期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 211, 期 13, 页码 2507-2517出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20140137
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资金
- SNF [31003A_ 135649]
- SNF Sinergia grant [CRSII3_ 141918]
- Japanese-Swiss Science and Technology Program grant
- Italian Association for Cancer Research (AIRC)
- Bangerter Foundation
- Grants-in-Aid for Scientific Research [24111001, 25251015, 24111007] Funding Source: KAKEN
- Swiss National Science Foundation (SNF) [CRSII3_141918] Funding Source: Swiss National Science Foundation (SNF)
Interactions between dendritic cells (DCs) and T cells control the decision between activation and tolerance induction. Thromboxane A2 (TXA2) and its receptor TP have been suggested to regulate adaptive immune responses through control of T cell-DC interactions. Here, we show that this control is achieved by selectively reducing expansion of low-avidity CD4(+) T cells. During inflammation, weak tetramer-binding TP-deficient CD4(+) T cells were preferentially expanded compared with TP-proficient CD4(+) T cells. Using intravital imaging of cellular interactions in reactive peripheral lymph nodes (PLNs), we found that TXA2 led to disruption of low-but not high-avidity interactions between DCs and CD4(+) T cells. Lack of TP correlated with higher expression of activation markers on stimulated CD4(+) T cells and with augmented accumulation of follicular helper T cells (T-FH), which correlated with increased low-avidity IgG responses. In sum, our data suggest that tonic suppression of weak CD4(+) T cell-DC interactions by TXA2-TP signaling improves the overall quality of adaptive immune responses.
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