Summary Foxp3+ CD4+ regulatory T cells (Tregs) are an immune cell lineage endowed with immunosuppressive functionality in a wide array of contexts, including both anti‐pathogenic and anti‐self responses. In the past decades, our understanding of the functional diversity of circulating or lymphoid Tregs has grown exponentially. Only recently, the importance of Tregs residing within non‐lymphoid tissues, such as visceral adipose tissue, muscle, skin and intestine, has been recognized. Not only are Tregs critical for influencing the kinetics and strength of immune responses, but the regulation of non‐immune or parenchymal cells, also fall within the purview of tissue‐resident or infiltrating Tregs. This review focuses on providing a systematic and comprehensive comparison of the molecular maintenance, local adaptation and functional specializations of Treg populations operating within different tissues.

Adler et al. (2016) raise some controversial issues about whether performance rating systems should be eliminated or not. We strongly believe that the decision to do away with performance ratings is premature because more research needs to be done, as suggested by “the better questions” that Adler et al. listed at the end of the focal article. We propose that those questions can be extended further by testing them in other cultures and supplemented with these questions: When, how, and why do cultural values influence performance management? Given the nature of our increasingly diverse workforce in which employees with different cultural values work together within the same organization, it is crucial to identify and document the influence of culture on performance appraisal practices. In this commentary, we briefly summarize research to date on the influence of cultural values on performance management and identify some important future research directions.

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Solar ultraviolet radiation (UVR) is a major source of skin damage, resulting in inflammation, premature ageing and cancer. While several UVR-induced changes, including extracellular matrix reorganisation and epidermal DNA damage, have been documented, the role of different fibroblast lineages and their communication with immune cells has not been explored. We show that acute and chronic UVR exposure led to selective loss of fibroblasts from the upper dermis in human and mouse skin. Lineage tracing and in vivo live imaging revealed that repair following acute UVR is predominantly mediated by papillary fibroblast proliferation and fibroblast reorganisation occurs with minimal migration. In contrast, chronic UVR exposure led to a permanent loss of papillary fibroblasts, with expansion of fibroblast membrane protrusions partially compensating for the reduction in cell number. Although UVR strongly activated Wnt-signalling in skin, stimulation of fibroblast proliferation by epidermal b-catenin stabilisation did not enhance papillary dermis repair. Acute UVR triggered an infiltrate of neutrophils and T cell subpopulations and increased pro-inflammatory prostaglandin signalling in skin. Depletion of CD4 and CD8 positive cells resulted in increased papillary fibroblast depletion, which correlated with an increase in DNA damage, pro-inflammatory prostaglandins and reduction in fibroblast proliferation. Conversely, topical COX-2 inhibition prevented fibroblast depletion and neutrophil infiltration after UVR. We conclude that loss of papillary fibroblasts is primarily induced by a deregulated inflammatory response, with infiltrating T cells supporting fibroblast survival upon UVR-induced environmental stress.