Further characterization of PNK-E: a monoclonal antibody enhancing porcine natural killer cell activity. Cell Immunol 1991 May;134(2):378-89
Date
05/01/1991Pubmed ID
2021974DOI
10.1016/0008-8749(91)90311-xScopus ID
2-s2.0-0025851601 (requires institutional sign-in at Scopus site) 11 CitationsAbstract
Monoclonal antibody PNK-E binds to approximately 15% of porcine peripheral blood lymphocytes (PBL) which are PT4 negative and PT8 positive. When cells from tissues of adult pigs are treated with PNK-E, enhancement of natural killer (NK) cell activity is observed from PBL and spleen cells, and a dramatic induction of NK activity is observed from bone marrow cells. With cells derived from tissues of neonatal piglets, PNK-E induces NK activity from PBL and bone marrow cells. To investigate the mechanism of PNK-E-mediated enhancement of NK, proliferation assays, calcium-pulse assays, single-cell assays, and kinetic analyses were performed. PNK-E did not induce proliferation of PBL. PNK-E could be added as late as 30 min prior to termination of Ca(2+)-pulse assays and still enhance NK activity. Using kinetic analysis PNK-E was found to increase the rate of NK lysis (Vmax) and rate of lytic programming per NK cell (k2). In addition, results from single-cell assays indicate that PNK-E activates a population of normally inactive effector cells. These results indicate that PNK-E enhances the lytic capacity of mature NK cells and induces a population of nonlytic cells to become highly cytolytic cells. Furthermore, the enhancing effects are immediate and do not require an induction period. Thus, PNK-E recognizes and activates a unique triggering molecule that is present on NK cells.
Author List
Johnson BD, Wierda WG, Kim YBAuthor
Bryon D. Johnson PhD Adjunct Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Age FactorsAnimals
Antibodies, Monoclonal
Cytotoxicity, Immunologic
Flow Cytometry
Humans
Killer Cells, Natural
Lymphocyte Activation
Mice
Swine









