While infection with HAV induces lifelong immunity in all cases and is mostly asymptomatic in children, it is often symptomatic in adolescents and adults causing acute hepatitis and

may, therefore, represent a substantial medical and economic burden. Prior to the development of HAV vaccines, human plasma immunoglobulin (Ig) from pooled donor IgG was administered as a pre- or post-exposure prophylactic measure, demonstrating the protective role of anti-HAV antibodies in humans. The concentrations of antibody achieved after passive transfer of immunoglobulin (or active induction by vaccination) are 10–100-fold lower than those produced in response to natural Selleckchem Afatinib infection, but are sufficient to protect against overt HAV disease. Experience regarding passive immunisation with Ig showed that individuals were protected with anti-HAV concentrations of 10–20 mIU/mL. However, since no absolute protective level has been defined for HAV, generally the lower limit of detection of the assay being used has been considered as the protective level. With this serological correlate Selleck Alectinib of protection, candidate vaccines against HAV

were rapidly developed and licensed; subsequently their efficacy has been confirmed in a number of studies and immunisation campaigns. Immune correlates of protection, when validated by a demonstrated clinical benefit, are extremely useful to the development of efficacious vaccines. In clinical terms, an AI disease may be defined as a disease in which tissue damage

is mediated by T cells and/or antibodies, resulting from a failure of self-tolerance. AI diseases may be organ-specific or systemic, depending on the organs and tissues affected. However, this is sometimes not a simple distinction, particularly in cases where there is apparent organ specificity despite autoreactive immune responses that target ubiquitous antigens. The innate immune system may contribute to the initial induction of antigen-specific autoreactivity and may participate in the effector mechanisms responsible for tissue damage, but activated T cells, antibodies, or both must also be detected many to establish a diagnosis of AI disease. From an immunological perspective, there is little evidence that vaccinations cause AI diseases – the pathological mechanisms underlying these diseases include complex features such as a genetic predisposition and chronic inflammation. Damage to target organs and tissues is usually the result of infiltration by activated immune cells and their subsequent cytokine production – the immune response is no longer regulated, leading to systemic disruption of physiological functions.