E. Kimby et al., EXPRESSION OF ADHESION MOLECULES CD11 CD18 (LEU-CAMS, BETA-2-INTEGRINS), CD54 (ICAM-1) AND CD58 (LFA-3) IN B-CHRONIC LYMPHOCYTIC-LEUKEMIA/, Leukemia & lymphoma, 13(3-4), 1994, pp. 297-306
Cell adhesion molecules (CAMs) are cell surface proteins with unique s
pecificities that allow intercellular adhesion. The importance of CAMs
for normal lymphocyte growth and differentiation is underscored by th
e association between neoplastic disease states and abnormal CAM expre
ssion. In the present study we analysed the cell surface expression of
several CAMs on peripheral blood lymphocytes from patients with progr
essive chronic lymphocytic leukemia of B-cell type (B-CLL) (n = 21) an
d stable monoclonal B-lymphocytosis of undetermined significance (B-ML
US) (n = 20). The CAM expression was analysed on the B-cell clone and
on normal T- and NK-cell populations separately using monoclonal antib
odies (MAbs). A phorbol ester-induced lymphocyte aggregation assay and
blocking MAbs were also used. The B-cell clone in B-CLL expressed ICA
M-1 (CD54) more frequently and at a higher density than in B-MLUS. The
brightest CD54 expression was noted in patients with prominent lympha
denopathy and/or splenomegaly. The beta 2 integrin CD11a (Leu-CAMa, LF
A-1) was detected on some B-cell clones and seemed to relate to tissue
localization of the disease. T and NK cells showed a low expression o
f CD11a in B-CLL patients, while in B-MLUS a high proportion of non-cl
onal cells coexpressed CD11a with a high staining intensity. The relat
ive numbers of both CD18+ as well as CD2+ cells showed a positive corr
elation with phorbol ester induced cell aggregation in B-MLUS patients
(p < 0.05). The aggregation was blocked by adding MAbs against CD18 i
n most cases but to a greater extent in B-CLL. These results extend an
d corroborate our earlier findings on surface phenotypic characteristi
cs of clonal and non-clonal lymphocytes in different clinical subtypes
of B-CLL. CAM expression on the monoclonal lymphocytes may play a rol
e in their interaction with regulatory immune cells and their tissue l
ocalization.