The Reticuloendothelial System: A Comprehensive Treatise Volume 5 Cancer PDF
Preview The Reticuloendothelial System: A Comprehensive Treatise Volume 5 Cancer
The Reticuloendothelial System A COMPREHENSIVE TREATISE Volume 5 Cancer The Reticuloendothelial System A COMPREHENSIVE TREATISE General Editors: Herman Friedman, University oj South Florida, Tampa, Florida Mario Escobar, Medical College oj Virginia, Richmond, Virginia and Sherwood M. Reichard, Medical College oj Georgia, Augusta, Georgia MORPHOLOGY Edited by Ian Carr and W. T. Daems BIOCHEMISTRY AND METABOLISM Edited by Anthony J. Sbarra and Robert R. Strauss PHYLOGENY AND ONTOGENY Edited by Nicholas Cohen and M. Michael Sigel IMMUNOPATHOLOGY Edited by Noel R. Rose and Benjamin V. Siegel CANCER Edited by Ronald B. Herberman and Herman Friedman PHYSIOLOGY Edited by Sherwood M. Reichard and James P. Filkins .. PHARMACOLOGY Edited by John Hadden and Andor Szentivanyi IMMUNOLOGY Edited by Joseph A. Bellanti and Herbert B. Herscowitz HYPERSENSITIVITY Edited by Peter Abramoff and S. Michael Phillips INFECTION Edited by John P. Utz and Mario R. Escobar The Reticuloendothelial System A COMPREHENSIVE TREATISE Volume 5 Cancer Edited by RONALD B. HERBERMAN Naiional Cancer Institute National Institutes of Health Fredrick, Maryland and HERMAN FRIEDMAN University of South Florida College of Medicine Tampa, Florida PLENUM PRESS • NEW YORK AND LONDON Library of Congress Cataloging in Publication Data Main entry under title: The Reticuloendothelial system. Includes bibliographies and indexes. CONTENTS: v. 1. Carr, I., Daems, W. T., and Lobo, A. Morphology.-v. 2. Sbarra, A. J., and Strauss, R. R. Biochemistry and metabolism.-v. 3. Cohen, N., and Sigel M. M. Phylogeny and Ontogeny.-v. 4. Rose, N. R., and Siegel, B. V. Immuno pathology.-v. 5. Herberman, R. B., and Friedman, H. Cancer. 1. Reticulo-endothelial system. 2. Macrophages.1. Friedman, Herman, 1931- II. Escobar, Mario R. III. Reichard, Sherwood M. [DNLM: 1. Reticuloendothelial system. WH650 R437] QP1l5.R47 591.2'95 79-25933 ISBN-13 :978-1-4684-4510-7 e-ISBN-13:978-1-4684-4508-4 001: 10.1007/978-1-4684-4508-4 Softcover reprint of the hardcover 1st edition 1983 © 1983 Plenum Press, New York A Division of Plenum Publishing Corporation 233 Spring Street, New York, N.Y. 10013 All rights reserved No part of this book may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the Publisher Contributors BETSY BENNETT • Department of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee IAN CARR • Department of Pathology, University of Manitoba, and St. Boniface Hospital, Winnipeg, Manitoba, Canada JEAN CARR· Department of Physiology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada GEORGE J. CIANCIOLO • Laboratory of Immune Effector Function, Howard Hughes Medical Institute, Division of Rheumatic and Genetic Diseases, Department of Medicine, Duke University Medical Center, Durham, North Carolina ROBERT D. COLLINS· Department of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee ROBERT EVANS· The Jackson Laboratory, Bar Harbor, Maine ISAIAH J. FIDLER • Cancer Metastasis and Treatment Laboratory, National Cancer Institute, Frederick Cancer Research Facility, Frederick, Maryland HERMAN FRIEDMAN • Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa, Florida ALAN D. GLICK • Department of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee STEPHEN HASKILL· Department of Obstetrics and.Gynecology, School of Medi cine, University of North Carolina, Chapel Hill, North Carolina RONALD B. HERBERMAN • Biological Therapeutics Branch, Biological Response Modifiers Program, National Cancer Institute, Frederick Cancer Research Facility, Frederick, Maryland v VI CONTRIBUTORS T. JUHANI LINNA· Central Research and Development Department, E. I. du Pont de Nemours and Company, Inc., Glenolden Laboratory, Glenolden, Pennsylvania ALBERTO MANTOVANI • Istituto di Ricerche Farmacologiche "Mario Negri," Milan, Italy VINCENT A. POLLACK • Cancer Metastasis and Treatment Laboratory, National Cancer Institute, Frederick Cancer Research Facility, Frederick, Maryland RALPH SNYDERMAN • Laboratory of Immune Effector Function, Howard Hughes Medical Institute, Division of Rheumatic and Genetic Diseases, Department of Medicine, Duke University Medical Center, Durham, North Carolina STEVEN SPECTER· Department of Medical Microbiology and Immunology, Uni versity of South Florida College of Medicine, Tampa, Florida KURT STERN • The Lautenberg Center for General and Tumor Immunology, The Hebrew University-Hadassah Medical School, Jerusalem, Israel ALDO TAGLIABUE • Istituto di Ricerche Farmacologiche "Mario Negri," Milan, Italy KENNETH D. THOMPSON· Departments of Pathology and Microbiology, Loyola University Medical Center, Maywood, Illinois LUIGI VA RESIO • Biological Therapeutics Branch, Biological Response Modifiers Program, National Cancer Institute, Frederick Cancer Research Facility, Frederick, Maryland Foreword This comprehensive treatise on the reticuloendothelial system is a project jointly shared by individual members of the Reticuloendothelial (RE) Society and bio medical scientists in general who are interested in the intricate system of cells and molecular moieties derived from these cells which constitute the RES. It may now be more fashionable in some quarters to consider these cells as part of what is called the mononuclear phagocytic system or the lymphoreticular system. Nevertheless, because of historical developments and current interest in the subject by investigators from many diverse areas, it seems advantageous to present in one comprehensive treatise current information and knowledge con cerning basic aspects of the RES, such as morphology, biochemistry, phylogeny and ontogeny, physiology, and pharmacology as well as clinical areas including immunopathology, cancer, infectious diseases, allergy, and hypersensitivity. It is anticipated that by presenting information concerning these apparently heterogeneous topics under the unifying umbrella of the RES attention will be focused on the similarities as well as interactions among the cell types constitut ing the RES from the viewpoint of various disciplines. The treatise editors and their editorial board, consisting predominantly of the editors of individual vol umes, are extremely grateful for the enthusiastic cooperation and enormous task undertaken by members of the biomedical community in general and especially by members of the American as well as European and Japanese Reticuloendothe lial Societies. The assistance, cooperation, and great support from the editorial staff of Plenum Press are also valued greatly. It is hoped that this unique treatise, the first to offer a fully comprehensive treatment of our knowledge concerning the RES, will provide a unified framework for evaluating what is known and what still has to be investigated in this actively growing field. The various vol umes of this treatise provide extensive in-depth and integrated information on classical as well as experimental aspects of the RES. It is expected that these volumes will serve as a major reference for day-to-day examination of various subjects dealing with the RES from many different viewpoints. Herman Friedman Mario R. Escobar Sherwood M. Reichard vii Introduction During the last few decades, the nature and mechanisms for development of malignancy have attracted a high level of interest and experimental study by numerous biomedical investigators. This tremendous. expansion of interest in the field of oncology has been based on the equally striking explosion of interest ~n all aspects of biomedical science. It also should be noted that, historically, the involvement of the reticuloendothelial system (RES) in the oncogenic process has been well recognized and widely investigated. Much of this has come about from the observation that defects in the RES may be involved in the potentiation or progression of the malignant process. Furthermore, the RES itself has been recognized as a target for the malignant process in that significant numbers of malignancies of both man and experimental animals appear to either arise in the organized RES tissues and/or are spread through and to the RES. Thus it ap peared appropriate to the editors of this treatise to include a comprehensive discussion of the reticuloendothelial system and malignancy. It may be of value to note that there are several general categories of malig nancy which appear to have different tissue sites of origin and different mechac nisms of induction by etiologic agents. Carcinomas are considered to be malig nancies arising from epithelial cells. In contrast, sarcomas are those malignancies which arise from mesothelial origin and include such diverse tu mors as fibrosarcomas, rhabdomyosarcomas, etc. Finally the lymphomas and leukemias are considered to be those malignancies which arise from the blood forming elements of the body, including the reticuloendothelial system. Despite a tremendous amount of investigative work over the past few dec ades concerning the malignant process, it is still apparent that the inability to fully define the malignant cell and to unequivocally determine the etiologic agents or events responsible for their development has hampered full expansion of knowledge in this field. A vast amount of information exists to describe what malignant cells do and to a lesser extent how they do it, but the fundamental characteristics that set them apart from normal cells are still not adequately understood. It is generally accepted that the RES consists of a complex of distinct cell types, including macrophages, reticular cells, lymphocytes, and plasmacytes. These cells are recognized as important in primary host defense mechanisms accounting for the clearance of foreign substances from the host, as well as the ix x INTRODUCTION regulation of cellular and metabolic activities. A fully functioning RES is impor tant in all aspects of host defenses including specific and nonspecific defense mechanisms against "foreign" invaders, such as parasites and microbes, as well as "internal" invaders, such as malignant cells as they arise and attempt to proliferate and disseminate throughout the body. Thus an understanding of how malignancies interact with the RES appears to be an important goal for those interested in the complex and interacting system of cells constituting the RE system. This volume of the RES treatise is concerned with several aspects of malig nancy. The introductory chapter discusses tumors arising in the RES system, their nature and characteristics. The pathology of tumors with an emphasis on infiltration of host lymphatic tissue by tumor cells is then discussed. It is widely recognized that the RES, including many important cellular components such as macrophages, plays an important role in control of tumors and this topic is the subject of detailed discussion. Specific antitumor effects by macrophages, both at the local and systemic level, are also reviewed. The role of macrophages in antitumor immunity is also presented in some detail, especially the ability of macrophages to mediate tumoricidal activity in various model systems. The function of macrophages within a tumor as compared to those in the general circulation of the individual or in other tissue sites is discussed in detail, since it is now quite apparent that those macrophages which may be infiltrating a tumor or interacting with tumor cells locally are functionally and immunobiologically distinct from macrophages in other sites. It is now widely accepted that some degree of immune alteration may be involved in tumor cell progression, if not initiation and selection. Various mech anisms involved in alterations of immunocompetence, as reflected by height ened susceptibility to tumors, are reviewed in this volume. It should be noted, however, that for many decades there was a lack of understanding of the role of the immune response in malignancy. Indeed, although there was a great deal of speculation and enthusiasm in the earlier part of this century that tumors could be brought under control by immunologic methods, such as by tumor vaccines, the excitement faded very rapidly when by the 1950s it was realized that most of the experimental antitumor vaccines really sensitized non-inbred animals to transplantation antigens and not tumor associated antigens. Nevertheless, in the mid-1950s it became dear that at least in some experimental animal tumor models, specific antitumor immune responses, although relatively weak, could be readily induced in syngeneic individuals. For example, transfer of meth ylcholanthrene-induced transplantable tumor cells to a susceptible, inbred syn geneic mouse, followed by excision of the tumor 1-2 weeks later, conferred on that animal the ability to resist reimplantation of somewhat larger numbers of tumor cells at a subsequent time. Innumerable studies in the 1950s and 1960s confirmed that specific anti tumor immunity could be induced by similar types of vaccines or antigen prepa rations derived from specific tumors. Indeed, it became apparent by the 1960s that oncogenic viruses elicited tumors in inbred animals and these tumors con tained virus-associated antigens; specific immune responses could be elicited to xi INTRODUCTION such antigens. Furthermore, chemically induced tumors also gave evidence of specific antigens, but these appeared to be unique to each induced tumor. Thus, the major question arose as to why tumors would progress in the face of poten tial stimulation of immune responses against tumor specific or associated anti gens. The idea of immunosurveillance and the role of the T lymphocyte system in monitoring the emergence of tumor cells containing tumor specific antigens became popular. It is not appropriate at this time to review in detail the emergence of the immunosurveillance theory, which was initially based upon the postulate that T lymphocytes and other cellular elements of the immune response systems devel oped to protect individuals against malignancies. Nevertheless, in the 1970s it was evident that the concept of failure of the immunosurveillance system lead ing to tumor development could not explain all features of how tumors can "escape" the immune system of the host. Indeed, in those instances in man where depressed immune responses have been associated with tumors, it be came evident that most tumors in such individuals invol~ the reticuloen dothelial system, whereas such tumors normally account for less than 5% of all tumors in man. Over the last ten years, increasing evidence also has accumulat ed to indicate that surveillance by immune T cells against immunogenic tumors does not provide a sufficiently comprehensive view of host resistance against tumors. An important role for natural immunity has emerged, with resistance being mediated by natural killer (NK) cells as well as by macrophages. Thus, a chapter summarizing the evidence for the role of NK cells in resistance to tumor growth has been included in this volume. It also has become quite evident over the last decade or so that tumor bearing individuals, either man or experimental animals, may not only have evidence of immunocompetence against the tumor per se, such as antibodies, sensitized T lymphocytes, and functionally active NK cells and macrophages, but also show evidence of "blocking" of immune competence by suppressive cells or factors, either specific or nonspecific. A wide variety of blocking factors, most notably soluble tumor antigens or antigen/antibody complexes, are present in many individuals with progressive tumors. Furthermore, suppressor cells of the immune system, including sup pressor macrophages and T lymphocytes, have been associated with many tu mors. In many experimental animal situations, development of suppressor cells precedes or parallels the progression of an experimental tumor, either trans planted or induced. Thus, these topics are discussed in some detail in this volume. Furthermore, it is well recognized that many tumor inducing agents, including chemical carcinogens, ultraviolet light, and irradiation may be immu nosuppressive, perhaps locally if not systemically. Most if not all tumor-induc ing viruses of experimental animals are now known to be immunosuppressive. These suppressive tumor viruses include the retroviruses. Thus, there is a dis cussion of tumor viruses and their immunosuppressive properties in this vol ume. In addition, many tumor cells may either directly or indirectly affect the immune system. Many of the leukemias, both in vivo and in vitro, secrete immu nosuppressive molecules, either unique or related to "normal" immunoregula-
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