{"title":"粒细胞特异性膜导向自身抗体在类风湿性关节炎中性粒细胞减少和自身免疫性中性粒细胞减少的病例中缺乏证据。","authors":"J Petersen, A Wiik","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>With the purpose of detecting granulocyte-specific membrane-directed autoantibodies, IgG was isolated from 14 patients with Felty's syndrome, from 5 patients with rheumatoid arthritis associated with neutropenia, and from 3 rheumatoid factor positive patients with autoimmune neutropenia. By means of indirect immunofluorescence suspensions of leukocytes from healthy controls were tested for their ability to bind whole IgG fractions or F(ab')2 fragments of IgG isolated from the neutropenic patients. By this method, whole IgG preparations from neutropenic patients and normal controls were invariably found to bind to the surface of granulocytes and a minor proportion of lymphocytes. In contrast. F(ab')2 fragments of IgG from the neutropenic patients failed to bind to the surface of granulocytes. Both whole IgG fractions and F(ab')2 fragments displayed displayed antinuclear antibody activity ruling out the possibility of loss of antibody reactivity during the preparation of F(ab')2 fragments. The neutropenia seen in rheumatoid arthritis with or without splenomegaly thus does not seem to be induced by granulocyte-specific membrane-directed IgG autoantibodies, but rather by a non-specific attachment of IgG most probably in immune complex bound form to Fc gamma receptors on neutrophils which thereby acquire surface properties facilitating removal from the circulating blood cell pool.</p>","PeriodicalId":77653,"journal":{"name":"Acta pathologica, microbiologica, et immunologica Scandinavica. Section C, Immunology","volume":"91 1","pages":"15-22"},"PeriodicalIF":0.0000,"publicationDate":"1983-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Lack of evidence for granulocyte specific membrane-directed autoantibodies in neutropenic cases of rheumatoid arthritis and in autoimmune neutropenia.\",\"authors\":\"J Petersen, A Wiik\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>With the purpose of detecting granulocyte-specific membrane-directed autoantibodies, IgG was isolated from 14 patients with Felty's syndrome, from 5 patients with rheumatoid arthritis associated with neutropenia, and from 3 rheumatoid factor positive patients with autoimmune neutropenia. By means of indirect immunofluorescence suspensions of leukocytes from healthy controls were tested for their ability to bind whole IgG fractions or F(ab')2 fragments of IgG isolated from the neutropenic patients. By this method, whole IgG preparations from neutropenic patients and normal controls were invariably found to bind to the surface of granulocytes and a minor proportion of lymphocytes. In contrast. F(ab')2 fragments of IgG from the neutropenic patients failed to bind to the surface of granulocytes. Both whole IgG fractions and F(ab')2 fragments displayed displayed antinuclear antibody activity ruling out the possibility of loss of antibody reactivity during the preparation of F(ab')2 fragments. The neutropenia seen in rheumatoid arthritis with or without splenomegaly thus does not seem to be induced by granulocyte-specific membrane-directed IgG autoantibodies, but rather by a non-specific attachment of IgG most probably in immune complex bound form to Fc gamma receptors on neutrophils which thereby acquire surface properties facilitating removal from the circulating blood cell pool.</p>\",\"PeriodicalId\":77653,\"journal\":{\"name\":\"Acta pathologica, microbiologica, et immunologica Scandinavica. Section C, Immunology\",\"volume\":\"91 1\",\"pages\":\"15-22\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1983-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Acta pathologica, microbiologica, et immunologica Scandinavica. Section C, Immunology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta pathologica, microbiologica, et immunologica Scandinavica. Section C, Immunology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Lack of evidence for granulocyte specific membrane-directed autoantibodies in neutropenic cases of rheumatoid arthritis and in autoimmune neutropenia.
With the purpose of detecting granulocyte-specific membrane-directed autoantibodies, IgG was isolated from 14 patients with Felty's syndrome, from 5 patients with rheumatoid arthritis associated with neutropenia, and from 3 rheumatoid factor positive patients with autoimmune neutropenia. By means of indirect immunofluorescence suspensions of leukocytes from healthy controls were tested for their ability to bind whole IgG fractions or F(ab')2 fragments of IgG isolated from the neutropenic patients. By this method, whole IgG preparations from neutropenic patients and normal controls were invariably found to bind to the surface of granulocytes and a minor proportion of lymphocytes. In contrast. F(ab')2 fragments of IgG from the neutropenic patients failed to bind to the surface of granulocytes. Both whole IgG fractions and F(ab')2 fragments displayed displayed antinuclear antibody activity ruling out the possibility of loss of antibody reactivity during the preparation of F(ab')2 fragments. The neutropenia seen in rheumatoid arthritis with or without splenomegaly thus does not seem to be induced by granulocyte-specific membrane-directed IgG autoantibodies, but rather by a non-specific attachment of IgG most probably in immune complex bound form to Fc gamma receptors on neutrophils which thereby acquire surface properties facilitating removal from the circulating blood cell pool.