Bioinformatic modeling of Egr2 and 3 regulatory program in T cells in association with infection and self-tolerance

Abstract

We found that transcription factors Egr2 and 3 have reciprocal functions in regulating proliferation and differentiation of T cells. Egr2 and 3 deficiency in T cells leads to severe infection and also the development of auto-immune diseases. Based on our knockout and knockin models, this project aims to analyse the data established from CHIP-seq, RNA-seq, and T cell repertoire seq of Egr2 positive T cells to define the target genes of Egr2, the pathways mediated by Egr2 in T cells under different responsive conditions and to create models of the regulatory program in T cell subsets with distinct functions.




References:
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Suling Li, Tizong Miao, Meera Sebastian, Punamdip Bhullar, Emma Ghaffari, Mengya Liu, Alistair L. J. Symonds, and Ping Wang, Egr-2 and -3 are essential for both the control of inflammatory autoimmune diseases and antigen receptor mediated activation of B and T cells, Immunity,19;37(4):685-96, 2012.

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Biological Areas:

Immunology
Biotechnology

BBSRC Area:

Animal disease, health and welfare