The relation of rheumatoid arthritis to hypogammaglobulinemia.
The following hypothesis is proposed. Hypogammaglobulinemia is produced by an excess of normal 7S complement-fixing anti-immunoglobulin which is specific for "altered" Fc portions of immunoglobulin. This is present lesser amount in normal blood, is not reactive with the native immunoglobulins of blood, and plays a part in controlling the normal level of antibody production. When it is present in excess, some patients respond by producing also an excess of normal non-complement-fixing 7S anti-immunoglobulin of the same specificity as well as classical 19S IgM rheumatoid factor. These latter agents successfully prevent the hypogammaglobulinemia but they produce "side effects". These "side effects" constitute classical rheumatoid arthritis.
D000361:Agammaglobulinemia / Q000150:complications* / Q000276:immunology; D000917:Antibody Formation; D000936:Antigen-Antibody Complex; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D001666:Binding Sites, Antibody; D003169:Complement Inactivator Proteins; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007075:Immunoglobulin M / Q000276:immunology; D007136:Immunoglobulins / Q000096:biosynthesis; D008214:Lymphocytes / Q000276:immunology
D000936:Antigen-Antibody Complex; D003169:Complement Inactivator Proteins; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007136:Immunoglobulins