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This study investigates the inter‐model spread of climatological extratropical westerly jets in boreal winter, using the historical simulation of 52 Coupled Model Intercomparison Project phase 6 (CMIP6) models from 1851 to 2014. The results show that there is a substantial spread in the latitude of the upper‐tropospheric westerly jet across models, characterised by large inter‐model standard deviations to both the poleward and equatorward sides of the jet axis, although the multi‐model ensemble mean (MME) performs well in simulating meridional position of westerly jets. Furthermore, we detect the consistency of inter‐model jet position spread between the Northern and Southern Hemispheres, based on the inter‐model empirical orthogonal function (EOF) decomposition and correlation of regional‐averaged zonal winds. Specifically, the models that simulate the westerly jets poleward/equatorward relative to the MME position in one hemisphere also tend to simulate the jets poleward/equatorward in the other hemisphere. Accordingly, we define a global jet spread index to depict the concurrence of jet shift in the two hemispheres. The results of inter‐model regression analyses based on this index indicate that the models positioning the jets poleward than the MME tend to simulate a wider Hadley Cell, a poleward‐shifted Ferrel Cell in the Southern Hemisphere, enhanced precipitation in the subtropics and suppressed precipitation in the tropics, and warmer sea surface temperatures in the subtropics and mid‐latitudes. The present results suggest that improving the simulation of jet positions in climate models requires a comprehensive consideration of thermal states in the tropics and subtropics/mid latitudes. [ABSTRACT FROM AUTHOR]

Fire is the primary form of terrestrial ecosystem disturbance on a global scale and an important Earth system process. Most Earth system models (ESMs) have incorporated fire modeling, with 19 of them submitting model outputs of fire-related variables to the Coupled Model Intercomparison Project Phase 6 (CMIP6). This study provides the first comprehensive evaluation of CMIP6 historical fire simulations by comparing them with multiple satellite-based products and charcoal-based historical reconstructions. Our results show that most CMIP6 models simulate the present-day global burned area and fire carbon emissions within the range of satellite-based products. They also capture the major features of observed spatial patterns and seasonal cycles, the relationship of fires with precipitation and population density, and the influence of the El Niño–Southern Oscillation (ENSO) on the interannual variability of tropical fires. Regional fire carbon emissions simulated by the CMIP6 models from 1850 to 2010 generally align with the charcoal-based reconstructions, although there are regional mismatches, such as in southern South America and eastern temperate North America prior to the 1910s and in temperate North America, eastern boreal North America, Europe, and boreal Asia since the 1980s. The CMIP6 simulations have addressed three critical issues identified in CMIP5: (1) the simulated global burned area being less than half of that of the observations, (2) the failure to reproduce the high burned area fraction observed in Africa, and (3) the weak fire seasonal variability. Furthermore, the CMIP6 models exhibit improved accuracy in capturing the observed relationship between fires and both climatic and socioeconomic drivers and better align with the historical long-term trends indicated by charcoal-based reconstructions in most regions worldwide. However, the CMIP6 models still fail to reproduce the decline in global burned area and fire carbon emissions observed over the past 2 decades, mainly attributed to an underestimation of anthropogenic fire suppression, and the spring peak in fires in the Northern Hemisphere mid-latitudes, mainly due to an underestimation of crop fires. In addition, the model underestimates the fire sensitivity to wet–dry conditions, indicating the need to improve fuel wetness estimation. Based on these findings, we present specific guidance for fire scheme development and suggest a post-processing methodology for using CMIP6 multi-model outputs to generate reliable fire projection products. [ABSTRACT FROM AUTHOR]

An important factor in the development of type 1 diabetes (T1D) is the deficiency of inhibitory immune checkpoint ligands, specifically programmed cell death ligand 1 (PD-L1) and galectin-9 (Gal-9), in β-cells. Therefore, modulation of pancreas-infiltrated T lymphocytes by exogenous PD-L1 or Gal-9 is an ideal approach for treating new-onset T1D. We genetically engineered macrophage cells to generate artificial extracellular vesicles (aEVs) overexpressing PD-L1 and Gal-9, which could restrict islet autoreactive T lymphocytes and protect β-cells from destruction. Intriguingly, overexpression of Gal-9 stimulated macrophage polarization to the M2 phenotype with immunosuppressive attributes. Alternatively, both PD-L1– and Gal-9–presenting aEVs (PD-L1–Gal-9 aEVs) favorably adhered to T cells via the interaction of programmed cell death protein 1/PD-L1 or T-cell immunoglobulin mucin 3/Gal-9. Moreover, PD-L1–Gal-9 aEVs prominently promoted effector T-cell apoptosis and splenic regulatory T (Treg) cell formation in vitro. Notably, PD-L1–Gal-9 aEVs efficaciously reversed new-onset hyperglycemia in NOD mice, prevented T1D progression, and decreased the proportion and activation of CD4+ and CD8+ T cells infiltrating the pancreas, which together contributed to the preservation of residual β-cell survival and mitigation of hyperglycemia. Article Highlights: Destruction of pancreatic β-cells by autoreactive CD4+ and CD8+ T cells is the main cause of type 1 diabetes (T1D); therefore, stunting autoreactive T cells is an effective strategy to alleviate T1D. Modulating the infiltration of T lymphocytes in the pancreas with exogenous programmed cell death ligand 1 (PD-L1) or galectin-9 (Gal-9) is an optimal treatment strategy for newly diagnosed T1D. PD-L1– and Gal-9–presenting (PD-L1–Gal-9) artificial extracellular vesicles (aEVs) exhibit characteristics of M2-type macrophages and efficaciously declined the proportion and activation of CD4+ and CD8+ T cells infiltrating the pancreas. PD-L1–Gal-9 aEVs demonstrated immunosuppressive therapeutic effects and effectively alleviated hyperglycemia in NOD mice with new-onset T1D. [ABSTRACT FROM AUTHOR]

Immune intervention of B cell activation to blockade the production of autoantibodies provokes intense interest in the field of systemic lupus erythematosus (SLE) therapy development. Although the survival rate for SLE is improved, many patients die untimely. Engineered cell membrane vesicles manifest remarkable capacity of targeted drug delivery and immunomodulation of immune cells such as B cells. Herein, this work engineered cellular nanovesicles (NVs) presenting CD40 (CD40 NVs) that can blunt B cells and thus alleviate SLE. CD40 NVs disrupt the CD40/CD40 ligand (CD40L) costimulatory signal axis through the blockade of CD40L on CD4+ T cells. Therefore, the CD40 NVs restrain the generation of the germinal center structure and production of antibodies from B cells. Furthermore, immunosuppressive drug mycophenolate mofetil (MMF) is also encapsulated in the vesicles (MMF‐CD40 NVs), which is employed to deplete immunocytes including B cells, T cells, and dendritic cells. Together, CD40 NVs are promising formulations for relieving autoimmunity and lupus nephritis in MRL/lpr mice. [ABSTRACT FROM AUTHOR]