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Prepublished online as a Blood First Edition Paper on April 30, 2002; DOI 10.1182/blood-2001-12-0303.
Submitted December 21, 2001
Accepted March 29, 2002
Engagement of ILT2/CD85j in Sezary syndrome cells inhibits their CD3/TCR signaling
Maria Nikolova, Philippe Musette, Martine Bagot, Laurence Boumsell, and Armand Bensussan*
INSERM Unite 448, Faculte de Medecine de Creteil, Creteil Cedex, France
INSERM 532, Institut de Recherche sur la Peau, Paris Cedex 10, France
* Corresponding author; email: Armand.Bensussan{at}im3.inserm.fr.
Extensive phenotype analysis of cutaneous T cell lymphoma (CTCL) malignant cell lines revealed surface expression of receptors usually not detected on normal circulating CD4+CD45RO+ lymphocytes. We previously found that CTCL malignant cells express the killer cell immunoglobulin-like receptor (KIR) KIR3DL2/CD158k, whereas, they fail to express the other KIRs. In the present study, we report for the first time that ILT2/CD85j receptor is found on Sezary cell lines and on circulating Sezary malignant CD4+ cells while it is hardly detectable on circulating CD4+ lymphocytes from normal individual. We demonstrate that ILT2 is functional on CTCL cells as its triggering leads to the recruitment of SHP-1 and to the specific inhibition of CTCL malignant cell proliferation induced by CD3/TCR stimulation. Interestingly, we found that separated CD4+ILT2+ circulating malignant Sezary cells are less susceptible to anti-CD3 mAb-induced cell death than autologous CD4+ILT2- lymphocytes. Therefore, the resistance to apoptosis of Sezary cells may result from distinct mechanisms including cytokine-induced high level of bcl-2 and specific expression of inhibitory receptors involved in lymphocyte survival.
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