IL-21 in Homeostasis of Resident Memory and Exhausted CD8 T Cells during Persistent Infection.

IL-21 in Homeostasis of Resident Memory and Exhausted CD8 T Cells during Persistent Infection.
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DOI:
10.3390/ijms21186966
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发表时间:
2020-09-22
影响因子:
5.6
通讯作者:
Lukacher AE
Lukacher AE
中科院分区:
生物学2区
文献类型:
--
作者:
Ren HM;Lukacher AE

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CD4 T cells guide the development of CD8 T cells into memory by elaborating mitogenic and differentiation factors and by licensing professional antigen-presenting cells. CD4 T cells also act to stave off CD8 T cell dysfunction during repetitive antigen stimulation in persistent infection and cancer by mitigating generation of exhausted T cells (TEX). CD4 T cell help is also required for establishing and maintaining tissue-resident memory T cells (TRM), the nonrecirculating memory T cell subset parked in nonlymphoid tissues to provide frontline defense against reinvading pathogens. Interleukin (IL)-21 is the signature cytokine secreted by follicular helper CD4 T cells (TFH) to drive B cell expansion and differentiation in germinal centers to mount high-affinity, isotype class-switched antibodies. In several infection models, IL-21 has been identified as the CD4 T help needed for formation and survival of TRM and TEX. In this review, we will explore the different memory subsets of CD8 T cells in persistent infections, the metabolic profiles associated with each, and evidence documenting the importance of CD4 T cell-derived IL-21 in regulating CD8 TRM and TEX development, homeostasis, and function.
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