Hypersensitivity pneumonitis: antigen diversity and disease implications

Article in PressHypersensitivity pneumonitis (HP) is an immune-mediated syndrome triggered by inhalation of a wide variety of allergens, to which an individual has previously been sensitized. More than 200 agents responsible for the disease have already been identified; however, HP occurs only in a small number of individuals exposed to causal antigens. The present report provides an overview of the role of antigen role in HP, highlighting its diversity, research methods, and prevention strategies, as well as the impact on disease prognosis following elimination of antigen. HP is an underdiagnosed disease and, therefore, it is difficult to accurately estimate its incidence. Triggering antigens can be divided into six broad categories: bacteria, fungi, mycobacteria, animal and plant proteins, chemicals, and metals, represented by disease prototypes. The identification of causal antigen is a major challenge; it is impossible to obtain in about 30-60% of cases. The acute form of HP, with early detection and immediate eviction of causal antigen, tends to have an excellent prognosis. In the chronic form, partial recovery of disease is still possible; however, some cases tend to progress to fibrosis, even after removal from exposure. In conclusion, HP diagnosis should be based on a proactive search for potential antigen sources, although their identification is hampered by the lack of standardized methods of demonstrating the specific antigen sensitization. Antigen avoidance is a critical determinant in disease prognosis.(undefined)info:eu-repo/semantics/acceptedVersio

Insulin-Specific IgG and IgE Antibody Response in Type I Diabetic Subjects Exclusively Treated with Human Insulin (recombinant DNA)

Bovine and porcine insulins elicit specific antibody response in diabetic subjects after a few months of treatment. In seven type I diabetic individuals who were exclusively treated with human insulin (recombinant DNA) each month, sera were examined for the development of insulin-specific IgG and IgE antibodies. In all patients (except one), IgG antibodies occurred after 2 mo and tended to further increase in concentration after 5–6 mo. IgE antibodies could be detected after 1 mo with a further increase after 2–3 mo and a marked decline thereafter. No patient exhibited allergic symptoms. The results indicate that physicochemical properties of insulin preparations used for treatment and the route of administration are of more importance for immunogenicity than species differences of insulin.</jats:p