About: CD8(+) T cells controlling pathogens or tumors must function at sites where oxygen tension is frequently low, and never as high as under atmospheric culture conditions. However, T‐cell function in vivo is generally analyzed indirectly, or is extrapolated from in vitro studies under nonphysiologic oxygen tensions. In this study, we delineate the role of physiologic and pathologic oxygen tension in vitro during reactivation and differentiation of tumor‐specific CD8(+) T cells. Using CD8(+) T cells from pmel‐1 mice, we observed that the generation of CTLs under 5% O(2), which corresponds to physioxia in lymph nodes, gave rise to a higher effector signature than those generated under atmospheric oxygen fractions (21% O(2)). Hypoxia (1% O(2)) did not modify cytotoxicity, but decreasing O(2) tensions during CTL and CD8(+) tumor‐infiltrating lymphocyte reactivation dose‐dependently decreased proliferation, induced secretion of the immunosuppressive cytokine IL‐10, and upregulated the expression of CD137 (4‐1BB) and CD25. Overall, our data indicate that oxygen tension is a key regulator of CD8(+) T‐cell function and fate and suggest that IL‐10 release may be an unanticipated component of CD8(+) T cell‐mediated immune responses in most in vivo microenvironments.

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About: CD8(+) T cells controlling pathogens or tumors must function at sites where oxygen tension is frequently low, and never as high as under atmospheric culture conditions. However, T‐cell function in vivo is generally analyzed indirectly, or is extrapolated from in vitro studies under nonphysiologic oxygen tensions. In this study, we delineate the role of physiologic and pathologic oxygen tension in vitro during reactivation and differentiation of tumor‐specific CD8(+) T cells. Using CD8(+) T cells from pmel‐1 mice, we observed that the generation of CTLs under 5% O(2), which corresponds to physioxia in lymph nodes, gave rise to a higher effector signature than those generated under atmospheric oxygen fractions (21% O(2)). Hypoxia (1% O(2)) did not modify cytotoxicity, but decreasing O(2) tensions during CTL and CD8(+) tumor‐infiltrating lymphocyte reactivation dose‐dependently decreased proliferation, induced secretion of the immunosuppressive cytokine IL‐10, and upregulated the expression of CD137 (4‐1BB) and CD25. Overall, our data indicate that oxygen tension is a key regulator of CD8(+) T‐cell function and fate and suggest that IL‐10 release may be an unanticipated component of CD8(+) T cell‐mediated immune responses in most in vivo microenvironments. Goto Sponge NotDistinct Permalink

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type	abstract
value	CD8(+) T cells controlling pathogens or tumors must function at sites where oxygen tension is frequently low, and never as high as under atmospheric culture conditions. However, T‐cell function in vivo is generally analyzed indirectly, or is extrapolated from in vitro studies under nonphysiologic oxygen tensions. In this study, we delineate the role of physiologic and pathologic oxygen tension in vitro during reactivation and differentiation of tumor‐specific CD8(+) T cells. Using CD8(+) T cells from pmel‐1 mice, we observed that the generation of CTLs under 5% O(2), which corresponds to physioxia in lymph nodes, gave rise to a higher effector signature than those generated under atmospheric oxygen fractions (21% O(2)). Hypoxia (1% O(2)) did not modify cytotoxicity, but decreasing O(2) tensions during CTL and CD8(+) tumor‐infiltrating lymphocyte reactivation dose‐dependently decreased proliferation, induced secretion of the immunosuppressive cytokine IL‐10, and upregulated the expression of CD137 (4‐1BB) and CD25. Overall, our data indicate that oxygen tension is a key regulator of CD8(+) T‐cell function and fate and suggest that IL‐10 release may be an unanticipated component of CD8(+) T cell‐mediated immune responses in most in vivo microenvironments.
subject	Immunology T cells Ecosystems Secretion Human cells »more»
part of	Phenotypic switch of CD8(+) T cells reactivated under hypoxia toward IL‐10 secreting, poorly proliferative effector cells
is abstract of	Phenotypic switch of CD8(+) T cells reactivated under hypoxia toward IL‐10 secreting, poorly proliferative effector cells
is hasSource of	covid:ann/target/57514228f5ef2a08688adc4c8c97fe96633d5432 covid:ann/target/5ea7de46c7e4602436733d45f862decd6a1e32e2 covid:ann/target/0ff7bf085ce1beb0bd800d7cb59466954f7ade48 covid:ann/target/0d57a08a78941ee451bb720069daada69b74e9b5 covid:ann/target/5579f4b16df5bc07577e0ad087652a32d3ebce06 »more»

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