A systematic study is presented of decadal climate variability in the North Pacific. In particular, the hypothesis is addressed that oceanic Rossby basin modes are responsible for enhanced energy at decadal and bidecadal time scales. To this end, a series of statistical analyses are performed on a 500-yr control integration of the Community Climate System Model, version 3 (CCSM3). In particular, a principal oscillation pattern (POP) analysis is performed to identify modal behavior in the subsurface pressure field. It is found that the dominant energy of sea surface temperature (SST) variability at 25 yr (the model equivalent of the Pacific decadal oscillation) cannot be explained by the resonant excitation of an oceanic basin mode. However, significant energy in the subsurface pressure field at time scales of 17 and 10 yr appears to be related to internal ocean oscillations. However, these oscillations lack the characteristics of the classical basin modes, and must either be deformed beyond recognition by the background circulation and inhomogeneous stratification or have another dynamical origin altogether. The 17-yr oscillation projects onto the Pacific decadal oscillation and, if present in the real ocean, has the potential to enhance the predictability of low-frequency climate variability in the North Pacific. © 2013 American Meteorological Society.

Using the Community Earth System Model, we explore the role of human land use and land cover change (LULCC) in modifying the terrestrial carbon budget in simulations forced by Representative Concentration Pathway 8.5, extended to year 2300. Overall, conversion of land (e.g., from forest to croplands via deforestation) results in a model-estimated, cumulative carbon loss of 490 Pg C between 1850 and 2300, larger than the 230 Pg C loss of carbon caused by climate change over this same interval. The LULCC carbon loss is a combination of a direct loss at the time of conversion and an indirect loss from the reduction of potential terrestrial carbon sinks. Approximately 40% of the carbon loss associated with LULCC in the simulations arises from direct human modification of the land surface; the remaining 60% is an indirect consequence of the loss of potential natural carbon sinks. Because of the multicentury carbon cycle legacy of current land use decisions, a globally averaged amplification factor of 2.6 must be applied to 2015 land use carbon losses to adjust for indirect effects. This estimate is 30% higher when considering the carbon cycle evolution after 2100. Most of the terrestrial uptake of anthropogenic carbon in the model occurs from the influence of rising atmospheric CO2 on photosynthesis in trees, and thus, model-projected carbon feedbacks are especially sensitive to deforestation.

Background

Psoriasis is an inflammatory, IL-17-driven skin disease in which autoantigen-induced CD8⁺ T cells have been identified as pathogenic drivers.

Objective

Our study focused on comprehensively characterizing the phenotypic variation of CD8⁺ T cells in psoriatic lesions.

Methods

We used single-cell RNA sequencing to compare CD8⁺ T-cell transcriptomic heterogeneity between psoriatic and healthy skin.

Results

We identified 11 transcriptionally diverse CD8⁺ T-cell subsets in psoriatic and healthy skin. Among several inflammatory subsets enriched in psoriatic skin, we observed 2 Tc17 cell subsets that were metabolically divergent, were developmentally related, and expressed CXCL13, which we found to be a biomarker of psoriasis severity and which achieved comparable or greater accuracy than IL17A in a support vector machine classifier of psoriasis and healthy transcriptomes. Despite high coinhibitory receptor expression in the Tc17 cell clusters, a comparison of these cells with melanoma-infiltrating CD8⁺ T cells revealed upregulated cytokine, cytolytic, and metabolic transcriptional activity in the psoriatic cells that differed from an exhaustion program.

Conclusion

Using high-resolution single-cell profiling in tissue, we have uncovered the diverse landscape of CD8⁺ T cells in psoriatic and healthy skin, including 2 nonexhausted Tc17 cell subsets associated with disease severity.