ILT4 drives B7-H3 expression via PI3K/AKT/mTOR signalling and ILT4/B7-H3 co-expression correlates with poor prognosis in non-small cell lung cancer

ILT4 通过 PI3K/AKT/mTOR 信号传导驱动 B7-H3 表达,且 ILT4/B7-H3 共表达与非小细胞肺癌预后不良相关

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作者:Pei Zhang, Shuwen Yu, Hongyu Li, Chuanyong Liu, Juan Li, Wenli Lin, Aiqin Gao, Linlin Wang, Wei Gao, Yuping Sun

Abstract

Immunoglobulin-like transcript (ILT) 4 is critical for the inhibitory function of certain immune cells. We previously demonstrated that ILT4 is over-expressed in human non-small cell lung cancer (NSCLC) cells and is involved in tumour evasion via an unknown mechanism. In this report, we demonstrate that ILT4 increases the expression of the co-inhibitory molecule B7-H3 through PI3K/AKT/mTOR signalling. In primary human NSCLC tissues, a significant positive relationship is observed between ILT4 and B7-H3 expression. ILT4/B7-H3 co-expression is significantly associated with a reduction in T infiltrating lymphoid cells and lower overall survival. In summary, ILT4 increases B7-H3 expression and ILT4/B7-H3 co-expression may be involved in NSCLC progression.

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