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Interleukin‐4 (IL‐4) Enhances Homotypic Adhesion of Activated B‐Chronic Lymphocytic Leukaemia (B‐CLL) Cells via a Selective Up‐Regulation of CD54
Author(s) -
CARLSSON M.,
SÖDERBERG O.,
NILSSON K.
Publication year - 1993
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1993.tb03328.x
Subject(s) - cell adhesion , cell adhesion molecule , microbiology and biotechnology , chemistry , cytokine , biology , cell , immunology , biochemistry
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‐1) and its ligand CD54 (ICAM‐1). A well‐characterized B‐chronic lymphocytie leukaemia (B‐CLL) clone (1–83) 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 aggregalion. The results from studying the expression of CD11a and CD18, the two suhunits 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.