Core B will be part of a multi-tiered expression analysis core set up to support all four projects of the PPG. We have been successful in our effort to develop an expression profiling resource at our center. In collaboration with Rick Young at the Massachusetts Institute of Technology and Aviv Regev at the Broad Institute of Genetics and Genomics, we have developed technologies to undertake multiplex expression profiling using newly acquired Nanostring nCounter technologies. With the support from MIT and the Broad Institute, our expression Core has the know-how, technologies, resources and analytical skills to support the research projects of this PPG. The Core allows for multiplex expression analysis of up to 500 genes in a single RNA sample using a recently acquired Nanostring nCounter, which saves time and materials. Furthermore, Nanostring nCounter technology is particularly suited for expression analysis of rare cells present or infiltrating into the CNS. The core has been set up so that expression data obtained from different projects and cell types can be readily analyzed and compared. The major aim of the core is undertake multiplexed gene expression profiling using Nanostring nCounter technologies.
Using the multiplexed gene expression resources of the core, together with ChlP-seq and RNA-seq data (undertaken in Project 2), will allow us to develop a molecular map to understand the development, function, and regulation of IL-27-driven Tri cells, which will lead to the identification of nodal points in Tri development. Identification of these nodal points could be used as essential drug targets for future immunomodulatory therapies for multiple sclerosis (MS).
|Hu, Dan; Notarbartolo, Samuele; Croonenborghs, Tom et al. (2017) Transcriptional signature of human pro-inflammatory TH17 cells identifies reduced IL10 gene expression in multiple sclerosis. Nat Commun 8:1600|
|Chihara, Norio; Madi, Asaf; Karwacz, Katarzyna et al. (2016) Differentiation and Characterization of Tr1 Cells. Curr Protoc Immunol 113:3.27.1-3.27.10|
|Anderson, Ana C; Joller, Nicole; Kuchroo, Vijay K (2016) Lag-3, Tim-3, and TIGIT: Co-inhibitory Receptors with Specialized Functions in Immune Regulation. Immunity 44:989-1004|
|Meyer Zu Horste, Gerd; Wu, Chuan; Wang, Chao et al. (2016) RBPJ Controls Development of Pathogenic Th17 Cells by Regulating IL-23 Receptor Expression. Cell Rep 16:392-404|
|Mayo, Lior; Cunha, Andre Pires Da; Madi, Asaf et al. (2016) IL-10-dependent Tr1 cells attenuate astrocyte activation and ameliorate chronic central nervous system inflammation. Brain 139:1939-57|
|Gaublomme, Jellert T; Yosef, Nir; Lee, Youjin et al. (2015) Single-Cell Genomics Unveils Critical Regulators of Th17 Cell Pathogenicity. Cell 163:1400-12|
|Wang, Chao; Yosef, Nir; Gaublomme, Jellert et al. (2015) CD5L/AIM Regulates Lipid Biosynthesis and Restrains Th17 Cell Pathogenicity. Cell 163:1413-27|
|Wang, Chao; Collins, Mary; Kuchroo, Vijay K (2015) Effector T cell differentiation: are master regulators of effector T cells still the masters? Curr Opin Immunol 37:6-10|
|Peters, Anneli; Fowler, Kevin D; Chalmin, Fanny et al. (2015) IL-27 Induces Th17 Differentiation in the Absence of STAT1 Signaling. J Immunol 195:4144-53|
|Xiao, Sheng; Brooks, Craig R; Sobel, Raymond A et al. (2015) Tim-1 is essential for induction and maintenance of IL-10 in regulatory B cells and their regulation of tissue inflammation. J Immunol 194:1602-8|
Showing the most recent 10 out of 14 publications