[HTML][HTML] 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

P Zhang, S Yu, H Li, C Liu, J Li, W Lin, A Gao, L Wang… - FEBS letters, 2015 - Elsevier
P Zhang, S Yu, H Li, C Liu, J Li, W Lin, A Gao, L Wang, W Gao, Y Sun
FEBS letters, 2015Elsevier
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 …
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.
Elsevier