CD161B:ClrB interactions mediate activation of enhanced lysis of tumor target cells following NK cell:DC co-culture

Co-culture of natural killer (NK) cells and dendritic cells (DCs) results in their reciprocal co-activation, and an enhancement of lysis of tumor target cells. The receptor:ligand pairings mediating this enhancement are unknown. Therefore, we investigated whether interactions of CD161, on NK cells,...

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Bibliographic Details
Published in:Immunologic research 2006-01, Vol.36 (1-3), p.43-50
Main Authors: Yang, Tianbing, Flint, Melanie S, Webb, Katie M, Chambers, William H
Format: Article
Language:English
Subjects:
Animals
Antigens, Surface - immunology
Antigens, Surface - metabolism
Cell Communication - immunology
Cell Line, Tumor
Cells
Cells, Cultured
Coculture Techniques
Cytotoxicity, Immunologic
Dendritic Cells - immunology
Flow Cytometry
Immunology
Killer Cells, Natural - immunology
Lectins, C-Type - immunology
Lectins, C-Type - metabolism
Neoplasms - immunology
Neoplasms - pathology
NK Cell Lectin-Like Receptor Subfamily B
Rats
Rats, Inbred F344
Reverse Transcriptase Polymerase Chain Reaction
Transduction, Genetic
Tumors
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Summary:Co-culture of natural killer (NK) cells and dendritic cells (DCs) results in their reciprocal co-activation, and an enhancement of lysis of tumor target cells. The receptor:ligand pairings mediating this enhancement are unknown. Therefore, we investigated whether interactions of CD161, on NK cells, with Clrs, on DCs, might have a role in this effect. Blocking expression of CD161B using siRNA resulted in a reduction in enhanced lytic activity following NK:DC co-culture. Conversely, blocking expression of CD161F with siRNA had no effect on enhanced lytic function following NK:DC co-culture. Blocking expression of ClrB/Ocil, a ligand for CD161B, resulted in a reduced level of enhanced lytic function following NK:DC co-culture. This is the first report of NK receptors responsible for interaction with DCs having a role in mediating enhanced lytic function following NK:DC interactions.
ISSN:0257-277X
0257-277X
1559-0755
DOI:10.1385/IR:36:1:43