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Prepublished online as a Blood First Edition Paper on May 15, 2003; DOI 10.1182/blood-2002-12-3898.
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Blood, 1 September 2003, Vol. 102, No. 5, pp. 1797-1805
IMMUNOBIOLOGY
Expression and function of KIR and natural cytotoxicity receptors in NK-type lymphoproliferative diseases of granular lymphocytes
Renato Zambello,
Michela Falco,
Mariella Della Chiesa,
Livio Trentin,
Davide Carollo,
Roberta Castriconi,
Giovanna Cannas,
Simona Carlomagno,
Anna Cabrelle,
Thierry Lamy,
Carlo Agostini,
Alessandro Moretta,
Gianpietro Semenzato, and
Massimo Vitale
From the Dipartimento di Medicina Clinica e Sperimentale, Immunologia
Clinica, Università di Padova e Centro di Eccellenza per la Ricerca
Biomedica Padova, Padua, Italy; Istituto Giannina Gaslini, Genova, Italy;
DIMES, Dipartimento di Medicina Sperimentale, Università di Genova,
Genoa, Italy; University of Rennes, Rennes, France; Centro di Eccellenza per
la Ricerca Biomedica di Genova, Genova, Italy; and IST, Istituto Scientifico
per la Ricerca sul Cancro Genova, Genoa, Italy.
Using monoclonal antibodies (mAbs) specific for different natural killer
(NK) receptors, we studied the lymphocyte population from 18 patients with
NK-type lymphoproliferative disease of granular lymphocytes (LDGL). The
analysis of both resting and cultured NK cell populations demonstrated that
these patients are frequently characterized by NK cells displaying a
homogeneous staining with given anti–killer Ig-like receptor (anti-KIR)
mAb (11 of 18 patients). In most patients NK cells were characterized by the
CD94/NKG2A+ phenotype, whereas only a minor fraction of the cases
expressed CD94/NKG2C. In 7 of these patients we could also assess the function
of the various NK receptors. Remarkably those KIR molecules that, in each
patient, homogeneously marked the NK cell expansion were found to display an
activating function as determined by cross-linking with specific anti-KIR mAb.
The KIR genotype analysis performed in 13 of 18 cases revealed that in NK-type
LDGL certain activating KIRs, as well as certain infrequent KIR genotypes,
were detected with higher frequencies as compared to previously analyzed
healthy donors. Moreover, most KIR genotypes included multiple genes coding
for activating KIRs. The analysis of non–HLA-specific triggering
receptors indicated that the natural cytotoxicity receptors (NKp46, NKp30)
were expressed at significantly low levels in freshly drawn NK cells from most
patients analyzed. However, in most instances the expression of NKp46 and
NKp30 could be up-regulated on culture in interleukin 2. Our data indicate
that in NK-LDGL the expanded subset is frequently characterized by the
expression of a given activating KIR, suggesting a direct role for these
molecules in the pathogenetic mechanisms of this disorder.
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