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The natural killer-related receptor for HLA-C expressed on T cells from
CD3+ lymphoproliferative disease of granular lymphocytes displays either
inhibitory or stimulatory function
A Cambiaggi, AM Orengo, R Meazza, S Sforzini, PL Tazzari, F Lauria, D Raspadori, R Zambello, G Semenzato, L Moretta and S Ferrini
Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy.
Four patients with lymphoproliferative disease of granular lymphocytes
(LDGL) coexpressing CD3 and the natural killer (NK)-related "p58" receptor
for HLA-C alleles were studied. These CD3+p58+ LDGLs have been detected
among a series of 44 CD3+ LDGLs analyzed. Two patients with LDGL (GI and
BA) expressed only the p58 molecule defined by the GL-183 and CH-L
monoclonal antibodies (MoAbs), while the cases of patients PU and MA also
coexpressed the molecular form identified by EB6 anti-p58 MoAb. Three LDGL
cases (GI, MA, and PU) displayed the CD8+4-CD16+ T- cell receptor
(TCR)alpha/beta+ phenotype, while one patient (BA) was CD8+4+CD16+
TCRalpha/beta+. Freshly isolated granular lymphocytes (GL) from these cases
displayed cytolytic activity in an anti-CD3 MoAb- triggered redirected
killing assay against the Fcgamma-receptor+ (Fcgamma-R+) P815 target cell
line. Lysis of P815 target cells, triggered by an anti-CD3 or by anti-CD16
MoAb, could be inhibited by the addition of anti-p58 MoAb in three fresh or
interleukin (IL)-2- cultured GL tested (GI, MA, and PU). Triggering of
cytotoxicity against the HLA-DR+ Fcgamma-R+ Daudi cell line induced by
appropriate superantigens could also be inhibited by anti-p58 MoAb in
patients PU and GI with LDGL. These data indicate that activation through
the CD16, CD3, and TCR molecules can be modulated by p58 receptors in these
LDGLs. On the contrary, IL-2-expanded cells of patient BA were induced to
lyse P815 target cells by anti-p58 MoAb. In addition, anti-p58 MoAB
enhanced anti-CD16 MoAb triggered lysis and did not inhibit activation via
CD3. These data indicate that, in this particular patient with LDGL, p58
displays a stimulatory effect on cell triggering, rather than the typical
inhibitory effect previously observed in p58+ T-cell clones derived from
healthy donors. The anti-p58 MoAb did not induce CA++ mobilization in p58+
LDGLs and in a p58+CD3+ normal T-cell clone equipped with inhibitory p58
molecules, while Ca++ mobilization could be observed in cultured GL from
patient BA, which could be activated by anti-58 MoAb. These findings
suggest that stimulatory and inhibitory p58 molecules are equipped with
different signal transducing properties, thus contributing to a better
knowledge of the normal counterpart.
Volume 87,
Issue 6,
pp. 2369-2375,
03/15/1996
Copyright © 1996 by The American Society of Hematology
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