Liposome modulation of surface immunoglobulins on rabbit spleen cells
Ostro, M.J.; Bessinger, B.; Summers, J.F.; Dray, S.
Journal of Immunology 124(6): 2956-2965
1980
ISSN/ISBN: 0022-1767 PMID: 7373057 Document Number: 157599
Treatment of rabbit spleen cells with lecithin liposomes caused a substantial decrease in the number of cells bearing surface immunoglobulin (Ig) as assessed by rosetting and immunofluorescent techniques. Immunofluorescent studies demonstrated that the decrease of surface Ig was the result of a capping phenomenon. A comparison of liposome vs. antibody-induced capping was made by monitoring the respective rates of recovery of displaced surface Ig on spleen cells. Cells treated with specific antibody recovered their surface Ig 6.5 h after antibody-cell incubation, while cells treated with liposomes required 24 h for a comparable recovery. The 2 phenomena appeared to be mechanistically distinct. Disruption of cytoskeletal function with lidocaine completely inhibited antibody-induced capping, while capping stimulated by liposomes was unaffected. Liposome-induced capping may be modulated by the cholesterol/phospholipid ratio in the lymphocyte membrane. Capping was inhibited by incremental addition of cholesterol to the liposomal membrane. Stimulation of the rate of cholesterol biosynthesis in spleen cells with dextran sulfate before the addition of liposomes reduced the time needed for the recovery of surface Ig on liposome-treated cells from 24 to 8 h. Inhibition of cholesterol biosynthesis by 25-hydroxycholesterol resulted in the failure of surface Ig to recover. There is apparently a relationship between the expression of lymphocyte surface Ig and cholesterol biosynthesis. The failure of lidocaine to inhibit liposome-induced capping suggests that surface Ig, under normal conditions, exists free in the lipid bilayer rather than anchored to the lymphocyte cytoskeleton.