polarization

Summary: Th17 cells contribute to the pathogenesis of inflammatory and autoimmune diseases and cancer. To reveal the Th17 cell-specific proteomic signature regulating Th17 cell differentiation and function in humans, we used a label-free mass spectrometry-based approach. Furthermore, a comprehensive...

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Bibliographic Details
Main Authors: Subhash K. Tripathi, Tommi Välikangas, Ankitha Shetty, Mohd Moin Khan, Robert Moulder, Santosh D. Bhosale, Elina Komsi, Verna Salo, Rafael Sales De Albuquerque, Omid Rasool, Sanjeev Galande, Laura L. Elo, Riitta Lahesmaa
Format: Article
Language:English
Published: Elsevier 2019-01-01
Series:iScience
Online Access:http://www.sciencedirect.com/science/article/pii/S2589004218302505
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Summary:Summary: Th17 cells contribute to the pathogenesis of inflammatory and autoimmune diseases and cancer. To reveal the Th17 cell-specific proteomic signature regulating Th17 cell differentiation and function in humans, we used a label-free mass spectrometry-based approach. Furthermore, a comprehensive analysis of the proteome and transcriptome of cells during human Th17 differentiation revealed a high degree of overlap between the datasets. However, when compared with corresponding published mouse data, we found very limited overlap between the proteins differentially regulated in response to Th17 differentiation. Validations were made for a panel of selected proteins with known and unknown functions. Finally, using RNA interference, we showed that SATB1 negatively regulates human Th17 cell differentiation. Overall, the current study illustrates a comprehensive picture of the global protein landscape during early human Th17 cell differentiation. Poor overlap with mouse data underlines the importance of human studies for translational research. : Immunology; Components of the Immune System; Omics; Proteomics Subject Areas: Immunology, Components of the Immune System, Omics, Proteomics
ISSN:2589-0042