Signaling capacity of FcgammaRII isoforms in B-CLL cells.

GAMBERALE R, FERNANDEZ-CALOTTI P, SANJURJO J, ARROSSAGARAY G, AVALOS JS, GEFFNER J, GIORDANO M.

LEUKEMIA RESEARCH

ELSEVIER

Lugar: USA; Año: 2005 vol. 21 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 reported that B cells from a subset of chronic lymphocytic leukemia (B-CLL) patients express not only FcgammaRIIB, as normal B lymphocytes, but also the myeloid FcgammaRIIA. The aim of this study was to evaluate the signaling capacity of both FcgammaRII isoforms in B-CLL cells. We found that FcgammaRIIA expressed by leukemic cells failed to induce Ca(2+) mobilization or protein tyrosine phosphorylation, suggesting that the receptor is not functional. By contrast, FcgammaRIIB effectively diminished BCR-triggered ERK 1 phosphorylation, which indicates that it is able to transduce inhibitory signals in B-CLL cells. Moreover, we found that FcgammaRIIB homoaggregation in either B-CLL or non-malignant tonsillar B cells did not result in apoptosis as was reported for murine B splenocytes. Together, these results show that FcgammaRIIB, but not FcgammaRIIA is biologically active in B-CLL cells and might influence leukemic cell physiology in vivo.