Abstract:
:Previous studies have suggested that T-lymphocyte dysfunction might be attributable to nitrative stress induced by reactive nitrogen species (RNS). In this manuscript, we explored this hypothesis and provided a direct demonstration of the inhibitory effects of RNS on human T-cell signaling, activation, and migration. We found that short exposure of human T cells to RNS induced tyrosine phosphorylation of several proteins, including the CD3ζ chain of the TCR complex, and release of Ca2+ from intracellular stores. When the exposure to RNS was prolonged, T cells became refractory to stimulation, downregulated membrane receptors such as CD4, CD8, and chemokine receptors, and lost their ability to migrate in response to chemokines. Since substantial protein nitration, a hallmark of nitrative stress, was observed in various human cancers, intratumoral generation of RNS might represent a relevant mechanism for tumor evasion from immune surveillance.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Kasic T,Colombo P,Soldani C,Wang CM,Miranda E,Roncalli M,Bronte V,Viola Adoi
10.1002/eji.201040868subject
Has Abstractpub_date
2011-07-01 00:00:00pages
1843-9issue
7eissn
0014-2980issn
1521-4141journal_volume
41pub_type
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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