期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 111, 期 35, 页码 12835-12840出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1406908111
关键词
T-cell activation; antigen presentation
资金
- Swiss National Science Foundation [310030_130674/1, CRSII3_136286/1, 310030_146187, 31003AB_131090]
- Sinergia Grant [CRS133_124819]
- Optimus Foundation
- European Molecular Biology Organization long term fellowship
- Swiss National Science Foundation (SNF) [310030_146187, CRSII3_136286, 31003AB_131090, 310030_130674] Funding Source: Swiss National Science Foundation (SNF)
Group 3 innate lymphoid cells (ILC3s) have emerged as important cellular players in tissue repair and innate immunity. Whether these cells meaningfully regulate adaptive immune responses upon activation has yet to be explored. Here we show that upon IL-1 beta stimulation, peripheral ILC3s become activated, secrete cytokines, up-regulate surface MHC class II molecules, and express costimulatory molecules. ILC3s can take up latex beads, process protein antigen, and consequently prime CD4(+) T-cell responses in vitro. The cognate interaction of ILC3s and CD4(+) T cells leads to T-cell proliferation both in vitro and in vivo, whereas its disruption impairs specific T-cell and T-dependent B-cell responses in vivo. In addition, the ILC3-CD4(+) T-cell interaction is bidirectional and leads to the activation of ILC3s. Taken together, our data reveal a novel activation-dependent function of peripheral ILC3s in eliciting cognate CD4(+) T-cell immune responses.
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