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- W181638963 abstract "Abstract Objective: Vasoactive intestinal peptide (VIP) and its synthetic analog VIP14-28 enhance NK cytotoxicity. This prompted us to study interaction of the naturally occurring peptide and orphan ligand VIP 10-28 with NK. Results: VIP10-28 stimulation (10-8-10-10 M, 30 min.) increased NK-92 cytotoxicity against K562 max. from 52% +/-2.6% SEM (control) to 68% +/-2.6% SEM (E:T 1:1), similar to long-term IL-2 stimulated NK from different donors (4/6), max. from 38% +/-4.2 SEM (control) to 51% +/-0.9% SEM (E:T 1:1). VIP10-28 did not seem to induce degranulation, since granzyme B levels remained unchanged in NK-92. However, stimulation with 10-8-10-10 M VIP10-28 for 5- 60 min. significantly induced tyrosine phosphorylation with ERK identified as one of the stimulated kinases. We used Informational Spectrum Method (ISM) to predict VIP10-28 NK receptor interactions. ISM results suggested potential binding of VIP10-28 to LFA-1α (F = 0.03, peptide residues 16-24) and with lower affinity to CD44 or MAC-1, but unlikely to NKG2D, -C, -A, NKp30, -44, -46, CD56, CD94, KIR2DL4, NKR-P1, CD45 or VIP receptors VPAC-1/ VPAC-2. Conclusion: The neuroendocrine peptide VIP10-28 induces increased NK cytotoxicity potentially through LFA-1 signaling pathways involving tyrosine kinase activation of ERK kinases." @default.
- W181638963 created "2016-06-24" @default.
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- W181638963 date "2009-04-01" @default.
- W181638963 modified "2023-10-18" @default.
- W181638963 title "Vasoactive intestinal peptide 10-28 enhances natural killer cell cytotoxicity (134.84)" @default.
- W181638963 doi "https://doi.org/10.4049/jimmunol.182.supp.134.84" @default.
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