Expression of adhesion molecules CD11/CD18 (Leu-CAMs, beta 2-integrins), CD54 (ICAM-1) and CD58 (LFA-3) in B-chronic lymphocytic leukemia.
Cell adhesion molecules (CAMs) are cell surface proteins with unique specificities that allow intercellular adhesion. The importance of CAMs for normal lymphocyte growth and differentiation is underscored by the association between neoplastic disease states and abnormal CAM expression. In the present study we analysed the cell surface expression of several CAMs on peripheral blood lymphocytes from patients with progressive chronic lymphocytic leukemia of B-cell type (B-CLL) (n = 21) and stable monoclonal B-lymphocytosis of undetermined significance (B-MLUS) (n = 20). The CAM expression was analysed on the B-cell clone and on normal T- and NK-cell populations separately using monoclonal antibodies (MAbs). A phorbol ester-induced lymphocyte aggregation assay and blocking MAbs were also used. The B-cell clone in B-CLL expressed ICAM-1 (CD54) more frequently and at a higher density than in B-MLUS. The brightest CD54 expression was noted in patients with prominent lymphadenopathy and/or splenomegaly. The beta 2 integrin CD11a (Leu-CAMa, LFA-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 of CD11a in B-CLL patients, while in B-MLUS a high proportion of non-clonal cells coexpressed CD11a with a high staining intensity. The relative numbers of both CD18+ as well as CD2+ cells showed a positive correlation with phorbol ester induced cell aggregation in B-MLUS patients (p < 0.05). The aggregation was blocked by adding MAbs against CD18 in most cases but to a greater extent in B-CLL. These results extend and corroborate our earlier findings on surface phenotypic characteristics of clonal and non-clonal lymphocytes in different clinical subtypes of B-CLL. CAM expression on the monoclonal lymphocytes may play a role in their interaction with regulatory immune cells and their tissue localization.
Kimby
E
E
Department of Medicine, Danderyd Hospital, Sweden.
Rincón
J
J
Patarroyo
M
M
Mellstedt
H
H
D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000096:biosynthesis* / Q000235:genetics; D018845:CD11 Antigens; D018821:CD18 Antigens; D018968:CD58 Antigens; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D015973:Gene Expression Regulation, Leukemic; D006801:Humans; D016023:Integrins / Q000096:biosynthesis / Q000235:genetics; D018799:Intercellular Adhesion Molecule-1; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000235:genetics / Q000378:metabolism*; D016131:Lymphocyte Subsets / Q000378:metabolism; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000235:genetics; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000096:biosynthesis* / Q000235:genetics
D015703:Antigens, CD; D018845:CD11 Antigens; D018821:CD18 Antigens; D018968:CD58 Antigens; D015815:Cell Adhesion Molecules; D016023:Integrins; D008562:Membrane Glycoproteins; D009363:Neoplasm Proteins; D018799:Intercellular Adhesion Molecule-1