Infectious agents, immunity, and rheumatic diseases.
It should again be cautioned that these hypotheses are just that--hypotheses, for which there are some suggestive but not conclusive data. I have described these hypotheses using B27 and AS, and DR4 and RA. We are all aware that AS occurs in individuals who are B27 negative, and RA occurs in individuals who lack DR4. Although space does not permit further elaboration here, these hypotheses can be modified to take these additional associations into account. It should also be noted that even if the mechanisms advanced in these hypotheses prove to be true, different mechanisms may apply to different diseases, and several of these mechanisms may act in concert to produce disease. Nevertheless, these hypotheses provide a framework against which future experiments can be designed to further elucidate the relationship among infectious agents, immunity, and rheumatic diseases.
Schwartz
B D
BD
Howard Hughes Medical Institute, St. Louis, Missouri.
D000941:Antigens / Q000502:physiology; D006680:HLA Antigens / Q000276:immunology; D015796:HLA-B27 Antigen / Q000276:immunology; D006684:HLA-DR Antigens / Q000276:immunology; D006801:Humans; D015394:Molecular Structure; D011991:Receptors, Virus / Q000276:immunology; D012216:Rheumatic Diseases / Q000209:etiology / Q000276:immunology* / Q000382:microbiology; D013601:T-Lymphocytes / Q000276:immunology; D014777:Virus Diseases / Q000150:complications / Q000276:immunology
D000941:Antigens; D006680:HLA Antigens; D015796:HLA-B27 Antigen; D006684:HLA-DR Antigens; D011991:Receptors, Virus