| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2047506 | FEBS Letters | 2015 | 9 Pages |
•ILT4 drives typical co-inhibitory molecule B7-H3 expression in NSCLC cells.•ILT4 activated PI3K/AKT/mTOR signalling in NSCLC cells.•ILT4 drives B7-H3 expression via PI3K/AKT/mTOR signalling in NSCLC cells.•ILT4 and B7-H3 are co-expressed in NSCLC cell lines and tissues.•ILT4 and B7-H3 co-expression is correlated with fewer T infiltrating lymphoid cells and worse survival.
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.
