The regulatory role of CD45 on rat NK cells in target cell lysis

Citation
Km. Giezeman-smits et al., The regulatory role of CD45 on rat NK cells in target cell lysis, J IMMUNOL, 163(1), 1999, pp. 71-76
Citations number
30
Categorie Soggetti
Immunology
Journal title
JOURNAL OF IMMUNOLOGY
ISSN journal
00221767 → ACNP
Volume
163
Issue
1
Year of publication
1999
Pages
71 - 76
Database
ISI
SICI code
0022-1767(19990701)163:1<71:TRROCO>2.0.ZU;2-1
Abstract
To investigate the role of CD45 in rat NK cell function, we developed new m Abs directed against rat CD45, mAb ANK12 binds to a high molecular isoform of CD45 and mAb ANK74 binds to the common part on all known CD45 isoforms, as has been described for the anti-rat CD45 mAb OX1. The ability of these m Abs to affect NK cell-mediated lysis was tested using the Fc receptor-posit ive target cell line P815, mAb ANK12 was found to significantly enhance the lysis of P815, whereas ANK74 and the anti-CD45 mAb OX1 did not. In additio n, cross-linking of the CD45 isoform by ANK12 induced tyrosine phosphorylat ion of specific proteins in NK cells. Subsequently, the involvement of CD45 in the negative signaling after "self" MHC class I recognition by rat NK c ells was investigated: The anti-CD45 mAbs were found to affect NK cell-medi ated lysis of syngeneic tumor cell lines, depending upon the expression lev el of MHC class I on target cells. mAbs ANK74 and OX1 only inhibited lysis of the syngeneic tumor cell lines that expressed low levels of MHC class I. Furthermore, both mAbs caused an inhibition of NK cell-mediated lysis of t hese tumor cell lines when MHC class I molecules on the tumor cell lines we re masked by an Ab, These results suggest that CD45 regulates the inhibitor y signal pathway after self MHC class I recognition, supposedly by dephosph orylation of proteins.