PurposeThis study investigates whether the COVID-19 pandemic has led to an acceleration of the digital transformation in the workplace.Design/methodology/approachThis study is based on a survey conducted during the COVID-19 pandemic from March to April 2020 on the crowdsourcing platform Amazon Mechanical Turk.FindingsThe findings show an increase of people working from home offices and that many people believe that digital transformation of work has accelerated in response to the COVID-19 pandemic. People who noted this acceleration can imagine working digitally exclusively in the future. Moreover, the importance of traditional jobs as a secure source of income has decreased, and digital forms of work as a secure source of income have increased because of the COVID-19 pandemic. Workers believe that digital work will play a more important role as a secure source of income in the future than traditional jobs.Research limitations/implicationsBecause the survey was conducted online, respondents may have had a certain affinity for digital work.Originality/valueThis study assesses the consequences of the COVID-19 pandemic on the future of work, showing that changes in the perception of digital transformation and the willingness to work exclusively in a digital manner have arisen as result of the COVID-19 pandemic. To estimate the long-term consequences of the pandemic on the digitisation of work, research that includes macroeconomic consequences in its forecast is necessary.

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Here we show that soluble CD83 induces the resolution of inflammation in an antigen-induced arthritis (AIA) model. Joint swelling and the arthritis-related expression levels of IL-1β, IL-6, RANKL, MMP9, and OC-Stamp were strongly reduced, while Foxp3 was induced. In addition, we observed a significant inhibition of TRAP+ osteoclast formation, correlating with the reduced arthritic disease score. In contrast, cell-specific deletion of CD83 in human and murine precursor cells resulted in an enhanced formation of mature osteoclasts. RNA sequencing analyses, comparing sCD83- with mock treated cells, revealed a strong downregulation of osteoclastogenic factors, such as Oc-Stamp, Mmp9 and Nfatc1, Ctsk, and Trap. Concomitantly, transcripts typical for pro-resolving macrophages, e.g., Mrc1/2, Marco, Klf4, and Mertk, were upregulated. Interestingly, members of the metallothionein (MT) family, which have been associated with a reduced arthritic disease severity, were also highly induced by sCD83 in samples derived from RA patients. Finally, we elucidated the sCD83-induced signaling cascade downstream to its binding to the Toll-like receptor 4/(TLR4/MD2) receptor complex using CRISPR/Cas9-induced knockdowns of TLR4/MyD88/TRIF and MTs, revealing that sCD83 acts via the TRIF-signaling cascade. In conclusion, sCD83 represents a promising therapeutic approach to induce the resolution of inflammation and to prevent bone erosion in autoimmune arthritis.

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