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Leukocyte membrane determinants regulating immune reactivity

  • Verlag: Elsevier Reference Monographs
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Leukocyte membrane determinants regulating immune reactivity

Leukocyte membrane determinants regulating immune reactivity

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    Format: ePUB
    Kopierschutz: AdobeDRM
    Seitenzahl: 798
    Sprache: Englisch
    ISBN: 9780323142472
    Verlag: Elsevier Reference Monographs
    Größe: 8854 kBytes
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Leukocyte membrane determinants regulating immune reactivity

CONTROL OF THE LATERAL MOBILITY OF MEMBRANE PROTEINS

J.M. Oliver, H.H. Yin and R.D. Berlin, Department of Physiology, University of Connecticut Health Center, Farmington, Connecticut 06032
Publisher Summary

This chapter presents studies on the mechanism by which one subcellular structure, cytoplasmic microtubule (MT) may interact with membranes to regulate surface topography. The degree of MT assembly and MT–membrane interaction in intact cells varies in a dynamic manner, depending on binding events occurring at the surface. The degree of assembly of MT and extent of MT–membrane interactions appears to be enhanced after ligand or particle binding with surface receptors. This enhancement may be mediated in part via the stimulation of cyclic GMP generation, which seems to increase MT stability. The mobility of proteins in cell membranes is regulated at least in part by MT. An intermediate step, the generation of cyclic GMP may follow ligand or particle binding and determine the stability of MT and/or of MT–membrane interaction. The immobilization of leukocyte membranes by phenylglyoxal is unrelated to changes in lipid fluidity. An arginine-rich intramembranous protein (or proteins) is involved in determining the mobility of proteins in leukocyte membranes and in controlling the deformability of the whole membrane. Although proteins are mobile in cell membranes, it is clear that they do not always diffuse at random in the lipid matrix of the membrane but rather are subject to considerable restraints on mobility.
INTRODUCTION

Characteristic changes in cell surface organization are induced by exposure of leukocytes to exogenous agents such as lectins, antibodies and phagocytic particles. These topographical changes very likely provide an initial signal for the cellular responses (metabolic stimulation, induction of cellular proliferation, etc.) that typically follow ligand binding. Thus, it is of particular importance to understand the molecular mechanisms that control the distribution and mobility of surface components.

In this paper we review our studies on the mechanism by which one subcellular structure, the cytoplasmic microtubule (MT) may interact with membranes to regulate surface topography. We also report on a new agent that can immobilize leukocyte membranes by interaction with a membrane protein. This agent is unlikely to act directly on subcellular structures such as MT or microfilaments (MF).
The Role of MT in Membrane Organization.

There is considerable evidence for a role of cytoplasmic MT in regulation of leukocyte surface topography. These data come from our studies with polymorphonuclear leukocytes (PMN) and Edelman's studies with lymphocytes. Most of the experiments have been reviewed (1,2) and so can simply be summarized here.

First, we have observed a segregative movement of surface proteins during phagocytic ingestion of polyvinyltoluene (PVT) particles or BSA-coated oil droplets in PMN. Transport proteins are selectively excluded from areas of the membrane that are internalized while glycoprotein receptors for two plant lectins, Concanavalin A (Con A) and Ricinus communis agglutinin (RCA) are concentrated in the membrane that is internalized during phagocytosis. Recent experiments by Berlin and Fera ( 3 ) indicate that this segregative movement also occurs with membrane lipids. They determined the viscosity of membranes isolated from PMN before and after phagocytosis from fluorescence polarization studies with two lipophilic probes, perylene and 1,6-diphenyl-1,3,5-hexatriene (DPH). Their results show a dramatic reduction in plasma membrane viscosity during phagocytosis. This suggests a selective removal or "freezing out" of lipids composed of more saturated fatty a

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