Identification of human IgG autoantibodies specific for IL-10

Since autoantibodies to IL-1α, interferon-alpha (IFN-α) and IL-6 have been described, this study concentrated on the search for autoantibodies to hIL-10 using an assay based on the precipitation of 125I-hIL-10 anti-IL-10 autoantibody complexes using Protein G-Sepharose. Among 1860 tested sera, only seven were found to specifically precipitate IL-10, thus indicating the rare occurrence of such autoantibodies. Four of those seven anti-IL-10 autoantibody sera were specific for hIL-10, two recognized both human and viral IL-10, while the last one recognized human, viral and murine IL-10, thus suggesting the existence of at least three different epitopic specificities. The purification of anti-IL-10 autoantibody from one serum demonstrated the existence of a single (IgG1, λ) autoantibody that neutralized IL-10 biological activity. Thus, autoantibodies to IL-10 may represent natural antagonists to IL-10

Association of pesticide exposure, vaccination response, and interleukin-1 gene polymorphisms

We performed a cross-sectional study involving workers from four European countries in which exposure to pesticides and immune parameters were evaluated over a short period of time. The total study population consisted of 238 workers occupationally exposed to pesticides and 198 nonoccupationally exposed workers. The study showed that pesticide exposure at levels encountered by workers under different conditions in Europe did not affect the ability of the immune system to respond to vaccination. We could, however, identify individuals within the group of pesticide exposed workers who were genetically characterized by the 2.2 IL-1alpha polymorphism and who showed a lower antibody response, pointing out the importance of the understanding of genetic variability and the interaction between genetic and environmental factors in the identification of high-risk individuals, which may eventually lead to preventive measures

Failure to detect an association with IL1 genotypes in European Caucasians with generalised early onset periodontitis

OBJECTIVES: In order to elucidate the genetic background to EOP it is useful to investigate associations with genetic polymorphisms of immune response genes, whose products play a r le in the inflammatory process. The aim of this study was to examine IL1A and IL1B genetic polymorphisms in unrelated European white Caucasian patients with generalised early-onset periodontitis (GEOP). MATERIAL AND METHODS: Polymerase chain reaction (PCR) amplification of the ILIA (-889) gene and IL1B (+3953) gene (56 patients, 56 controls) was carried out and PCR products subjected to restriction fragment length polymorphism (RFLP) analysis. RESULTS: There were no significant differences between patients and controls for any of the genotype or allele frequencies investigated (p = 1.0). Smoking status was also included as a covariate but this did not alter the results. Furthermore, expression of the composite genotype described by Kornman and coworkers was also investigated in these subjects. No significant differences were found between patients and controls whether smoking was included as a covariate or not. CONCLUSION: The lack of any association between the IL1 polymorphisms and GEOP, in the population presented here, brings into doubt the usefulness of these candidate genes as markers of susceptibility to this form of periodontitis