GENETIC CONTROL OF THE ANTIBODY RESPONSE TO MICROBIAL ANTIGENS

对微生物抗原的抗体反应的遗传控制

• 批准号: 3803095
• 负责人: P J BAKER
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3803095
• 关键词: Pseudomonas aeruginosa; active immunization; antibody formation; antigen presentation; bacterial antigens; bacterial polysaccharides; genetic strain; immunogenetics; immunoglobulin G; immunoglobulin isotypes; interferons; laboratory mouse; leukocyte activation /transformation; lipopolysaccharides; microorganism immunology; receptor binding; suppressor T lymphocyte

Lipopolysaccharide-responsive (LPS(r)) and LPS-defective (LPS(d)) strains of C3H mice differ greatly in the capacity of bacterial monophosphoryl lipid A (MPL) to inactivate suppressor T cell (Ts) function generated after exposure to Type III pneumococcal polysaccharide (SSS-III). This suggests that the activated Ts of such mice differ with respect to (a) a cell surface receptor required for the binding and subsequent internalization of MPL and/or (b) the presence of a biochemical pathway that is extremely sensitive to inactivation by MPL. The predominant isotype of antibody against Pseudomonas aeruginosa LPS in several strains of inbred mice is IgG3. Treatment with Gamma-interferon resulted in an increase in IgG2a antibody, regardless of major histocompatibility complex (MHC) haplotype. Thus the isotypic pattern produced in mice immunized with this antigen is not MHC restricted and is influenced greatly by lymphokines.

脂多糖反应（LPS(r)）和脂多糖缺陷（LPS(d)）