| 摘要 |
We previously reported that NKG2A, a key inhibitory ligand for HLA-E, is expressed on activated TH2, but not TH1, cells. Here we measured cytokine expression in ex vivo TH2 cells and in a mouse model of asthma upon activation with antiCD3/28 and challenge with an NKG2A-specific agonist We show that signaling through NKG2A modulates Th2 cell effector function. This new molecular pathway data provides a novel explanation and treatment for respiratory virus-associated asthma. RSV and hMPV suppress IFN-gamma and HLA-E expression and therefore decrease NKG2A signaling in activated TH2 cells. This results in a relatively robust Th2 response and an unfavorable shift in Th1/Th2 balance. The data presented here suggest that increasing signaling via the NKG2A receptor suppresses Th2 effector function and could positively impact Th1/Th2 balance in asthma.
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