TY - JOUR
T1 - Mechanism of activation of natural killer and CD8 T cells by interleukin 15 in the prostate cancer microenvironment
T2 - Spring Meeting for Clinician Scientists in Training February 2014
AU - Elhage, Oussama
AU - Sakellariou, Christina
AU - Ukimura, Osamu
AU - Gill, Inderbir
AU - Smith, Richard A
AU - Galustian, Christine
AU - Dasgupta, Prokar
PY - 2014/2/26
Y1 - 2014/2/26
N2 - The prostate cancer microenvironment profoundly inhibits effector immune-cell activity. We have shown that interleukin (IL) 15, unlike other cytokines proposed for anti-tumour immunotherapy such as IL12 and IL21, can increase natural killer (NK) cell and CD8 T-cell activity within the prostate cancer microenvironment. To investigate mechanisms of this activation, we studied the effects of IL15 on inhibitory and activatory receptors on NK cells and their corresponding ligands on prostate cancer cells. NK receptors known as killer-Ig-like receptors (KIRs) have a crucial role in NK-mediated killing of tumour cells. NK-receptor ligands on tumour cells can attenuate NK activity by binding their corresponding inhibitory receptors. Conversely, increased HLA-related ligand expression can increase the recognition and killing of tumour cells by T cells.
AB - The prostate cancer microenvironment profoundly inhibits effector immune-cell activity. We have shown that interleukin (IL) 15, unlike other cytokines proposed for anti-tumour immunotherapy such as IL12 and IL21, can increase natural killer (NK) cell and CD8 T-cell activity within the prostate cancer microenvironment. To investigate mechanisms of this activation, we studied the effects of IL15 on inhibitory and activatory receptors on NK cells and their corresponding ligands on prostate cancer cells. NK receptors known as killer-Ig-like receptors (KIRs) have a crucial role in NK-mediated killing of tumour cells. NK-receptor ligands on tumour cells can attenuate NK activity by binding their corresponding inhibitory receptors. Conversely, increased HLA-related ligand expression can increase the recognition and killing of tumour cells by T cells.
U2 - 10.1016/S0140-6736(14)60310-X
DO - 10.1016/S0140-6736(14)60310-X
M3 - Meeting abstract
SN - 0140-6736
VL - 383
SP - S47
JO - The Lancet
JF - The Lancet
IS - Supplement 1
M1 - N/A
ER -