Distribution of the anti-gamma globulin factors in the synovial membrane and other tissues in various diseases.

Bonomo, Lorenzo; Tursi, A.; Gillardi, U

doi:10.1136/ard.27.2.122

Cited by 25 publications

(8 citation statements)

References 22 publications

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“…These findings resemble those observed in rheumatoid arthritis synovia, which have been found to contain deposits of IgG, complexes of IgG-rheumatoid factor, or of IgG and C3, extracellularly or within macrophages (Hollander et al, 1965;Bonomo et al, 1968;1970a, b). It is possible, though yet to be proved, that these complexes activate complement, as does the aggregated IgG without antigen, and contribute to the other substances perpetuating the inflammation.…”

Section: Discussionsupporting

confidence: 76%

Studies on vasculitis

1976

Clin Experimental Allergy

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Human cutaneous vasculitis lesions tend to be chronic in contrast to ephemeral experimental Arthus responses. Human lesions were examined for fixed antiglobulin antibodies, as occur in rheumatoid joint synovia, which could bind globulins to form tissue-damaging complexes and perpetuate the inflammation.The immunofluorescence procedure was modified by pretreating sections with 5% bovine serum albumin, and by using fluorescein conjugates of F(ab)2 portions of antibodies to avoid the antigen-nonspecific binding that sometimes occurs in inflamed or necrotic tissue.Previous findings of immunoglobulins in lesions were confirmed by the more discriminating technique. IgG and IgM was present more frequently in lesions with mainly mononuclear cell changes, than in those with mainly neutrophil changes, leucocytoclastic or necrotizing vascuhtis. Fab occurred in some lesions without Fc of IgG or IgM.Three lesions containing IgM or IgM and IgG, specifically bound heat-aggregated whole IgG or Fc of IgG. None bound IgM.The results indicate that the immunoglobulin in some cutaneous vasculitis lesions is locally formed or fixed antiglobulin, which will bind aggregated IgG possibly forming complexes perpetuating the lesion.

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Section: Discussionsupporting

confidence: 76%

Studies on vasculitis

1976

Clin Experimental Allergy

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“…Immunoglobulins, rheumatoid factor (RF), and complement components have all been found in the intimal cells of the synovium (Rodman, William, Bilka, and Muller-Eberhard, 1967;Bonomo, Tursi, and Gillardi, 1968;Brandt, Cathcart, and Cohen, 1968) and within cytoplasmic inclusions of leucocytes of the synovial fluid (Zucker-Franklin, 1966;Vaughan, Barnett, Sobel, and Jacox, 1968) from patients with rheumatoid arthritis. The fact that we have been able to demonstrate the presence of IgM, IgG, and fl, within macrophages and polymorphs adhering to skin-window coverslips in rheumatoid patients (Vernon-Roberts and Jessop, 1972) could suggest that similar immunological factors may influence the function of inflammatory cells at extra-articular sites.…”

Section: Discussionmentioning

confidence: 99%

Effects of gold salts and prednisolone on inflammatory cells. I. Phagocytic activity of macrophages and polymorphs in inflammatory exudates studied by a “skin-window” technique in rheumatoid and control patients.

Jessop¹,

Vernon‐Roberts²,

Harris³

1973

Annals of the Rheumatic Diseases

123

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“…The cells contain factors active against both human and rabbit gammaglobulin or predominantly against the latter (Bonomo, Tursi, and Gillardi, 1968). Rheumatoid factor reacting with altered human gammaglobulin is seldom aggregated in families.…”

Section: Rheumatoid Factormentioning

confidence: 99%