FcγRIIb expression in early stage chronic lymphocytic leukemia

Abstract

In normal B-cells, B-cell antigen receptor (BCR) signaling can be negatively regulated by the low-affinity receptor FcγRIIb (CD32b). To better understand the role of FcγRIIb in chronic lymphocytic leukemia (CLL), we correlated its expression on 155 samples from newly-diagnosed Binet A patients with clinical characteristics and outcome. FcγRIIb expression was similar in normal B-cells and leukemic cells, this being heterogenous among patients and within CLL clones. FcγRIIb expression did not correlate with well known prognostic markers [disease stage, serum beta-2 microglobulin (B2M), IGHV mutational status, expression of ZAP-70 and CD38, and cytogenetics] except for a weak concordance with CD49d Moreover, patients with low FcγRIIb expression (69/155, 44.5%) required therapy earlier than those with high FcγRIIb expression (86/155, 55.5%) (median 151.4 months vs. not reached; p=0.071). These results encourage further investigation on the role of FcγRIIb in CLL biology and prognostic significance in larger series of patients.

Deep-Sea-Derived Butyrolactone I Suppresses Ovalbumin-Induced Anaphylaxis by Regulating Mast Cell Function in a Murine Model

“…FcγRIIB is also expressed on cells of the innate immune system and on B cells. Bosch et al 48 reported that FcγRIIB was the only subtype of FcγR expressed on B lymphocytes and that it had potent inhibitory activity against B cells. 49 In our study, the B cell population and IgE levels declined in mice given BTL-I.…”

Association of blood IgG with tumor necrosis factor-alpha and clinical course of chronic lymphocytic leukemia

“…In normal human B cells, IVIG can bind the inhibitory Fc receptor CD32B, which recruits phosphatases such as SHIP-1 to prevent BCR-mediated activation of kinase cascades [ 40 ]. CD32B is the only Fc receptor expressed by CLL cells [ 7 ]. Consistent with this, the CD32 antibody AT10 [ 37 ] partially reversed the inhibitory effects of Hizentra at 15 g/L on BCR-mediated expression of CD83 in some patients (Supplementary Fig.…”

Clinical observation of chronic myeloid leukemia with variant translocation and supplementary rearrangement t(1;8)(q23;q24.3)

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