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The Journal of Immunology, Vol 154, Issue 1 80-87, Copyright © 1995 by American Association of Immunologists

ARTICLES

Selective loss of NK cytotoxicity in antisense NK-TR1 rat LGL cell lines. Abrogation of antibody-independent tumor and virus-infected target cell killing

SL Giardina, SK Anderson, TJ Sayers, WH Chambers, GA Palumbo, HA Young and JR Ortaldo
Biologic Carcinogenesis and Development Program, Program Resource, Inc./DynCorp, Frederick, MD 21702.

We have shown that NK-TR1, a protein containing a cyclophilin-like domain, is associated with a receptor/triggering molecule on the surface of human large granular lymphocytes (1). In the present study, we have further defined the role of NK-TR1 in target cell recognition/killing by generating antisense NK-TR1 transfectants in the rat LGL cell line, RNK-16. Stable transfectants were identified by analyzing permeabilized cells with the anti-NK-TR1 mAb, 4F9. Transfectants with low levels of 4F9 staining showed drastically reduced levels of killing against three NK-susceptible target cell lines. Lytic activity against vaccinia virus-infected cell lines also was dramatically reduced. In contrast, transfected cells showing normal levels of NK-TR1 expression demonstrated normal killing of all target cells. The ability of all transfectants to form conjugates was identical to that observed with the wild-type RNK cell line. Lectin- dependent cytotoxicity, reverse ADCC via NKR-PI, and ADCC-mediated killing were comparable in both high or low NK-TR1 expressing clones, demonstrating that the lytic machinery was still intact. BLT-esterase activity, PF levels, and surface marker phenotype were not significantly affected. These results provide strong evidence that NK- TR1 is an essential element in a signaling pathway leading to MHC unrestricted killing of tumor and virus-infected cells.


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M. Kozlowski, J. Schorey, T. Portis, V. Grigoriev, and J. Kornbluth
NK Lytic-Associated Molecule: A Novel Gene Selectively Expressed in Cells with Cytolytic Function
J. Immunol., August 15, 1999; 163(4): 1775 - 1785.
[Abstract] [Full Text] [PDF]


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