The Reticuloendothelial System

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.

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1. Neoplasms of the Mononuclear Phagocyte System.- 1. Acute Myelomonocytic Leukemia (AMML, French-American-British Classification, FAB-M4).- 2. Acute Monocytic Leukemia (AMoL, FAB-M5).- 3. Chronic Myelomonocytic Leukemia (CMML).- 4. Malignant Histiocytoses, without Langerhans Granules.- 4.1. Histiocytic Medullary Reticulosis.- 4.2. Malignant Histiocytoses, Not Otherwise Specified.- 5. Malignant Histiocytoses, with Langerhans Granules.- 6. Proliferations of MPS, Not Proven to Be Malignant Neoplasms.- 6.1. Histiocytoses of Cells without Langerhans Granules.- 6.2. Histiocytoses of Cells with Langerhans Granules.- 7. Other Neoplasms Considered to Be of MPS Origin.- 8. Differential Diagnosis.- References.- 2. Lymphatic Metastasis of Neoplasms.- 1. Lymph Node Metastasis in Human Cancer.- 2. Invasion and Metastasis.- 3. The Normal Lymphatic Vessel and Its Cellular Content.- 4. Experimental Lymphatic Metastasis.- 5. Penetration of the Lymphatic Capillary.- 6. Cells in Lymph-Draining Tumors.- 7. Reaction in the Draining Node.- 8. Barrier Function of Lymph NodesTumor Cell Killing.- 9. Chemotherapy and Immunotherapy of Lymphatic Metastasis.- References.- 3. Control of Tumors by the RES.- 1. Introduction.- 1.1. Local and Host Factors in Resistance to Cancer.- 1.2. Involvement of the RES in Cancer: Supportive Evidence.- 1.3. Interactions between the RES and Cancer.- 2. The RES in Development of Cancer.- 2.1. Functional Parameters.- 2.2. Genetic Determinants of RE Functions.- 2.3. Specific Models of Carcinogenesis.- 2.4. Comments.- 3. The RES in Progression of Cancer.- 3.1. Morphologic Features.- 3.2. Functional Changes in the Cancer Host.- 3.3. Macrophages in Tumors.- 3.4. Effects of Macrophages on Metastatic Dissemination.- 3.5. Comments.- 4. Mechanisms Mediating Antineoplastic Activity of the RES.- 4.1. Participation in Immune Responses.- 4.2. Activation of Macrophages: Cytostatic and Cytocidal Macrophages.- 4.3. Regulation of Growth.- 4.4. Comments.- 5. Factors Affecting Antineoplastic Activities of the RES.- 5.1. Heterogeneity of Macrophages.- 5.2. Humoral Factors (Opsonins).- 5.3. Hormones.- 5.4. Nutrition.- 5.5. Macromolecules.- 5.6. Microbial Agents.- 5.7. Comments.- 6. Modulation of the RES and Cancer.- 6.1. Stimulation of the RES.- 6.2. Depression of the RES.- 6.3. Subversion of the RES by Cancer.- 7. The RES and the Concept of Immune Surveillance.- 8. Conclusions.- References.- 4. Activities of Macrophages Within and Peripheral to the Tumor Mass.- 1. Introduction.- 2. Mechanisms Controlling Accumulation of TAM.- 3. Peripheral Blood Monocytes, TAM, and Heterogeneity.- 3.1. Macrophage Heterogeneity.- 4. Tumor Immunogenicity, Host Immunity, and TAM.- 5. Macrophages and Intratumor Functions.- 5.1. Macrophage-Mediated Cytolosis or Cytostasis.- 5.2. Antibody-Dependent Cytotoxicity.- 5.3. Stimulation of Tumor Growth.- 5.4. Involvement in Therapy.- 5.5. TAM and Induction of Immunity.- 5.6. Other Functions of TAM in situ.- 6. Conclusions.- References.- 5. Stimulation of the RES and Control of Cancer Metastasis.- 1. The Pathogenesis of Cancer Metastasis.- 2. Host Immunity and Metastasis.- 3. Rationale for Control of Micrometastasis by Activated Cytotoxic Macrophages.- 4. Activation of Macrophages by Agents Encapsulated within Liposomes.- References.- 6. Neoplasia and Mononuclear Phagocyte Function.- 1. Introduction.- 2. Role of Macrophages in Tumor Growth.- 3. Increase in Monocyte/Macrophage Numbers in Tumor-Bearing Animals.- 4. Enhancement of Macrophage Migration by Tumor Factors.- 5. Chemotactic Factor Inactivators Associated with Neoplasia.- 6. Monocyte/Macrophage Migratory Dysfunction in Tumor-Bearing Hosts: Evidence for the Presence of Tumor-Associated Inhibitory Factors.- 7. Isolation and Characterization of Inhibitors of Mononuclear Phagocyte Function Associated with Neoplasia.- 8. Summary.- References.- 7. Suppressor Cells and Cancer: Inhibition of Immune Functions by Macrophages.- 1. Introduction.- 2. Approaches for the Demonstration of Suppressor Macrophages.- 3. Suppression of Lymphoproliferative Responses.- 3.1. Tumor-Bearing Mice.- 3.2. Suppression of Proliferative Responses in Other Experimental Tumor Systems.- 3.3. Suppressor Cells in Humans.- 4. Suppression of the Generation of Cytotoxic T Lymphocytes.- 5. Suppression of Antibody Responses.- 6. Suppression of Lymphokine Production.- 7. Suppression of NK Cell Activity.- 8. Suppressor Macrophages in Normal as Well as in Tumor-Bearing Individuals.- 9. Do Macrophages Inhibit Every Aspect of the Immune Response?.- 10. Generation of Suppressor Macrophages.- 11. In Vivo Role of Suppressor Macrophages.- 12. Summary and Concluding Remarks.- References.- 8. Modulation of Mononuclear Phagocytes by Cancer Chemotherapeutic Agents.- 1. Introduction.- 2. Effects of Chemotherapeutic Agents on Mononuclear Phagocytes.- 2.1. Glucocorticoids.- 2.2. Antimetabolites.- 2.3. Alkylating Agents.- 2.4. Intercalating Agents.- 2.5. Plant Alkaloids.- 3. Antitumor Efficacy and Modulation of Mononuclear Phagocytes.- 4. Concluding Remarks.- References.- 9. Natural Killer Cells and Other Effector Cells, and Their Roles in Resistance against Cancer.- 1. Introduction.- 2. Effector Mechanisms That May Be Involved in Resistance against Tumor Growth.- 2.1. Tumor-Associated Antigens and Their Recognition by T and B Cells.- 2.2. Macrophages and Polymorphonuclear Leukocytes.- 2.3. NK Cells.- 3. Is the Immune Surveillance Hypothesis Valid?.- 3.1. Possible Role of Macrophages in Immune Surveillance.- 3.2. Possible Role of NK Cells or Other Related Natural Effector Cells in Immune Surveillance.- 3.3. Possible Role of ADCC in Immune Surveillance.- 4. Use of Assays for Monitoring of Immunotherapy Trials.- 5. Concluding Remarks.- References.- 10. Immunosuppressive Factors Produced by Tumors and Their Effects on the RES.- 1. Tumor-Produced Suppressor Factors.- 2. Blocking FactorsImmune Complexes.- 3. Tumor and Fetal Tissue Antigens.- 4. Plasma/Serum Factors.- 5. Tumor-Derived Suppressive Factors.- 6. Mastocytoma.- 7. Plasmacytoma.- 8. Factors from Chemically Induced Tumors.- 9. L1210 Leukemias.- 10. Tumor Cell Lines.- 11. Conclusions and Discussion.- 12. Summary.- References.- 11. Tumorigenic Virues Affecting the RES.- 1. Avian Virus-Induced Tumors of the RES.- 1.1. Avian RNA Viruses.- 1.2. Marek's Disease.- 2. Virus-Induced Tumors of the RES in Mammals.- 2.1. Murine …