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Characterization of signaling pathways in the inflammatory infiltrate in mouse tumor models associated to HPV16

Grant number: 11/01650-3
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): April 01, 2011
Effective date (End): December 31, 2011
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal researcher:Ana Paula Lepique
Grantee:André Bento Chaves Santana
Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Cervical cancer is one of the main causes for women death in developing countries. Persistent infection with high risk Human Papillomavirus (HPV) is the main cause for cervical tumors development. Most infected women naturally clear infection and precursor lesions. However, a fraction of these women stains persistent infection and may develop tumors. The immune system in essential for the control of HPV associated tumor progression. Our laboratory has been working with a mouse tumor model associated to HPV16. Using this model we were able to characterize the tumor inflammatory infiltrate, where macrophages capable of inducing regulatory phenotype in T cells are the most abundant population. We have shown that regulatory phenotype induction is dependent on IL-10 expressed by tumor macrophages (Lepique et al, 2009; Bolpetti et al, 2010). We have also characterized cytokine expression profile in tumors, tumor inflammatory infiltrate and tumor bearing mice spleens. Besides GM-CSF, expressed by tumor cells, all tumor populations express CCL2 and TGFb. In the spleens of tumor bearing mice, we have seen downregulation of CXCL10 expression. In this project, we intend to study the signaling pathways activation, in antigen presenting cells in tumors and spleens of mice with tumors, triggered by the receptors of the cytokines above. This project will give us information on how the tumor environment influences the phenotype of antigen presenting cells, therefore influencing T cell anti-tumor responses.

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