Abstract:
:CD69 is an early activation marker on the surface of T lymphocytes undergoing activation by cognate antigen. We observed intense expression of CD69 on tumor-infiltrating T-lymphocytes that reside in the hypoxic tumor microenvironment and hypothesized that CD69 could be, at least partially, under the control of the transcriptional hypoxia response. In line with this, human and mouse CD3-stimulated lymphocytes cultured under hypoxia (1% O2) showed increased expression of CD69 at the protein and mRNA level. Consistent with these findings, mouse T lymphocytes that had recently undergone hypoxia in vivo, as denoted by pimonidazole staining, were more frequently CD69+ in the tumor and bone marrow hypoxic tissue compartments. We found evidence for HIF-1α involvement both when using T-lymphocytes from inducible HIF-1α-/- mice and when observing tumor-infiltrating T-lymphocytes in mice whose T cells are HIF-1α-/-. Direct pro-transcriptional activity of HIF-1α on a newly identified hypoxia response element (HRE) found in the human CD69 locus was demonstrated by ChIP experiments. These results uncover a connection between the HIF-1α oxygen-sensing pathway and CD69 immunobiology.
journal_name
Oncoimmunologyjournal_title
Oncoimmunologyauthors
Labiano S,Meléndez-Rodríguez F,Palazón A,Teijeira Á,Garasa S,Etxeberria I,Aznar MÁ,Sánchez-Paulete AR,Azpilikueta A,Bolaños E,Molina C,de la Fuente H,Maiso P,Sánchez-Madrid F,de Landázuri MO,Aragonés J,Melero Idoi
10.1080/2162402X.2017.1283468subject
Has Abstractpub_date
2017-01-19 00:00:00pages
e1283468issue
4eissn
2162-4011issn
2162-402Xpii
1283468journal_volume
6pub_type
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