Signaling capacity of FcgRII isoforms in B-CLL cells

ROMINA GAMBERALE; PAULA FERNANDEZ CALOTTI; JULIETA SANJURJO; GUILLERMO ARROSSAGARAY; JULIO SANCHEZ AVALOS; JORGE GEFFNER; MIRTA GIORDANO

LEUKEMIA RESEARCH

Año: 2005 vol. 29 p. 1277 - 1284

0145-2126

Two main isoforms of Fcgamma receptor II (CD 32) have been described in humans:activatory FcgammaRIIA and inhibitory FcgammaRIIB. We have previously reportedthat B cells from a subset of chronic lymphocytic leukemia (B-CLL) patientsexpress not only FcgammaRIIB, as normal B lymphocytes, but also the myeloidFcgammaRIIA. The aim of this study was to evaluate the signaling capacity ofboth FcgammaRII isoforms in B-CLL cells. We found that FcgammaRIIA expressed byleukemic cells failed to induce Ca(2+) mobilization or protein tyrosinephosphorylation, suggesting that the receptor is not functional. By contrast,FcgammaRIIB effectively diminished BCR-triggered ERK 1 phosphorylation, whichindicates that it is able to transduce inhibitory signals in B-CLL cells.Moreover, we found that FcgammaRIIB homoaggregation in either B-CLL ornon-malignant tonsillar B cells did not result in apoptosis as was reported formurine B splenocytes. Together, these results show that FcgammaRIIB, but notFcgammaRIIA is biologically active in B-CLL cells and might influence leukemiccell physiology in vivo.