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Peatlands play an important role in the global carbon cycle as they contain a large soil carbon stock. However, current climate change could potentially shift peatlands from being carbon sinks to carbon sources. Remote sensing methods provide an opportunity to monitor carbon dioxide (CO2) exchange in peatland ecosystems at large scales under these changing conditions. In this study, we developed empirical models of the CO2 balance (net ecosystem exchange, NEE), gross primary production (GPP), and ecosystem respiration (ER) that could be used for upscaling CO2 fluxes with remotely sensed data. Two to three years of eddy covariance (EC) data from five peatlands in Sweden and Finland were compared to modelled NEE, GPP and ER based on vegetation indices from 10 m resolution Sentinel-2 MSI and land surface temperature from 1 km resolution MODIS data. To ensure a precise match between the EC data and the Sentinel-2 observations, a footprint model was applied to derive footprint-weighted daily means of the vegetation indices. Average model parameters for all sites were acquired with a leave-one-out-cross-validation procedure. Both the GPP and the ER models gave high agreement with the EC-derived fluxes (R2 = 0.70 and 0.56, NRMSE = 14% and 15%, respectively). The performance of the NEE model was weaker (average R2 = 0.36 and NRMSE = 13%). Our findings demonstrate that using optical and thermal satellite sensor data is a feasible method for upscaling the GPP and ER of northern boreal peatlands, although further studies are needed to investigate the sources of the unexplained spatial and temporal variation of the CO2 fluxes.

The high-resolution Sentinel-2 data potentially enable the estimation of gross primary productivity (GPP) at finer spatial resolution by better capturing the spatial variation in a heterogeneous landscapes. This study investigates the potential of 10 m resolution reflectance from the Sentinel-2 Multispectral Instrument to improve the accuracy of GPP estimation across Nordic vegetation types, compared with the 250 m and 500 m resolution reflectance from the Moderate Resolution Imaging Spectroradiometer (MODIS). We applied linear regression models with inputs of two-band enhanced vegetation index (EVI2) derived from Sentinel-2 and MODIS reflectance, respectively, together with various environmental drivers to estimate daily GPP at eight Nordic eddy covariance (EC) flux tower sites. Compared with the GPP from EC measurements, the accuracies of modelled GPP were generally high (R2 = 0.84 for Sentinel-2; R2 = 0.83 for MODIS), and the differences between Sentinel-2 and MODIS were minimal. This demonstrates the general consistency in GPP estimates based on the two satellite sensor systems at the Nordic regional scale. On the other hand, the model accuracy did not improve by using the higher spatial-resolution Sentinel-2 data. More analyses of different model formulations, more tests of remotely sensed indices and biophysical parameters, and analyses across a wider range of geographical locations and times will be required to achieve improved GPP estimations from Sentinel-2 satellite data.

T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We aimed to characterize the function of the lincRNA Myocardial Infarction Associated Transcript (MIAT) during early human Th17 cell differentiation. We found MIAT to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. STAT3, a key regulator of Th17 differentiation, directly bound to the MIAT promoter and induced its expression during the early stages of Th17 cell differentiation. MIAT resides in the nucleus and regulates the expression of several key Th17 genes, including IL17A, IL17F, CCR6 and CXCL13, possibly by altering the chromatin accessibility of key loci, including IL17A locus. Further, MIAT regulates the expression of protein kinase C alpha (PKCα), an upstream regulator of IL17A. A reanalysis of published single-cell RNA-seq data showed that MIAT was expressed in T cells from the synovium of RA patients. Our results demonstrate that MIAT contributes to human Th17 differentiation by upregulating several genes implicated in Th17 differentiation. High MIAT expression in T cells of RA patient synovia suggests a possible role of MIAT in Th17 mediated autoimmune pathologies.