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Plasma membrane lipid packing and leukocyte function‐associated antigen‐1‐dependent aggregation of lymphocytes
Author(s) -
Smith Douglas M.,
Williamson Patrick L.,
Schlegel Robert A.
Publication year - 1993
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041560124
Subject(s) - population , chemistry , biophysics , microbiology and biotechnology , lymphocyte function associated antigen 1 , lipid bilayer , antigen , monoclonal antibody , lymphocyte , in vitro , membrane , cell adhesion , biology , antibody , cell , biochemistry , immunology , demography , sociology
A simple model system for study of adhesion mediated by leukocyte function‐associated antigen‐1 (LFA‐1) is aggregation of lymphocytes stimulated in vitro. Although aggregation is blocked by monoclonal antibodies to LFA‐1, not all lymphocytes expressing LFA‐1 aggregate, indicating that LFA‐1 is necessary but not sufficient for aggregation. To investigate whether the lipid bilayer plays a role in the functional activation of LFA‐1, human peripheral blood lymphocytes and murine splenic lymphocytes were stimulated in culture, and measurements made of aggregation vs. packing of plasma membrane lipids. Progression of cells into aggregates was paralleled by a decrease in lipid packing of the population as a whole, as monitored by increased staining with the fluorescent probe merocyanine 540. Cells from aggregates stained more intensely than nonaggregated cells from the same population, indicating that aggregates are preferentially formed from cells in the population with the loosest packed membrane. In contrast, aggregated cells were found to express equivalent or even lower amounts of LFA‐1 than nonaggregated cells. Looser lipid packing is therefore associated with the development of LFA‐1‐dependent aggregation, and might be involved in the functional activation of this cell adhesion molecule. © 1993 Wiley‐Liss, Inc.