Record Display for the EPA National Library Catalog


Main Title Induction of Activation Antigens on Human Natural Killer Cells Mediated Through the Fc-Gamma Receptor.
Author Harris, D. T. ; Travis, W. W. ; Koren., H. S. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Clinical Research Branch. ;Duke Univ. Medical Center, Durham, NC. ;North Carolina Univ. at Chapel Hill.
Publisher c1989
Year Published 1989
Report Number EPA/600/J-89/467;
Stock Number PB91-116004
Additional Subjects Antigens ; Deoxyribonucleic acids ; Reprints ; Natural killer cells ; Fluorescent antibody technic ; Cross-linking reagents ; Interleukin-2 ; Monoclonal antibodies ; Endogenous substances receptors
Library Call Number Additional Info Location Last
NTIS  PB91-116004 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 8p
NK cells, defined here as lymphocytes bearing the CD16 Ag found on the NK cell Fc-gamma receptor (FcR), are known to enter a proliferative and activated state in response to stimulation with IL-2 as assessed by clonal expansion, short-term DNA synthesis, and de novo expression of lymphocyte-associated activation Ag. We have found that the FcR of NK cells acts as a signaling pathway through which IL-2-dependent activation may be greatly enhanced, allowing for more rapid induction of activation Ag and recruitment of an increased percentage of cells expressing surface markers of cellular activation. FcR-interactive agents, such as solid phase immobilized immune complexes or cross-linked CD16-specific mAb, work synergistically with rIL-2 to elicit a rapid expression of IL2R and transferrin receptors on greater than 5% of purified NK cells as early as day 3 of culture. IL-2 or FcR-interactive stimuli alone were weak or ineffective stimulators by comparison. In contrast to the induction of de novo activation Ag, DNA synthesis was elicited by IL-2 alone, but was not substantially or consistently enhanced by the subsequent addition of FcR-interactive stimuli. (Copyright (c) 1989 by the American Association of Immunologists).