TY - JOUR
T1 - IL-4 inhibits binding and cytotoxicity of NK cells to vascular endothelium
AU - Paganin, Carla
AU - Matteucci, Christian
AU - Cenzuales, Salvatore
AU - Mantovani, Alberto
AU - Allavena, Paola
PY - 1994
Y1 - 1994
N2 - We investigated the influence of IL-4 on the interaction between Natural Killer (NK) cells and vascular endothelial cells (EC). Pretreatment of NK cells with IL-4 inhibited the adhesion of NK cells on resting or IL-1-activated EC. The inhibitory action of IL-4 was observed on both unstimulated NK cells as well as on cells concomitantly activated with IL-2 or with phorbol ester. IL-4 also inhibited the cytotoxicity of IL-2 activated NK cells on EC. Binding of NK cells to vascular EC involves the LFA1/ICAM-1 and 2, and VLA-4/VCAM-1 adhesion pathway. Anti-CD18 mAb had a lower inhibitory effect in IL-4-treated NK cells compared to control. The levels of inhibition with resting vs IL-1-activated EC, as well as antibody blocking experiments, suggested that IL-4 exerts an inhibitory influence predominantly on the β2-integrin (CD18)-dependent adhesion pathway; nevertheless IL-4 did not affect the expression of CD18/CD11a and VLA-4 on the NK cell surface, as assessed by flow cytometry. NK cells are potent producers of IFN-γ and there is evidence that they play a role in orienting immunity to the TH1-type responses. The inhibition by IL-4 of NK cell binding to EC and subsequent recruitment and activation may thus contribute to development of TH2 responses.
AB - We investigated the influence of IL-4 on the interaction between Natural Killer (NK) cells and vascular endothelial cells (EC). Pretreatment of NK cells with IL-4 inhibited the adhesion of NK cells on resting or IL-1-activated EC. The inhibitory action of IL-4 was observed on both unstimulated NK cells as well as on cells concomitantly activated with IL-2 or with phorbol ester. IL-4 also inhibited the cytotoxicity of IL-2 activated NK cells on EC. Binding of NK cells to vascular EC involves the LFA1/ICAM-1 and 2, and VLA-4/VCAM-1 adhesion pathway. Anti-CD18 mAb had a lower inhibitory effect in IL-4-treated NK cells compared to control. The levels of inhibition with resting vs IL-1-activated EC, as well as antibody blocking experiments, suggested that IL-4 exerts an inhibitory influence predominantly on the β2-integrin (CD18)-dependent adhesion pathway; nevertheless IL-4 did not affect the expression of CD18/CD11a and VLA-4 on the NK cell surface, as assessed by flow cytometry. NK cells are potent producers of IFN-γ and there is evidence that they play a role in orienting immunity to the TH1-type responses. The inhibition by IL-4 of NK cell binding to EC and subsequent recruitment and activation may thus contribute to development of TH2 responses.
KW - Adhesion molecules
KW - Cytokines
KW - NK cells
KW - Vascular endothelium
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U2 - 10.1016/1043-4666(94)90034-5
DO - 10.1016/1043-4666(94)90034-5
M3 - Article
C2 - 7913345
AN - SCOPUS:0027932258
VL - 6
SP - 135
EP - 140
JO - Cytokine
JF - Cytokine
SN - 1043-4666
IS - 2
ER -