Role of receptor ST2 in the development of Ehrlich tumor

• Grant number: 13/00825-0
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: March 01, 2013
• End date: November 30, 2013
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Ana Paula Campanelli
• Grantee: Nathalia Christina Gallo
• Host Institution: Faculdade de Odontologia de Bauru (FOB). Universidade de São Paulo (USP). Bauru , SP, Brazil

Abstract

Recent studies have shown that there is a direct association between a Th1-related immune response and a better prognosis in patients with cancer. These findings have led us to hypothesize that the protective Th1-type immune response toward cancer might be inhibited by immunoregulatory factors. One example is ST2L, which when activated by the cytokine IL-33 promotes Th2-type responses and impairs Th1-type innate immune responses (Ramaprakash et al., AJP, 2010). Moreover, ST2L is constitutively expressed on natural killer (NK) cells but its role in these cells during anti-tumor and anti-metastatic responses remains to be fully elucidated. Based on these findings, our hypothesis is that immunoregulatory signaling mediated via IL-33/ST2L impairs the Th1-type immune response thereby leaving the development of cancer. Our two specific aims are as follows:1. to analyze the development and progression of Ehrlich tumor in ST2 deficient mice.2. to analyze the effect of IL-33 on the cytotoxic activity of NK cells. (AU)