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Contact-dependent delivery of IL-2 by dendritic cells to CD4 T cells in the contraction phase promot

本站小编 Free考研考试/2022-01-02

Dan Tong1,
Li Zhang1,
Fei Ning1,
Ying Xu1,
Xiaoyu Hu1,,
Yan Shi1,2,
1 Tsinghua Institute for Immunology and Department of Basic Medical Sciences, Beijing Key Lab for Immunological Research on Chronic Diseases, School of Medicine, Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing 100084, China;
2 Department of Microbiology, Immunology and Infectious Diseases, Snyder Institute, University of Calgary, Calgary, Canada
Funds: We thank Drs. Li Wu, Hai Qi, and Chen Dong for providing mice and reagents and Dr. Fei Shu for help in Listeria monocytogens infection and adoptive transfer experiments. Y.S. is supported by the joint Peking-Tsinghua Center for Life Sciences and the National Natural Science Foundation of China grants 81621002, 31630023, 31370878 and 20171312479. X.H. is supported by Ministry of Science and Technology of China National Key Research Projects 2015CB943201, National Natural Science Foundation of China grants 31821003, 31725010, 81661130161, 91642115 and 81571580.

Received Date: 2019-08-05
Rev Recd Date:2019-09-18
Publish Date:2020-02-10




Abstract
Common γ chain cytokines are important for immune memory formation. Among them, the role of IL-2 remains to be fully explored. It has been suggested that this cytokine is critically needed in the late phase of primary CD4 T cell activation. Lack of IL-2 at this stage sets for a diminished recall response in subsequent challenges. However, as IL-2 peak production is over at this point, the source and the exact mechanism that promotes its production remain elusive. We report here that resting, previously antigen-stimulated CD4 T cells maintain a minimalist response to dendritic cells after their peak activation in vitro. This subtle activation event may be induced by DCs without overt presence of antigen and appears to be stronger if IL-2 comes from the same dendritic cells. This encounter reactivates a miniature IL-2 production and leads a gene expression profile change in these previously activated CD4 T cells. The CD4 T cells so experienced show enhanced reactivation intensity upon secondary challenges later on. Although mostly relying on in vitro evidence, our work may implicate a subtle programing for CD4 T cell survival after primary activation in vivo.
Keywords: dendritic cell,
contact dependence,
long term survival,
T cell memory,
IL-2



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