The mechanisms leading to the onset and perpetuation of systemic and tissue-specific autoimmune diseases are complex, and numerous hypotheses have been proposed or confirmed over the past 12 months. It is particularly of note that the number of articles published during 2011 in the major immunology and autoimmunity journals increased by 3 % compared to the previous year. The present article is dedicated to a brief review of the reported data and, albeit not comprehensive of all articles, is aimed at identifying common and future themes. First, clinical researchers were particularly dedicated to defining refractory forms of diseases and to discuss the use and switch of therapeutic monoclonal antibodies in everyday practice. Second, following the plethora of genome-wide association studies reported in most multifactorial diseases, it became clear that genomics cannot fully explain the individual susceptibility and additional environmental or epigenetic factors are necessary. Both these components were widely investigated, both in organ-specific (i.e., type 1 diabetes) and systemic (i.e., systemic lupus erythematosus) diseases. Third, a large number of 2011 works published in the autoimmunity area are dedicated to dissect pathogenetic mechanisms of tolerance breakdown in general or in specific conditions. While our understanding of T regulatory and Th17 cells has significantly increased in 2011, it is of note that most of the proposed lines of evidence identify potential targets for future treatments and should not be overlooked
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