Interleukin-4 (IL-4) Enhances Homotypic Adhesion of Activated B-Chronic Lymphocytic Leukaemia (B-CLL) Cells via a Selective Up-Regulation of CD54.

It is well established that cell-to-cell contact modifies cytokine signalling but little is known on the role of homotypic cell adhesion for proliferation and differentiation of B cells. Homotypic adhesion involves mainly the interaction between the adhesion molecules Leukocyte Function Antigen-1 (LFA-I) and its ligand CD54 (ICAM-1). A well-characterized B-chronic lymphocytic leukaemia (B-CLL) clone (I-83) was used as a source of monoclonal B cells inducible to DNA synthesis and differentiation by using 12-O-tetradecanoyl-phorbol-13-acetate(TPA) in combination with intcrleukin-4(IL-4) and thioredoxin (Trx)-containing supernatant from a T-cell hybridoma (BSF-MP6). This paper shows that IL-4 alone was able to induce aggregation of B-CLL cells and to strongly enhance TPA+ BSF-MP6-induced aggregation. The results from studying the expression of CD1 la and CD18, the two subunits of LFA-1, and CD54 during stimulated DNA synthesis and differentiation suggest that IL-4-induced, or enhanced, aggregation was mainly mediated by a selective up-regulation of CD54. It was further demonstrated by antibody blockade to either CD11a, CD18 or CD54 that aggregation could be inhibited without affecting induced DNA synthesis or differentiation. [ABSTRACT FROM AUTHOR]