Pharmacologic inhibition of experimentally induced SLE-like deposition of immunoglobulins in skin nuclei.
Binding of autologous immunoglobulins to epidermal nuclei can be induced in mice sensitized to ultraviolet-irradiated DNA following total body uv irradiation. The lesions, which resemble those observed in human systemic lupus erythematosus (SLE), are characterized histologically by the accumulation of polymorphonuclear (PMN) cells at different skin sites. In the present investigation this experimental model has been employed to study whether currently used anti-inflammatory (chloroquine, hydrocortisone, indomethacin) and polyvalent antiprotease (trasylol) drugs can either abolish or reduce the development of this murine pathology. The results of this study demonstrate that while trasylol, chloroquine, and indomethacin are able to inhibit, with variable effectiveness, the experimental skin lesions, hydrocortisone does not manifest any therapeutic activity.
D000818:Animals; D007611:Aprotinin / Q000627:therapeutic use; D001666:Binding Sites, Antibody; D002738:Chloroquine / Q000627:therapeutic use; D003176:Complement C3 / Q000276:immunology; D005260:Female; D006854:Hydrocortisone / Q000627:therapeutic use; D007074:Immunoglobulin G / Q000276:immunology*; D007213:Indomethacin / Q000627:therapeutic use; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000517:prevention & control; D051379:Mice; D008810:Mice, Inbred C57BL; D012867:Skin / Q000276:immunology*; D014466:Ultraviolet Rays; D014916:Whole-Body Irradiation
D003176:Complement C3; D007074:Immunoglobulin G; D002738:Chloroquine; D007611:Aprotinin; D006854:Hydrocortisone; D007213:Indomethacin