Immunome Research

Immunome Research
Open Access

ISSN: 1745-7580

+44-77-2385-9429

Investigating molecular mechanism regulating EGR2 expression and its role in the immune response


International Congress on Vaccines, Immunology & Antibiotics

December 06-07, 2018 | Amsterdam, Netherlands

Nima Taefehshokr and Su-Ling Li

Brunel University London, England

Posters & Accepted Abstracts: Immunome Res

Abstract :

The immune system is evolved to defend the body against pathogens and is composed of thousands of complicated and intertwined approaches, which are highly controlled by regulatory processes such as transcription and repression of cellular genes. Early growth response gene (EGR2) is important for maintaining immune stability and it has a vital role in controlling inflammation and preventing the development of autoimmune diseases. A recent study by our group demonstrated the function of EGR2 as a checkpoint molecule controlling the proliferation and differentiation of the T cells, confirming its regulatory role, which is essential for optimal immune responses against pathogens; however the EGR2 expression mechanism is still unclear. EGR2 and EGR3 play indispensable roles in T cell immune response, but its role in tumor regression is less well known. In this study, we have found that EGR2 expression is regulated by antigens and cytokines, including INFg and IL-6 which is mediated by INFg/STAT1 and IL6/STAT3 signaling pathways. Furthermore, it is shown that EGR2 can be significantly expressed in tumor infiltrating lymphocytes (TILs) as we observed in a mouse melanoma tumor model. Also, tumor growth is delayed in WT mice model in comparison with EGR2/3 KO counterpart, which is followed by higher TILs expansion in WT model. This was supported by IL-2 and Ki-67 significant expression in WT CD8+ TILs, suggesting the positive role of EGR2 in CD8+ TILs expansion and tumor regression. Collectively, our results demonstrate that EGR2 is an intrinsic regulator of adaptive immunity and tumor microenvironment.

Biography :

  

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