FcgRII isoforms in chronic lymphocytic leukemia B cells.

GAMBERALE R, FERNÁNDEZ-CALOTTI P, GABELLONI ML, GALLETTI J, SÁNCHEZ AVALOS J, GEFFNER J, GIORDANO M

Córdoba, Argentina

Congreso; VII Congreso Latinoamericano de Inmunología; 2005

Sociedad Latinoamericana de Inmunología

We have previously reported that B cells from a subset of chronic lymphocytic leukemia (CLL) patients express not only receptors for the Fc portion of IgG type IIB (FcgRIIB), as normal B lymphocytes, but also a non-functional form of the myeloid FcgRIIA. In this study we aimed to determine whether FcgRIIA expression is associated to the poor prognostic markers, CD38 and ZAP-70, and  to evaluate the signaling capacity of FcgRIIB.   The expression of FcgRIIA, ZAP-70 and CD38 in B-CLL cells was determined by flow cytometry. The inhibitory capacity of FcgRIIB was assessed by western blot. Apoptosis induction through FcgRIIB was determined by flow cytometry and fluorescence microscopy.   We found that FcgRIIA expression is not associated with CD38 or ZAP-70 positivity (n=27). Regarding FcgRIIB, our results showed that its homoaggregation in either B-CLL (n=15) or non-malignant B cells (n=4) did not result in apoptosis as was reported for murine B splenocytes. However, it effectively diminished BCR-triggered ERK1 phosphorylation (n=6, p<0.05), indicating that it is able to transduce inhibitory signals in CLL cells. Because a significant proportion of CLL clones express polyreactive BCR, it is possible that IgG immune complexes activate FcgRIIB inhibitory signaling and influence leukemic cell physiology in vivo.