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MethodsTwo T helper cell clones recognizing the gp 120 envelope protein of HIV were generated from the peripheral blood of a healthy seropositive individual. These cells were type specific as they proliferated and produced IL 2 when stimulated by an epitope in the amino-terminal half of gp 120 of HIVsF2, but not by a similar region of HIVz,6, a Zairian HIV-1 isolate. These two viruses differ by 26% in the deduced amino sequence of the gp 120 protein. Moreover, the antigenic site(s) recognized by the cloned T cells are distinct from those recognized by envelope-specific antibodies. These observations have important implications for the development and use of anti-HIV vaccines.
MethodsTwo T helper cell clones recognizing the gp 120 envelope protein of HIV were generated from the peripheral blood of a healthy seropositive individual. These cells were type specific as they proliferated and produced IL 2 when stimulated by an epitope in the amino-terminal half of gp 120 of HIVsF2, but not by a similar region of HIVz,6, a Zairian HIV-1 isolate. These two viruses differ by 26% in the deduced amino sequence of the gp 120 protein. Moreover, the antigenic site(s) recognized by the cloned T cells are distinct from those recognized by envelope-specific antibodies. These observations have important implications for the development and use of anti-HIV vaccines.
Indigenous micro-organisms in the oral cavity can cause two major diseases, dental caries and periodontal diseases. There is neither agreement nor consensus as to the actual mechanisms of pathogenesis of the specific virulence factors of these micro-organisms. The complexity of the bacterial community in dental plaque has made it difficult for the single bacterial agent of dental caries to be determined. However, there is considerable evidence that Streptococcus mutans is implicated as the primary causative organism of dental caries, and the cell-surface protein antigen (SA I/Il) as well as glucosyltransferases (GTFs) produced by S. mutans appear to be major colonization factors. Various forms of periodontal diseases are closely associated with specific subgingival bacteria. Porphyromonas gingivalis has been implicated as an important etiological agent of adult periodontitis. Adherence of bacteria to host tissues is a prerequisite for colonization and one of the important steps in the disease process. Bacterial coaggregation factors and hemagglutinins likely play major roles in colonization in the subgingival area. Emerging evidence suggests that inhibition of these virulence factors may protect the host against caries and periodontal disease. Active and passive immunization approaches have been developed for immunotherapy of these diseases. Recent advances in mucosal immunology and the introduction of novel strategies for inducing mucosal immune responses now raise the possibility that effective and safe vaccines can be constructed. In this regard, some successful results have been reported in animal experimental models. Nevertheless, since the public at large might be skeptical about the seriousness of oral diseases, immunotherapy must be carried out with absolute safety. For this goal to be achieved, the development of safe antibodies for passive immunization is significant and important. In this review, salient advances in passive immunization against caries and periodontal diseases are summarized, and the biotechnological approaches for developing recombinant and human-type antibodies are introduced. Furthermore, our own attempts to construct single-chain variable fragments (ScFv) and human-type antibodies capable of neutralizing virulence factors are discussed.
The article contains sections titled: 1. Introduction 1.1. Historical Aspects 1.2. Principles and Definitions 1.2.1. Antigens 1.2.2. Antibodies 1.2.3. Immune Response 1.2.4. Active Immunization 1.2.5. Passive Immunization 1.2.6. Genetic Engineering 2. Bacterial Vaccines 2.1. Diphtheria Vaccine 2.2. Tetanus Vaccine 2.3. Pertussis Vaccine 2.4. Typhoid Fever Vaccine 2.5. Streptococcus pneumoniae Vaccine 2.6. Shigella Vaccines 2.7. CholeraVaccine 2.8. Vaccines Against Nosocomial Pathogenes 2.9. Meningococcal Meningitis Vaccine 2.10. Tuberculosis Vaccine 2.11. Escherichia coli Vaccines 2.12. Neisseria gonorrhoeae Vaccine 2.13. Hemophilus influenzae Type b Vaccines 3. Viral vaccines 3.1. Measles Vaccine 3.2. Mumps Vaccine 3.3. Rubella Vaccine 3.4. Combined Measles ‐ Mumps ‐ RubellaVaccine 3.5. Polio vaccine 3.6. Hepatitis b Vaccine 3.7. Rabies Vaccine 3.8. Influenza Vaccine 3.9. Varicella Vaccine 3.10. Yellow Fever Vaccine 3.11. Tick‐Borne Encephalitis Vaccine 3.12. Japanese Encephalitis Vaccine 3.13. Smallpox Vaccine 3.14. Rift Valley Fever Vaccine 4. Vaccines against Parasites 4.1. Vaccines against Helminths 4.1.1. Vaccines against Schistosoma 4.1.2. Vaccines against Nematodes 4.1.2.1. Gastrointestinal Nematodes 4.1.2.2. Tissue‐Invading Nematodes (Filariidae) 4.1.3. Vaccines against Cestodes 4.2. Malaria Vaccine 4.2.1. Strategy for Malaria Vaccine Development 4.2.2. Sporozoite Vaccines 4.2.3. Asexual Blood Stage Vaccine 4.2.3.1. Merozoite Surface Antigens 4.2.3.2. Rhoptry antigens 4.2.3.3. Antigens Associated with the Membrane of Infected Erythrocytes 4.2.3.4. Other Proteins and Synthetic Peptides 4.2.4. Sexual Stages‐Transmission Blocking Immunity 5. Immunotherapy 5.1. Gamma Globulin Preparations 5.1.1. Standard Immune Serum Globulin 5.1.2. Immunoglobulin for Intravenous Use 5.1.3. Hyperimmune Globulins and Antitoxins 5.1.4. Production Requirements 5.2. Prophylaxis with Immune Serum Globulin 5.3. Prophylaxis with Hyperimmune Globulins 5.4. Therapy with Immune Serum Globulin 5.5. Prophylaxis and Therapy with Intravenous Immunoglobulin (IVIG) 5.5.1. Viral Infection 5.5.2. Bacterial Infection 5.5.3. Noninfectious Diseases 5.5.3.1. Therapeutic Effect of IVIG 5.5.3.2. Mechanism of Action 5.6. Prophylaxis and Therapy with Plasma and Other Blood Products 5.7. Adverse Effects of Gamma Globulin Preparations 5.8. Future Prospects 6. Immunotherapeutic Uses of Monoclonal Antibodies 6.1. Introduction 6.2. Bacterial Targets 6.3. Viral and Chlamydial targets 6.4. Parasite Targets
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