T helper type 17 cells contribute to anti‐tumour immunity and promote the recruitment of T helper type 1 cells to the tumour. Issue 1 (8th April 2013)

• Record Type: Journal Article
• Authors: Nuñez, Sarah; Saez, Juan Jose; Fernandez, Dominique; Flores‐Santibañez, Felipe; Alvarez, Karla; Tejon, Gabriela; Ruiz, Paulina; Maldonado, Paula; Hidalgo, Yessia; Manriquez, Valeria; Bono, Maria Rosa; Rosemblatt, Mario; Sauma, Daniela
• Is Part Of: Immunology. Volume 139:Issue 1(2013:May)
• Page Start: 61
• Page End: 71
• Publication Date: 2013-04-08
• Subjects: Immunology -- Periodicals
• DOI: 10.1111/imm.12055
• Languages: English
• ISSNs: 0019-2805

Abstract

<abstract abstract-type="main" xml:lang="en" id="imm12055-abs-0001"> <title>Summary</title> <p>T helper type 17 (Th17) lymphocytes are found in high frequency in tumour‐burdened animals and cancer patients. These lymphocytes, characterized by the production of interleukin‐17 and other pro‐inflammatory cytokines, have a well‐defined role in the development of inflammatory and autoimmune pathologies; however, their function in tumour immunity is less clear. We explored possible opposing anti‐tumour and tumour‐promoting functions of Th17 cells by evaluating tumour growth and the ability to promote tumour infiltration of myeloid‐derived suppressor cells (MDSC), regulatory T cells and CD4⁺ interferon‐γ⁺ cells in a retinoic acid‐like orphan receptor γt (RORγt) ‐deficient mouse model. A reduced percentage of Th17 cells in the tumour microenvironment in RORγt‐deficient mice led to enhanced tumour growth, that could be reverted by adoptive transfer of Th17 cells. Differences in tumour growth were not associated with changes in the accumulation or suppressive function of MDSC and regulatory T cells but were related to a decrease in the proportion of CD4⁺ T cells in the tumour. Our results suggest that Th17 cells do not affect the recruitment of immunosuppressive populations but favour the recruitment of effector Th1 cells to the tumour, thereby promoting anti‐tumour responses.</p> </abstract>