Origin of the Game of Chess.

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doi:10.1016/s0140-6736(02)83674-1

Immunotherapy and Vaccines

Cryz

¹

,

Granström²,

Gottstein

³

et al. 2000

Ullmann's Encyclopedia of Industrial Chemistry

2

0

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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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Highly restricted spread of HIV-1 and multiply infected cells within splenic germinal centers

Gratton

¹

,

Cheynier

²

,

Dumaurier

³

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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The tremendous dynamics of HIV infection finds expression in the tempo of sequence diversification. Genetic diversity calculations require the clearance of a majority of infected cells, the obvious predator being anti-HIV immune responses. Indeed, infiltration of germinal centers (GCs) by HIV-specific CD8 ؉ cytotoxic T lymphocytes has been described. A corollary to this description would be limited diffusion of virus within lymphoid structures. HIV efficiently infects and replicates mainly in activated CD4 ؉ T lymphoblasts. These cells are found within GCs after their activation in the adjacent periarteriolar lymphoid sheath (PALS). Here GCs and PALS have been dissected from consecutive 10-m sections through splenic tissue from three HIV-1-infected patients. Nested PCR amplification of the two first hypervariable regions of the env gene indicated that 38 -78% of sections contained HIV-infected cells. Since there are several hundred CD4 ؉ T cells per GC section, approximately 0.09 -0.64% harbor proviral DNA. Such a low frequency not only suggests that virions on the follicular dendritic cell surfaces do not readily infect adjacent T cells but also indicates highly restricted spread of HIV within GCs and the PALS. Sections were heavily infiltrated by CD8 ؉ cells, which, together with a large body of extant data, suggests that the majority of infected cells are destroyed by HIV-specific cytotoxic T lymphocytes before becoming productively infected. Finally, sequence analysis revealed that those HIV-positive cells were multiply infected, which helps explain widespread recombination despite a low overall frequency of infected cells.spleen ͉ pathogenesis ͉ viral dynamics ͉ multiple infection ͉ recombination P roductive HIV replication requires activation of resting T cells. As antigenic stimulation is the driving force, secondary lymphoid organs are the main sites for HIV replication in vivo (1, 2). CD4 T lymphocytes are the principal targets for HIV, although macrophages and dendritic cells are infected at lower frequencies (3). Splenic white pulps are sites of intense immunological activity. HIV and T cell founder effects within white pulps suggested the local recruitment of antigen-specific T cells paralleled by de novo replication of HIV (1).White pulps consist of T cell-rich areas, the periarteriolar lymphoid sheaths (PALS), and the B cell-rich follicles, including the germinal centers (GCs). T cells are stimulated in the PALS upon activation by their specific antigen presented by interdigitating dendritic cells. Together with activated B cells, they induce the formation of antigen-specific follicles. GCs are secondary follicles responsible for B cell memory formation and plasmocyte maturation. By immunohistological staining GCs are easily recognized by their follicular dendritic cell (FDC) networks (4). Under physiological conditions, most T cells within a GC are antigen specific and express CD4 and specific markers for activated and memory cells (5, 6). Within GCs, HIV proviruses are mainly present within CD4 T...

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