I. Role of Histocompatibility Antigens in Cell-Cell Interaction.- 1 Histocompatibility Antigens and the T-Cell Repertoire.- 1. Introduction.- 2. H-2 Restriction.- 2.1. H-2 Restriction of T Cells.- 2.2. B Cells Are Not H-2-Restricted.- 3. H-2-Linked Ir Genes.- 3.1. Influence on the T-Cell Repertoire.- 3.2. H-2-Gene Complementation.- 3.3. The B-Cell Repertoire Is Not Directly Influenced by H-2-Linked Ir Genes.- 4. Frequency of Cells Specific for Allogeneic H-2 Antigens.- 4.1. Allospecific T Cells.- 4.2. Allospecific B Cells.- 5. T-Cell Repertoire for Restricting Elements vs. the Repertoire for Allogeneic H-2 Antigens.- 6. T-Cell vs. B-Cell Repertoire.- 6.1. Probing of the Repertoire by Responsiveness.- 6.2. Probing of the Repertoire by v-Gene Markers on Responding Cells.- 7. Conclusions.- References.- 2 Continuously Proliferating Allospecific T-Cell Lines: A Model to Study T-Cell Functions and Receptors.- 1. Introduction.- 2. Properties of Allospecific T-Cell Lines.- 2.1. Initiation of Allospecific T-Cell Lines.- 2.2. Requirements for Cell Proliferation in Long-Term T-Cell Cultures.- 2.3. Cytotoxic Potential of Allospecific T-Cell Lines.- 2.4. Selection of Allospecific T-Cell Lines over Extended Periods of Time.- 2.5. Cell-Surface Molecules of Allospecific T-Cell Lines.- 3. Outlook.- References.- 3 The Dual Specificity of Virus-Immune T Cells: Functional Indications That Virus and H-2 Molecules May Associate on the Cell Membrane.- 1. Introduction.- 2. The Influenza Model.- 2.1. Characteristics of Influenza Viruses.- 2.2. Specificity of Influenza-Immune T Cells.- 2.3. Responder-Nonresponder Situations.- 2.4. Blocking Cytotoxicity with Monospecific Antisera.- 3. Negative Selection of Alloreactive Precursors.- 3.1. Rationale.- 3.2. Responsiveness in Allogeneic Situations.- 4. General Discussion.- 5. Summary.- References.- 4 Hapten Recognition by Cytotoxic T Cells: The Modifying Influence of the Major Histocompatibility Complex.- 1. Introduction.- 2. Materials and Methods.- 2.1. Preparation of Liposomes.- 2.2. Preparation of Haptenated Bovine Serum Albumin.- 2.3. Purified Anti-DNP Antibody.- 2.4. [125I]-Anti-DNP Antibody.- 2.5. Membrane-Vesicle Preparation.- 2.6. Binding of [125I]-Anti-DNP Antibody to Haptenated Cells.- 2.7. C-Mediated and K-Cell-Mediated Cytolysis.- 2.8. Generation of Hapten-Specific Cytotoxic Responses.- 2.9. T-Cell Mediated Cytolytic Assays.- 3. Results.- 3.1. Hapten Presentation on Target Cells after Direct Chemical Modification and after Interaction with Dinitrophenylated Liposomes and Dinitrophenylated Protein.- 3.2. Generation of a Primary Hapten-Specific Cytotoxic Response in Vitro Using a Variety of Hapten-Bearing Stimulator Cells.- 3.3. Target Cells “Haptenated” by Various Procedures: Their Susceptibility to Lysis by H-2-Restricted, Hapten-Specific Cytotoxic T Lymphocytes.- 3.4. Attempts to Inhibit Hapten-Specific Cytolysis with Haptenated Cells.- 4. Discussion.- References.- 5 New Thoughts on the Control of Self-Recognition, Cell Interactions, and Immune Responsiveness by Major Histocompatibility Complex Genes.- 1. Introduction.- 2. Self-Recognition and Cell-Cell Interactions.- 3. Concept of Adaptive Differentiation.- 4. Relevance of the Proposed Mechanisms of Adaptive Differentiation to Certain Unresolved Immunological Puzzles.- 5. Recognition Mechanisms in the Immune System.- 6. Some Current Thoughts on Ir Genes.- 7. Some New Observations on Ir-Gene Mechanisms.- 8. Conclusions.- References.- 6 The Role of Cell-Surface Antigens in Progressive Tumor Growth (Immunological Surveillance Re-revisited).- 7 Self-HLA-D-Region Products Restrict Human T-Lymphocyte Activation by Antigen.- 1. Introduction.- 2. The HLA-D/DR and Rodent I-Region Cell-Membrane Products Are Analogous.- 3. Self-HLA-D/DR Restriction of T Cells Sensitized in Vivo.- 3.1. The T-Cell Proliferative Response to PPD in Vitro Is Macrophage-Dependent.- 3.2. The Antigen-Presenting Macrophages Must Share at Least One HLA-D/DR Determinant with the T-Cell Donor.- 3.3. Lack of Cooperation between Cells from HLA-D-Disparate Donors Is Not Due to Suppression or Cytotoxicity Caused by the Allogeneic Responses.- 3.4. Anti-DR Antibodies Will Specifically Inhibit the Antigen-Specific Response.- 3.5. Clonal Distribution of HLA-D/DR-Restricted Antigen-Specific T-Cells.- 3.6. B Lymphocytes Expressing Self-HLA-D Are Not Able to Substitute for Macrophages in Antigen Activation.- 4. Self-HLA-D/DR Restriction of T Cells Sensitized in Vitro.- 4.1. In Vitro Priming against TNP-Treated Autologous Cells.- 4.2. HLA-D/DR Restriction of the TNP-Specific Response.- 4.3. Is the TNP-Specific Response Also Restricted by HLA-A,B,C?.- 4.4. Can B Cells Substitute for Macrophages in the Secondary TNP-Specific Response?.- 5. Comments.- 6. Implications.- 7. Conclusion.- References.- 8 How Strict is the MHC Restriction of T Cells?.- 1. Introduction.- 2. Materials and Methods.- 2.1. Mice.- 2.2. Virus and Immunization.- 2.3. Chimeras.- 2.4. Cell Preparations and H-2 Typing.- 2.5. Cytotoxicity Assay.- 2.6. Antiviral Protection Assay in Vivo.- 2.7. Statistical Methods.- 3. Results.- 3.1. Quantitation of the Restriction Specificity Expressed in Vivo and in Vitro by Virus-Specific Cytotoxic T Cells from Unmanipulated Mice.- 3.2. Comparison of the Restriction Specificities Expressed by Virus-Specific Cytotoxic T Cells from Chimeric Mice.- 4. Discussion.- References.- II. Clinical Aspects of Transplantation: Association with Disease.- 9 The Role of Histocompatibility Antigens in Clinical Transplantation.- 1. Introduction.- 2. HLA-A and -B Matching.- 3. HLA-D Matching.- 4. Blood Transfusions.- References.- 10 HLA-Linked Regulation of Immune Responsiveness in Man: Role of I-Region-Gene Products.- 1. Introduction.- 2. Association between HLA and Immune Response.- 2.1. Response to Ethical Antigens.- 2.2. Response to Skin-Test Antigens.- 2.3. Conclusion.- 3. Immunogenetics of Response to Streptococcal Antigens.- 3.1. Purification and Characterization.- 3.2. PSA-C Response in Families.- 3.3. Mechanisms of Response to Streptococcal Antigens.- 3.4. Conclusion.- References.- 11 Clinical Histocompatibility Testing in Renal Transplantation: Potential Keys to Alloimmune Specificity and Reactivity.- 1. Introduction.- 2. Pretransplant Immunological Assessment.- 2.1. Donor-Specific Resistance.- 2.2. General (Nonspecific) Host Immune Competence.- 3. Posttransplantation Immunological Assessment.- 3.1. Donor-Specific Immune Monitoring.- 3.2. Nonspecific Immune Monitoring.- 4. Summary.- References.- 12 Human Ia-like Alloantigens and Their Medical Significances.- 1. Introduction.- 2. Human Ia-like Alloantigens.- 3. Merrit Alloantigenic System.- 4. Relationship of Ia-like Alloantigenic Systems to the HLA Complex.- 5. Seventh International Histocompatibility Workshop and HLA-DRw Specificities.- 6. Correlation between HLA-D and DRw.- 7. Ia-like Alloantigenic Segregants Distinct from HLA-DR.- 8. Leukemia Cells and Ia-like Alloantigens.- 9. Ia-like Alloantigens and Nonmalignant-Disease Associations.- 10. HLA and Cancer: New Considerations.- 11. Major Histocompatibility Complex, Aging, and DNA Repair.- References.- 13 The Enigma of Good Kidney-Graft Survival in the Face of Poor HLA Matches: HLA Matching for Kidney Transplantation Makes Sense.- 1. Introduction.- 2. Blood Transfusion.- 3. HLA-DR Matching.- 4. Incompatibility for Non-HLA Determinants.- 5. Discussion and Conclusions.- References.- 14 Histocompatibility Antigens and Susceptibility to Disease—Genetic Considerations.- 1. Introduction.- 2. General Considerations.- 2.1. HLA Association at the Population Level.- 2.2. Distribution of HLA Phenotypes within the Patient Sample.- 2.3. Studies of Linkage.- 2.4. Affected Sibpair Method.- 3. Relationships between HLA and Specific Diseases.- 3.1. Complement Factor 2 Deficiency.- 3.2. Congenital Adrenal Hyperplasia Due to 21-Hydroxylase Deficiency.- 3.3. Idiopathic Hemotochromatosis.- 3.4. Ankylosing Spondylitis.- 3.5. Insulin-Dependent Diabetes.- 3.6. Multiple Sclerosis and Optic Neuritis.- 4. Concluding Remarks.- References.