T helper type 17 cells contribute to anti-tumour immunity and promote the recruitment of T helper type 1 cells to the tumour
Author
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Nuñez, Sarah
Author
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Saez, Juan José
es_CL
Author
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Fernández, Dominique
es_CL
Author
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Flores Santibañez, Felipe
es_CL
Author
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Álvarez, Karla
es_CL
Author
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Tejón, Gabriela
es_CL
Author
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Ruiz, Paulina
es_CL
Author
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Maldonado, Paula
es_CL
Author
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Hidalgo, Yessia
es_CL
Author
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Manriquez, Valeria
es_CL
Author
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Bono Merino, María Rosa
es_CL
Author
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Rosemblatt Silber, Mario César
es_CL
Author
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Sauma Mahaluf, Daniela
es_CL
Admission date
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2014-01-28T13:24:23Z
Available date
dc.date.available
2014-01-28T13:24:23Z
Publication date
dc.date.issued
2013
Cita de ítem
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Immunology, 139, 61–71
en_US
Identifier
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doi:10.1111/imm.12055
Identifier
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https://repositorio.uchile.cl/handle/2250/119715
General note
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Artículo de publicación ISI
en_US
Abstract
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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-c+ cells in a
retinoic acid-like orphan receptor ct (RORct) -deficient mouse model. A
reduced percentage of Th17 cells in the tumour microenvironment in
RORct-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.