BackgroundAutism is a complex polygenic neurodevelopmental disorder characterized by deficits in communication and social interactions as well as specific stereotypical behaviors. Both genetic and environmental factors appear to contribute to the pathogenesis of autism. Accumulating data including changes in immune responses, linkage to major histocompatibility complex antigens, and the presence of autoantibodies to neural tissues/antigens suggest that the immune system plays an important role in its pathogenesis.SummaryIn this brief review, we discuss the data regarding changes in both innate and adaptive immunity in autism and the evidence in favor of the role of the immune system, especially of maternal autoantibodies in the pathogenesis of a subset of patients with autism. The rationale for possible therapeutic use of intravenous immunoglobulin is also discussed.

Yellow nail syndrome (YNS) is a rare disorder of unknown aetiology that is characterized by yellow nails associated with lymphoedema and chronic respiratory manifestations. There are no detailed immunological studies in YNS. In this study, we present first extensive immunological analysis of both adaptive and innate immunity in two patients with YNS. One patient has common variable immunodeficiency, whereas second patient has specific antibody deficiency syndrome. Severe lymphopaenia, a striking deficiency of naïve CD4+ and CD8+ T cells and total B cells, and increased transitional B cells were observed. T cell proliferative response to mitogens and antigens was significantly reduced in both patients. Both patients failed to make specific antibody response to pneumococci. Complement, natural killer cell activity and neutrophil oxidative burst were normal. Immunoglobulin administration resulted in decreased frequency and severity of infections, and an impressive effect was observed on lymphoedema and on the recurrence of pleural effusion. Our data show that YNS is associated with both T and B cell defects. Furthermore, Immunoglobulin may be beneficial in clinical manifestations of lymphoedema.

Infection of newborn mice with Herpesvirus hominis type 2 (HVH-2) was used as an experimental model of disseminated HVH infection in newborn humans. Mice were challenged with 103 plaque-forming units of HVH-2 intranasally and were then given 0.2 ml of rabbit serum intraperitoneally. Passive immunization with rabbit anti-HVH-2 serum resulted in a significant decrease in mortality and prolongation of survival time. This effect correlated with the neutralizing antibody titer of the serum against HVH-2 and was more pronounced when immune serum was administered 1 h after infection as compared with 24 h. These results suggest that administration of high-titer anti-HVH-2 immunoglobulins shortly after delivery could afford significant protection to the newborn of a mother with genital HVH-2 infection.