Autoimmunity in 2012

The initiation and perpetuation of autoimmunity recognize numerous checkpoints, from the genomic susceptibility to the breakdown of tolerance. This latter phenomenon includes the loss of B cell anergy and T regulatory cell failure, as well as the production of autoantibodies and autoreactive T cells. These mechanisms ultimately lead to tissue injury via different mechanisms that span from the production of proinflammatory cytokines to the chemotaxis of immune cells to the target sites. The pathways to autoimmunity have been widely investigated over the past year and resulted in a number of articles in peer-reviewed journals that has increased by nearly 10 % compared to 2011. We herein follow on the attempt to provide a brief discussion of the majority of articles on autoimmune diseases that were published in the major immunology journals in the previous solar year. The selection is necessarily arbitrary and may thus not be seen as comprehensive but reflects current research trends. Indeed, 2012 articles were mostly dedicated to define new and old mechanisms with potential therapeutic implications in autoimmunity in general, though based on specific clinical conditions or animal models. As paradigmatic examples, the environmental influence on autoimmunity, Th17 changes modulating the autoimmune response, serum autoantibodies and B cell changes as biomarkers and therapeutic targets were major issues addressed by experimental articles in 2012. Further, a growing number of studies investigated the sex bias of autoimmunity and supported different working hypotheses to explain the female predominance, including sex chromosome changes and reproductive life factors. In conclusion, the resulting scenario illustrates that common factors may underlie different autoimmune diseases and this is well represented by the observed alterations in interferon-α and TGFβ or by the shared signaling pathways.