期刊
IMMUNITY
卷 16, 期 1, 页码 51-65出版社
CELL PRESS
DOI: 10.1016/S1074-7613(02)00266-2
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资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI039646] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [N01AR062227, R01AR044565] Funding Source: NIH RePORTER
- NIAID NIH HHS [P01-AI39646] Funding Source: Medline
- NIAMS NIH HHS [AR44565, N01-AR-6-2227, AR35304] Funding Source: Medline
- NIH HHS [A1/GF41520-01] Funding Source: Medline
We identified intracellular adhesion molecule-2 (ICAM-2) in a genetic screen as an activator of the PI3K/AKT pathway leading to inhibition of apoptosis. ICAM-2 induced tyrosine phosphorylation of ezrin and PI3K kinase membrane translocation, resulting in phosphatidylinositol 3,4,5 production, PDK-1 and AKT activation, and subsequent phosphorylation of AKT targets BAD, GSK3, and FKHR. ICAM-2 clustering protected primary human CD19(+) cells from TNFalpha- and Fas-mediated apoptosis as determined by single-cell analysis. ICAM-2 engagement by CD19(+) cells of its natural receptor, LFA-1, on CD4(+) naive cells specifically induced AKT activity in the absence of an MHC-peptide interaction. These results attribute a novel signaling function to ICAM-2 that might suggest mechanisms by which ICAM-2 signals intracellular communication at various immunological synapses.
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