Five experiments were conducted with a twofold aim: firstly, examine the normativeness of some important features of Western individualism, and secondly, determine what aspect of social value serves as the anchor for their potential normativeness. Five key constituents of individualism were studied. A questionnaire composed of five sub-questionnaires was used, each one referring to an 'individualistic' constituent and to its opposing 'collectivistic' referent. Two main paradigms in the judgment-norm approach were implemented, one implying self-presentation strategies and the other implying social judgments. Together, the results revealed that only three constituents of individualism can be considered normative-self-sufficiency, individual anchoring, and internality-and that one of the constituents-the primacy of individual goals-is not normative at all, and may be even counternormative. The results pointed out an individualistic pattern that is much less homogeneous than often assumed.

m e norm of internality is defined as a social valorization

A 44-year-old Caucasian woman with no history of diabetes was admitted to the emergency department in 2014 for vomiting and confusion, with polyuria, polydipsia, and a very recent weight loss (15 days). Biological tests revealed severe hyperglycemia and diabetic ketoacidosis (glycemia 50.45 mmol/L, ketones 31, pH 7.25, HCO 3 2 3 mEq/L), with acute renal failure (39 mL/min/1.73 m 2

Interstitial lung disease (ILD) is a complex and heterogeneous disorder that is often associated with autoimmune syndromes (1). Despite the connection between ILD and autoimmunity, it remains unclear whether ILD can develop from an autoimmune response that specifically targets the lung parenchyma. Here, we utilized a severe form of autoimmune disease, Autoimmune Polyglandular Syndrome Type 1 (APS1), to establish a strong link between an autoimmune response to the lung-specific protein BPIFB1 and clinical ILD. Screening of a large cohort of APS1 patients revealed autoantibodies to BPIFB1 in 9.6% of APS1 subjects overall and in 100% of APS1 subjects with ILD. Further investigation of ILD outside the APS1 disorder revealed BPIFB1 autoantibodies specifically present in 14.6% of patients with connective tissue disease-associated ILD and in 12.0% of patients with idiopathic ILD. Utilizing the animal model for APS1 to examine the mechanism of ILD pathogenesis, we found that Aire−/− mice harbor autoantibodies to a similar lung antigen named BPIFB9 that are a marker for ILD, and determined that a defect in thymic tolerance is responsible for the production of BPIFB9 autoantibodies and the development of ILD. Importantly, we also found that immunoreactivity targeting BPIFB1 independent of a defect in Aire also leads to ILD, consistent with our discovery of BPIFB1 autoantibodies in non-APS1 patients. Overall, our results demonstrate that autoimmunity targeting the lung-specific antigen BPIFB1 may be important to the pathogenesis of ILD in patients with APS1 and in subsets of patients with non-APS1 ILD, demonstrating the role of lung-specific autoimmunity in the genesis of ILD.