Contemporary Topics in Immunobiology (Paperback, Softcover Repri)

'1 Cancer: A Problem in Somatic Cell Evolution.- I. Introduction.- II. Is Escape from Senescence on the Pathway to Cancer?.- III. Are Metastases or Angiogenesis on the Pathway to Cancer?.- IV. Is Anchorage-Independent Growth on the Pathway to Cancer?.- A. Introduction.- B. Models for the Expression of Anchorage-Dependent Growth.- C. The Mutation from Anchorage-Dependent to Anchorage-Independent Growth.- D. The Coordinate Expression of Anchorage-Independent Growth and Tumorigenicity.- E. The Expression of Anchorage-Independent Growth as a Result of Mutation vs. Anchorage-Independent Growth as a Result of Differentiation.- V. Can We Put Order in the Data Concerning the Immune Response to Tumors?.- A. An Immunological Framework within Which Tumor-Immune System Evolution Can Be Rationalized.- B. The Tumor-Host Immune System Interaction.- VI. Natural Killer Activity and Cancer.- VII. The Bottom Line.- A. Transformation.- B. Evasion.- C. Are There Universals?.- VIII. References.- 2 The Genetic and Cellular Basis of Regulation of the Immune Response to Tumor Antigens.- I. Introduction.- II. Cellular Interactions.- A. Synergy of T Cells in Vitro and in Vivo.- B. Suppressor-T-Cell-Effector-T-Cell Interactions.- C. Macrophage-Lymphocyte Interactions.- III. Genetic Basis of the Immune Response to Tumor Antigens.- A. Genetic Resistance to Virus-Induced Tumors.- B. Genetic Basis of the Response to Other Tumor Types.- C. H-2 Products and Tumor Antigens.- D. Alloantigens and the Relationship to Tumor Antigen.- IV. Effector T Cells.- V. Suppressor T Cells.- A. Suppressor Factors and Suppressor Cell Circuits.- B. Suppression of Myeloma Cell Function.- C. The Ultraviolet-Light-Induced Tumor System.- D. Immunological Modulation of Tumor Responses in Vivo.- VI. Summary.- VII. References.- 3 Monoclonal Antibodies to Tumor Antigens.- I. Introduction.- II. Methodology.- A. Generation of Spleen Cell-Myeloma Cell Hybrids.- B. Isolation of Hybridomas Producing Specific Antibodies.- C. Production, Purification, and Characterization of Hybridoma Antibodies.- D. Serological Analysis of Cell Surface Antigens Identified by Hybridoma Antibodies.- E. Purification and Structural Analysis of Cell Surface Antigens Identified by Hybridoma Antibodies.- III. Antigens of Mouse Tumors.- A. Differentiation Antigens.- B. Antigens of Chemically Transformed Fibroblasts.- C. Murine Leukemia Virus Antigens.- IV. Antigens of Human Tumors.- A. Melanoma Antigens.- B. Neuroblastoma Antigens.- C. Colon Carcinoma Antigens.- D. Leukemia Antigens.- V. Conclusions.- VI. References.- 4 Continuous Cytotoxic T-Cell Lines.- I. Introduction.- II. Cytolytic T-Lymphocyte Lines.- A. The Creation of Cloned, Monospecific CTLL.- B. Human CTLL.- C. CTLL Immunotherapy.- III. Methods for Culturing T Cells.- A. The TCGF(IL2) Assay.- B. The Production of TCGF(IL2).- C. The Initiation and Maintenance of T-Cell Lines.- IV. The Immunobiologic Significance of TCGF(IL2).- V. Conclusions.- VI. References.- 5 The Role of MuLV Receptors on T-Lymphoma Cells in Lymphoma Cell Proliferation.- I. Introduction.- II. Each T Lymphoma Will Bear Surface Receptors Which Specifically Recognize Its Inducing MuLV.- A. Cell Surface Retrovirus Binding Can Be Detected by FACS Analysis.- B. Retrovirus Binding to T-Lymphoma Cells May Lead to Infection.- III. Retrovirus Receptors Can Be Used to Distinguish Incipient T Lymphomas from Other T Cells.- IV. Substances Which Interfere with Receptor Binding Inhibit T-Lymphoma Proliferation.- V. T-Lymphoma Receptors Should Have Variable Regions Analogous to Immunoglobulins and Normal T-Cell Receptors.- VI. Continuous in Vivo Antigenic Stimulation of Appropriate Normal T-Cell Clones Should Also Be Lymphomagenic.- VII. Concluding Remarks.- VIII. References.- 6 On Network Theory and H-2 Restriction.- I. Introduction.- II. The Cross-Linking Postulate and Symmetry in the System.- A. First C