No abstract

Serum immunoglobulins, complement and a,-antitrypsin were assayed in forty-eight patients with chronic urticaria. Thirteen cases had chronic cold urticaria and thirtytwo had chronic idiopathic urticaria. Elevated mean serum IgM was found in chronic cold urticaria. Seven patients had partial immunoglobulin deficiencies. IgE was elevated in sixteen cases of chronic idiopathic and in two with chronic cold urticaria. Eight patients had depressed serum total haemoiytic complement activity. Low C3 and normal C4 serum protein concentrations in four cases suggested alternative complement pathway activation. Twenty of forty-six patients were atopic, although specific allergies responsible for the urticaria were not identified in any of them, a^antitrypsin levels were normal in all patients. The data suggest that the aetiology and pathogenesis of chronic urticarias in this study are heterogeneous. No evidence of abnormality of the protease inhibitor system in either chronic idiopathic or chronic cold urticaria was found.

No abstract

The ability of monoclonal IgM anti‐DNA auto‐antibodies derived from normal human lymphoid cells to bind to cellular constituents of human epithelial cells (HEp‐2) was examined by immunofluorescence. Hybridoma supernatants from 10 different clones were studied. Four of them gave a strong fibrillar cytoplasmic staining that resembled cytoskeletal staining, 1 showed strong nuclear staining only, 3 showed weak nucleolar staining only, and 2 showed no staining. The hybridoma supernatants that reacted with HEp‐2 cytoskeleton were either polyspecific for various nucleic acid antigens, such as single‐stranded DNA, DNA, poly(dA:dT), poly(dG)·poly(dC), RNA, and cardiolipin, or were restricted to cardiolipin. Cytoskeletal staining identical to the hybridoma supernatant staining was also seen with mouse monoclonal anti‐vimentin antibody B11.5.1. Inhibition of the cytoskeletal staining was accomplished in 3 of the 4 hybridoma supernatants by preabsorption of these hybridoma supernatants with cardiolipin and/or single‐stranded DNA, or by preincubation of the HEp‐2 cells with the mouse monoclonal anti‐vimentin antibody.