TGF-β is responsible for NK cell immaturity during ontogeny and increased susceptibility to infection during mouse infancy.
TGF-β is responsible for NK cell immaturity during ontogeny and increased susceptibility to infection during mouse infancy.
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我们对婴儿免疫的理解中的一个主要差距是为什么自然杀伤（NK）细胞反应不足，使婴儿更容易受到病毒感染。在这里，我们证明了转化生长因子-β（TGF-β）是婴儿期NK细胞不成熟的原因。在CD 11 cdnR小鼠中发现了更高数量的完全成熟的NK细胞，其NK细胞缺乏TGF-βR信号传导。重要的是，在没有TGF-β信号传导的情况下，NK细胞的个体发育成熟进展得更快，导致在生命早期形成成熟的NK细胞库。因此，婴儿CD 11 cdnR小鼠有效地控制了病毒感染。因此，这些数据表明TGF-β在个体发育中具有前所未有的作用，可以解释为什么NK细胞应答在生命早期缺乏。
A major gap in our understanding of infant immunity is why natural killer (NK) cellresponses are deficient, making infants more prone to viral infection. Here we demonstrate that transforming growth factor-β (TGF-β) was responsible for NK cell immaturity during infancy. Higher numbers of fully mature NK cells were found in CD11cdnR mice, whose NK cells lack TGF-βR signaling. Importantly, ontogenic maturation of NK cells progressed faster in the absence of TGF-β signaling, resulting in the formation of mature NK cell pool early in life. As a consequence, infant CD11cdnR mice efficiently controlled viral infections. These data thus demonstrate an unprecedented role for TGF-β in ontogeny that can explain why NK cell responses are deficient early in life.