Cell Biology and Immunology of Leukocyte Function

Efraim Racker

• Verlag: Academic Press
• Jahr: 2012
• ISBN:
  9780323141864
• Thema: Scienze biologiche
• Thema: Zoologia

Cell Biology and Immunology of Leukocyte Function is a collection of papers presented at the 12th International Leukocyte Culture Conference, held in Beersheba, Israel on June 1978. This book is organized into seven parts encompassing 111 chapters. The contributors cover the different aspects of cell biology and immunology and the unique leukocyte function. Part I describes the mechanism of lymphocyte activation, the structure and function of the plasma membrane, and the macromolecular synthesis during lymphocyte activation. This part also deals with the interaction of lymphocytes with mitogenic lectins, the comparison of the mitogenic and nonmitogenic lectin binding, and the role of macrophages in the response of lymphocytes to lectins. Part II explores the thymic factors and the development of characteristic markers, antigens, and receptors. This part particularly emphasizes lymphocyte differentiation. Parts III and IV examine the genetic control and intercellular interactions involved in leukocyte function and the parameters of the immune response under in vitro conditions. Chapters on cytotoxicity, the mechanisms of phagocytic killing, autoimmunity, and the responses of leukocytes to tumor cells are included in these parts. Part V discusses the interactions of viruses and leukocytes and provides data on the physical mapping and analysis of sarcoma and leukemia viruses, while Part VI considers the application of leukocyte culture to problems of clinical medicine. Part VII involves the study of radiation effects, with an emphasis on the application of total lymphoid irradiation to the induction of transplantation tolerance. This part also looks into the role of the DNA repair process. Cell biologists, immunologists, and biomedical scientists and researchers will greatly benefit from this book.

CHAPTER I

LYMPHOCYTE ACTIVATION

Outline

Chapter 1: THE LYMPHOCYTE MEMBRANE AND THE CYTOSKELETON

Chapter 2: TRIGGERING SIGNALS FOR T-CELL ACTIVATION

Chapter 3: STUDIES OF LYMPHOCYTE ACTIVATION

Chapter 4: FUNCTIONAL ORGANIZATION OF THE LYMPHOCYTE PLASMA MEMBRANE RELATING TO CELL ACTIVATION

Chapter 5: INVESTIGATIONS ON THE ROLE OF CA2+ AS A POTENTIAL SECOND MESSENGER FOR T AND B LYMPHOCYTE ACTIVATION AND ITS RELEVANCE IN DNA SYNTHESIS

Chapter 6: A MODEL FOR THE CONTROL OF POTASSIUM TRANSPORT IN PHA-STIMULATED HUMAN BLOOD LYMPHOCYTES

Chapter 7: EFFECT OF CON-A ON THE CATION AFFINITY OF THE Na+- K+ PUMP IN LYMPHOCYTES

Chapter 8: ACTIVATION OF LYMPHOCYTES WITHOUT MITOGENS BY INCREASING THE CALCIUM CONCENTRATION IN THE CELL CULTURE MEDIUM

Chapter 9: MEMBRANE MECHANISMS IN LYMPHOCYTE ACTIVATION WORKSHOP SUMMARY

Chapter 10: SYNTHESIS AND PROCESSING OF RNA IN STIMULATED FIBROBLASTS AND LYMPHOCYTES

Chapter 11: REGULATION OF PROTEIN SYNTHESIS DURING LYMPHOCYTE ACTIVATION BY PHYTOHAEMAGGLUTININ

Chapter 12: EVIDENCE FOR AND AGAINST UNUSUAL SPECIES OF DNA IN LYMPHOCYTE ACTIVATION

Chapter 13: STUDIES ON mRNA IN RESTING AND GROWING LYMPHOCYTES

Chapter 14: V- AND C-PARTS OF IMMUNOGLOBULIN n-CHAIN GENES ARE SEPARATE IN MYELOMA

Chapter 15: EVIDENCE FOR A NON-MESSENGER RNA WHICH IS RATE LIMITING FOR PROTEIN SYNTHESIS IN RESTING LYMPHOCYTES

Chapter 16: ADENYLATE CYCLASE IN NORMAL AND LEUKEMIC HUMAN LYMPHOCYTES

Chapter 17: ON THE COMMITMENT OF LYMPHOCYTES TO DNA REPLICATION: A POSSIBLE ROLE FOR TRANSGLUTAMINASE

Chapter 18: COOPERATION REQUIREMENTS OF MITOGEN STIMULATED LYMPHOCYTES IN AGAROSE-GEL CULTURES

Chapter 19: LECTIN-BINDING SURFACE PROTEINS OF HUMAN T-LYMPHOCYTES. A COMPARISON BETWEEN MITOGENIC AND NONMITOGENIC LECTINS

Chapter 20: PARALLEL INDUCTION OF T-CELL STIMULATION: POSITIVE CONTROL OF T-CELL RESPONSE BY MITOGEN TREATED MACROPHAGES

SECTION 1

PLASMA MEMBRANE STRUCTURE AND FUNCTION

Outline

Chapter 1: THE LYMPHOCYTE MEMBRANE AND THE CYTOSKELETON

Chapter 2: TRIGGERING SIGNALS FOR T-CELL ACTIVATION

Chapter 3: STUDIES OF LYMPHOCYTE ACTIVATION

Chapter 4: FUNCTIONAL ORGANIZATION OF THE LYMPHOCYTE PLASMA MEMBRANE RELATING TO CELL ACTIVATION

Chapter 5: INVESTIGATIONS ON THE ROLE OF CA2+ AS A POTENTIAL SECOND MESSENGER FOR T AND B LYMPHOCYTE ACTIVATION AND ITS RELEVANCE IN DNA SYNTHESIS

Chapter 6: A MODEL FOR THE CONTROL OF POTASSIUM TRANSPORT IN PHA-STIMULATED HUMAN BLOOD LYMPHOCYTES

Chapter 7: EFFECT OF CON-A ON THE CATION AFFINITY OF THE Na+- K+ PUMP IN LYMPHOCYTES

Chapter 8: ACTIVATION OF LYMPHOCYTES WITHOUT MITOGENS BY INCREASING THE CALCIUM CONCENTRATION IN THE CELL CULTURE MEDIUM

Chapter 9: MEMBRANE MECHANISMS IN LYMPHOCYTE ACTIVATION WORKSHOP SUMMARY

THE LYMPHOCYTE MEMBRANE AND THE CYTOSKELETON

Francis Loor, Basel Institute for Immunology, Basel, Switzerland

Publisher Summary

This chapter focuses on the lymphocyte membrane and the cytoskeleton. Biochemistry and immunofluorescence studies have shown that the lymphocyte contains all the various structural and mechanochemical proteins known to constitute the cytoskeleton of most eukaryotic cells, that is, tubulin, actin, myosin, α-actinin, and so on. In the resting lymphocyte, thin section electron microscopy shows a narrow, dense network of thin microfilaments (MF), probably made of actin. Myosin is present in the cortical cytoplasm but does not seem to be organized as thick filaments. Microtubules (MT) are frequent. Most MT are connected with the centrioles. Some MT run parallel to the plasma membrane (PM) but remain separated from it by the MF network. Few MT are oriented toward the PM and terminate at it or close to it. Thus, there can be many more direct interactions between MF and PM than between MT and PM. Membrane component clustering by external, cross-linking ligands suggests membrane fluidity. Clustering is a prerequisite for capping to occur. Extensive crosslinking of membrane glycoproteins by some lectins inhibits capping.

INTRODUCTION

Structural and physiological aspects of the lymphocyte surface have recently been a subject of several reviews (1–4). Lately, a number of important observations have still appeared. Since the first description of membrane component spotting and capping by external ligands, and the original proposal of the “fluid mosaic membrane“ model, our understanding of lymphocyte surface organization has significantly changed and the models need revision. In particular, they have to fit the important fact that cytoskeletal structures influence the organization of the lymphocyte surface, namely the expression of microvilli (MV) and the formation of the cap and of the uropode. The experimental evidence comes from morphological observations with the fluorescence and electron microscopes, from the use of drugs which disorganize the cytoskeleton, and, more recently, from the biochemical analysis of lymphocyte membrane components. The new concept of plasma membrane (PM) organization constitutes the central part of this paper. I shall discuss both the model, its bases and its implications in extenso elsewhere (Loor, manuscript in preparation).

A SUMMARY OF THE DATA

Biochemistry and immunofluorescence have shown that the lymphocyte contains all the various structural and mechanochemical proteins known to constitute the cytoskeleton of most eukaryotic cells, i.e. tubulin, actin, myosin, α-actinin, and so on. In the resting lymphocyte, thin section electron microscopy shows a narrow, dense network of thin microfilaments (MF), probably made of actin. Myosin is present in the cortical cytoplasm but does not seem to be organized as thick filaments. Microtubules (MT) are frequent. Most MT, perhaps all, are connected with the centrioles. Some MT run parallel to the PM, but remain separated from it by the MF network. Few MT (a maximum of about a hundred per lymphocyte) are oriented towards the PM and terminate at it or close to it (1–4). Thus, there can be many more direct interactions between MF and PM than between MT and PM.

Typical studies on the capping phenomenon have shown the following (1–4). Membrane component clustering by external, cross-linking ligands suggests membrane fluidity. Clustering is a prerequisite for capping to occur. Extensive cross-linking of membrane glycoproteins by some lectins inhibits capping. Capping requires active metabolism. Capping is inhibited by agents which interfere with MF function, e.g. cytochalasins. If anything, depolymerization of MT, e.g. by drugs such as colchicine and vinblastine, helps capping? in fact, it even relieves from the inhibition of capping caused by high doses of lectins. Capping occurs on the uropode. One finds an accumulation of actin, tubulin, myosin, MF and MT under the cap. Actin and myosin are clustered as “sub-patches” in the submembranous cortical cytoplasm, under the patches of whatever clustered PM component, (e.g. ref. 5). Thus, capping appears as a contractile phenome...