| Literature DB >> 30455400 |
Surojit Sarkar1,2,3,4, Yevgeniy Yuzefpolskiy2,4, Hanxi Xiao2, Florian M Baumann5, Soojin Yim6, David J Lee6, Dominik Schenten7, Vandana Kalia1,2.
Abstract
IL-1, generally considered an amplifier of adaptive immune responses, has been proposed for use as adjuvant during immunization with weak immunogens. However, its effects on memory T cell function remain largely undefined. Using the murine model of acute viral infection, in this paper, we show that in addition to augmenting the size of the Ag-specific pool, IL-1 signals act directly on CD8 T cells to promote the quality of effector and memory responses. Ablation of IL-1R1 or MyD88 signaling in T cells led to functional impairment; both the ability to produce multiple cytokines on a per cell basis (polyfunctionality) and the potential for recall proliferation in response to antigenic restimulation were compromised. IL-1 supplementation during priming augmented the expansion of Ag-specific CD8 T cells through the MyD88-IRAK1/4 axis, resulting in a larger memory pool capable of robust secondary expansion in response to rechallange. Together, these findings demonstrate a critical role of the IL-1-MyD88 axis in programming the quantity and quality of memory CD8 T cell responses and support the notion that IL-1 supplementation may be exploited to enhance adoptive T cell therapies against cancers and chronic infections.Entities:
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Year: 2018 PMID: 30455400 DOI: 10.4049/jimmunol.1800906
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422