Cell-mediated immunity in rheumatoid arthritis: Discrimination between specific and non-specific effects of native and aggregated IgGs on leucocyte migration

PubMedID: 6698622Leucocyte migration inhibition (LMI) by paired samples of autologous serum and synovial fluid IgG as well as homologous IgG and also heat-aggregated forms of all three IgGs was studied for patients with rheumatoid arthritis (RA) and compared with the response to these antigens by leucocytes from healthy individuals. Autologous and homologous serum IgGs did not markedly affect leucocyte migration, whereas synovial fluid IgGs caused occasional pronounced LMI with autologous (rheumatoid) leucocytes. Although aggregated IgG produced LMI in both RA patients and controls, the means of the migration indexes were significantly different between both groups. Peripheral blood mononuclear cells from RA patients and healthy controls were also cultured with both native rheumatoid and normal IgG; only supernatants from RA cells incubated with rheumatoid IgG showed LMI activity, in contrast to the other culture supernatants. These results indicate that LMI to native IgG in RA may represent a form of specific cell-mediated immunity, although LMI to aggregated IgG might be explained by non-specific factors. © 1984 S. Karger AG, Basel

Binding of Wheat Gliadin in Vitro to Reticulin in Normal and Dermatitis Herpetiformis Skin

We have demostrated by indirect immunofluorescence that wheat gliadin in vitro to reticulin-like fibrils present in cryostat sections of human skin, and rat liver, kidney and stomach.Gliadin was seen to bind to fibrils throughout the dermis of both normal and dermatitis herpetiformis skin,and this was particularly striking in the dermal papillae. Serum form 2 dermatitis herpetiformis patients who did when not have antireculin staining when retested by immunofluorescence on cryostat sections of rat tissue pretreated with gliadin. Gliadin treated sections may prove useful in screening patients with gluten sensitive enteropathy for antigladin antibody. Binding of gliadin to skin sites in dermatitis herpetiformis patients and subsequent deposition of antigliadin antibody at these sites may be involved in the development of skin lesions