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T helper type 17 cells contribute to anti‐tumour immunity and promote the recruitment of T helper type 1 cells to the tumour
Author(s) -
Nuñez Sarah,
Saez Juan Jose,
Fernandez Dominique,
FloresSantibañez Felipe,
Alvarez Karla,
Tejon Gabriela,
Ruiz Paulina,
Maldonado Paula,
Hidalgo Yessia,
Manriquez Valeria,
Bono Maria Rosa,
Rosemblatt Mario,
Sauma Daniela
Publication year - 2013
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12055
Subject(s) - adoptive cell transfer , immunology , cytotoxic t cell , cancer research , biology , retinoic acid , rar related orphan receptor gamma , t cell , immune system , foxp3 , in vitro , cell culture , genetics , biochemistry
Summary T helper type 17 ( T h17) 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 T h17 cells by evaluating tumour growth and the ability to promote tumour infiltration of myeloid‐derived suppressor cells ( MDSC ), regulatory T cells and CD 4 +  interferon‐γ + cells in a retinoic acid‐like orphan receptor γt ( ROR γt) ‐deficient mouse model. A reduced percentage of T h17 cells in the tumour microenvironment in ROR γt‐deficient mice led to enhanced tumour growth, that could be reverted by adoptive transfer of T h17 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 CD 4 + T cells in the tumour. Our results suggest that T h17 cells do not affect the recruitment of immunosuppressive populations but favour the recruitment of effector T h1 cells to the tumour, thereby promoting anti‐tumour responses.

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