Capping of surface immunoglobulin on 'hairy cells' is independent of energy production

• Published in: Journal of cell science Vol. 36; no. 1; pp. 45 - 59
• Main Authors: Splinter, T A, Collard, J G, De Wildt, A, Temmink, J H, Décary, F
• Format: Journal Article
• Language: English
• Published: England 01.04.1979
• Subjects: Adult; Aged; Colchicine - pharmacology; Cytochalasin B - pharmacology; Energy Metabolism; Humans; Immunologic Capping - drug effects; Leukemia, Hairy Cell - immunology; Leukemia, Hairy Cell - ultrastructure; Leukocytes - immunology; Leukocytes - metabolism; Male; Receptors, Antigen, B-Cell; Receptors, Concanavalin A - immunology; Temperature
• ISSN: 0021-9533; 1477-9137
• DOI: 10.1242/jcs.36.1.45

Capping, independent of metabolic energy, of surface immunoglobulin (S-Ig) on 'Hairy cells' from patients with Hairy cell leukaemia (HCL) is described. As controls leukaemic cells from a patient with a prolymphocytic leukaemia (PLL) and blood lymphocytes from healthy individuals were used. The specificity of the energy-independent capping of the HCL-cells as compared to the controls was tested by incubation of the cells at 4 degrees C in the presence of 0.1 M sodium azide with different FITC-labelled ligands. In order to find an explanation for this phenomenon, the influence of cytochalasin B, colchicine and the combination of both drugs on capping of S-Ig and concanavalin (Con-A)-receptors at 37 degrees C was investigated. Furthermore the effect of Con A on S-Ig capping and vice versa was studied. The results show that only S-Ig on HCL cells could form caps at 4 degrees C in the presence of sodium-azide. Cytochalasin B alone induced a strong inhibition of Con A capping on all 3 cell types, whereas S-Ig capping was unaffected. Colchicine alone had practically no effect. Anti-Ig inhibited subsequent patch and cap formation with Con A on both HCL cells and PLL cells, whereas Con A caps and patches were redistributed by anti-Ig on PLL cells, but not on HCL cells. Conversely, Con A could link S-Ig to other receptors, leading to inhibition of S-Ig capping at 4 degrees C on HCL cells and to co-capping of S-Ig at 37 degrees C on both cell types. In addition Con A induced redistribution of S-Ig caps. The combination of co-capping of S-Ig by Con A, followed by redistribution of the caps by FITC-anti-Ig simulated inhibition of S-Ig capping by Con A on PLL cells. The major conclusions are: in some cases inhibition of capping may actually be caused by redistribution of caps; the energy-independent capping cannot be explained by free diffusion of S-Ig in the membrane through lack of any connexion with receptor-mobility regulating systems. It is proposed that the energy requirement of capping is needed to inactivate a specific mechanism,w which restrains receptor mobility and which is non-operative in HCL cells.