Purpose of review: System biology is an interdisciplinary approach with the purpose to evaluate the experimental results of ‘-omics’ sciences as a whole. The ‘-omics’ sciences do not start generally from a-priori assumptions and are aimed to study the constituents of a specific biological domain (genome, transcriptome, proteome and metabolome) in a given state, using different high-throughput technologies (as polymerase chain reaction, arrays, liquid chromatography, mass spectrometry, etc.) and allowing a hermeneutical integration and recomposition of the experimental information. The aim of the present review is to explore the main new findings of system biology studies applied to sarcoidosis in the last year. Recent findings: The main new findings of sarcoidosis that were highlighted by different studies in the last year (including miRNAs, TGF-β pathway, TNF-α and related proteins, vesicle trafficking, vitamin D and lipid metabolism, analyzed by system biology) are presented in this article. Summary: System biology is a useful approach to combine different experimental results to study the pathogenesis of sarcoidosis and to identify groups of new molecules and mediators with potential clinical application as biomarkers.

Purpose of review: We review the newly formulated and published research classification criteria for interstitial pneumonia with autoimmune features and appraise these criteria in light of findings from recent investigations. Recent findings: Previous studies demonstrated that interstitial pneumonia may be caused by an autoimmune process with a variety of names and criteria utilized for this entity. To standardize terminology and provide a definition for future research, a multidisciplinary task force formulated criteria by which patients with interstitial lung disease and autoimmune features might be recognized. The interstitial pneumonia with autoimmune features criteria require the presence of an interstitial pneumonia on chest imaging or surgical lung biopsy, exclusion of an alternate cause, the absence of a defined connective tissue disease and at least one feature suggestive of autoimmunity from at least two of three domains: clinical with specific extra-thoracic features, serologic with positive autoantibodies and morphologic as demonstrated by chest imaging, histopathology, or multicompartment involvement. Although recent studies provide insight into features of significance, these criteria have not undergone formal validation. Summary: A uniform name and set of research criteria for interstitial pneumonia with autoimmune features may identify patients with treatment responsive interstitial lung disease and an improved prognosis. These criteria require validation before they can be applied in the clinical setting.

Purpose of review: In a chronic, progressive and ultimately fatal disease like idiopathic pulmonary fibrosis (IPF), the maintenance of patients’ quality of life should be regarded as a major aim of treatment. Although better knowledge and two antifibrotic drugs are now available in IPF, the individual response to treatment and its acceptance remain poorly explored. This review summarizes recent advances in research on patient-reported outcomes and their measures, indispensable instruments to investigate how patients feel and function, and how the disease impacts their lives. Recent findings: In IPF, there is a paucity of specific well-validated patient-reported outcome measures (PROMs). The use of generic PROMs in past IPF trials revealed a poor correlation of such questionnaires with established endpoints of treatment response. Several attempts are currently ongoing to develop specific IPF PROMs. The King's Brief Interstitial Lung Disease health status questionnaire and the Tool to Assess Quality of Life in IPF are promising questionnaires developed by using institutional recommendations and are currently being validated in large cohorts. Summary: Well-validated relevant PROMs can be employed for multiple purposes: as outcome measures for daily care or for driving therapeutic decisions, as efficacy endpoints in clinical trials, or as tools to collect useful data for healthcare policy makers in order to improve access and quality of care.

Purpose of review: The pathogenesis of genetically complex granulomatous diseases, such as sarcoidosis and latent tuberculosis, remains largely unknown. With the recent advent of more powerful research tools, such as genome-wide expression platforms, comes the challenge of making sense of the enormous data sets so generated. This manuscript will provide demonstrations of how in-silico (computer) analysis of large research data sets can lead to novel discoveries in the field of granulomatous lung disease. Recent findings: The application of in-silico research tools has led to novel discoveries in the fields of noninfectious (e.g., sarcoidosis) and infectious granulomatous diseases. Computer models have identified novel disease mechanisms and can be used to perform ‘virtual’ experiments rapidly and at low cost compared with conventional laboratory techniques. Summary: Granulomatous lung diseases are extremely complex, involving dynamic interactions between multiple genes, cells, and molecules. In-silico interpretation of large data sets generated from new research platforms that are capable of comprehensively characterizing and quantifying pools of biological molecules promises to rapidly accelerate the rate of scientific discovery in the field of granulomatous lung disorders.