title: Incidence of autoantibodies against type I and type II interferons in a cohort of systemic lupus erythematosus patients in Slovakia.
abstract: Autoantibodies against interferon (IFN) can be found in patients with systemic lupus erythematosus (SLE). However, detailed information about the occurrence of type-specific antihuman IFN antibodies is not available. In this study, we investigated the incidence of autoantibodies specifically recognizing various type I IFNs (alpha1, alpha2, beta, omega) and type II IFN (gamma). Sera from 100 SLE patients were screened for the presence of IFN-binding antibodies by ELISA, using various types of recombinant IFNs as antigen. On the whole, autoantibodies against type I or type II or both IFNs were detected in 45% (45 of 100) of the serum samples investigated. More than half (56%) of the positive samples (25 of 45) contained antibodies specific only for type I IFNs, and 36% of positive sera (16 of 45) had autoantibodies only against type II IFN. Antibodies against both type I and type II IFNs were detected in 8% (4 of 45) of the positive samples. Among autoantibodies to type I IFNs, the most abundant were those against the type IFN-omega (15%) and the subtype IFN-alpha2 (11%). Autoantibodies binding subtype IFN-alpha1 and type IFN-beta were detected at a relatively lower incidence of about 3%-4%. The highest occurrence (20%) showed autoantibodies to the proinflammatory cytokine, IFN-gamma. We did not find any correlation between the production of autoantibodies against particular IFN species and an antibody response to other IFN species. We further observed that 84% (38 of 45) of the positive sera bound only one IFN species, and 13% (6 of 45) of positive samples contained antibodies against two IFN species of five different combinations (alpha1/beta, alpha1/omega, alpha2/omega, alpha2/gamma, omega/gamma). One sample uniquely showed reactivity with three IFN species (alpha2/omega/gamma). Our findings suggest that formation of autoantibodies could reflect humoral immune responses to increased spontaneous production of the respective IFN species in SLE patients.
authors.affiliation: Institute of Virology, Slovak Academy of Sciences, 842 45 Bratislava, Slovakia.
authors.forename: Monika
authors.initials: M
authors.lastname: Slavikova
authors.forename: Hana
authors.initials: H
authors.lastname: Schmeisser
authors.forename: Eva
authors.initials: E
authors.lastname: Kontsekova
authors.forename: Frantisek
authors.initials: F
authors.lastname: Mateicka
authors.forename: Ladislav
authors.initials: L
authors.lastname: Borecky
authors.forename: Peter
authors.initials: P
authors.lastname: Kontsek
mesh_terms: D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000097:blood*; D015331:Cohort Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D015994:Incidence; D007370:Interferon Type I / Q000276:immunology*; D016898:Interferon-alpha / Q000276:immunology; D016899:Interferon-beta / Q000276:immunology; D007371:Interferon-gamma / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011485:Protein Binding; D018154:Slovakia / Q000453:epidemiology
chemical_list: D001323:Autoantibodies; D007370:Interferon Type I; D016898:Interferon-alpha; C063743:interferon omega 1; D016899:Interferon-beta; D007371:Interferon-gamma