Upregulation of IL-17 immunity and detrimental effects of IL-17 on human islets have been implicated in human type 1 diabetes. In animal models, the plasticity of Th1/Th17 cells contributes to the development of autoimmune diabetes. In this study, we demonstrate that the upregulation of the IL-17 pathway and Th1/Th17 plasticity in peripheral blood are markers of advanced β cell autoimmunity and impaired β cell function in human type 1 diabetes. Activated Th17 immunity was observed in the late stage of preclinical diabetes in children with β cell autoimmunity and impaired glucose tolerance, but not in children with early β cell autoimmunity. We found an increased ratio of IFN-γ/IL-17 expression in Th17 cells in children with advanced β cell autoimmunity, which correlated with HbA1c and plasma glucose concentrations in an oral glucose tolerance test, and thus impaired β cell function. Low expression of Helios was seen in Th17 cells, suggesting that Th1/Th17 cells are not converted thymus-derived regulatory T cells. Our results suggest that the development of Th1/Th17 plasticity may serve as a biomarker of disease progression from β cell autoantibody positivity to type 1 diabetes. These data in human type 1 diabetes emphasize the role of Th1/Th17 plasticity as a potential contributor to tissue destruction in autoimmune conditions.

Vegetative dormancy, that is the temporary absence of aboveground growth for ≥ 1 year, is paradoxical, because plants cannot photosynthesise or flower during dormant periods. We test ecological and evolutionary hypotheses for its widespread persistence. We show that dormancy has evolved numerous times. Most species displaying dormancy exhibit life-history costs of sprouting, and of dormancy. Short-lived and mycoheterotrophic species have higher proportions of dormant plants than long-lived species and species with other nutritional modes. Foliage loss is associated with higher future dormancy levels, suggesting that carbon limitation promotes dormancy. Maximum dormancy duration is shorter under higher precipitation and at higher latitudes, the latter suggesting an important role for competition or herbivory. Study length affects estimates of some demographic parameters. Our results identify life historical and environmental drivers of dormancy. We also highlight the evolutionary importance of the little understood costs of sprouting and growth, latitudinal stress gradients and mixed nutritional modes.

The 5-year cumulative incidence of childhood CD is significantly higher in Finland than in Estonia. Sequential infections early in life may increase the risk for developing CD.

The prevalence of immune-mediated diseases, such as allergies and type 1 diabetes, is on the rise in the developed world. In order to explore differences in the gene expression patterns induced in utero in infants born in contrasting standards of living and hygiene, we collected umbilical cord blood RNA samples from infants born in Finland (modern society), Estonia (rapidly developing society) and the Republic of Karelia, Russia (poor economic conditions). The whole blood transcriptome of Finnish and Estonian neonates differed from their Karelian counterparts, suggesting exposure to toll-like receptor (TLR) ligands and a more matured immune response in infants born in Karelia. These results further support the concept of a conspicuous plasticity in the developing immune system: the environmental factors that play a role in the susceptibility/protection towards immune-mediated diseases begin to shape the neonatal immunity already in utero and direct the maturation in accordance with the surrounding microbial milieu.

Summary Many perennial plants experience prolonged dormancy, meaning they do not grow above‐ground for one or several growing seasons. When plants disappear (fail to sprout) and have not been recorded to re‐emerge, they either have died or are alive and dormant. In demographic studies of such species, researchers have been forced to make assumptions about death versus dormancy. Little is known about the consequences of these assumptions for predictions from the population models used in the studies. Here, we define survival of dormancy‐prone plants in three distinct ways: Separate, Instant and Slow death. In the Separate death model, plants are assumed to die either in emergent or in dormant stages. Death can also be described as a process of disappearance followed by dying, either in the first year below‐ground (Instant death) or with constant mortality rate in any given dormant year (Slow death). Using simulated data with known parameter values, we test whether survival and re‐emergence rates are confounded in these life‐history models. Using a general model and models for two orchid species (Epipactis atrorubens and Isotria medeoloides), we test how different assumptions about dormancy (Instant and Slow death) affect predictions about population dynamics: population growth rate, generation time, relative reproductive values, life expectancies, and sensitivity and elasticity of population growth rate to stage transitions and vital rates. Our results confirm that survival and re‐emergence rates of dormancy‐prone plant species are difficult to estimate; parameters were separable only with the assumptions of Instant and Slow death. Both theoretical and empirical analyses show that the predictions of population growth rate and generation time do not depend on the assumptions made about the fate of the plants after their disappearance. Synthesis. Assumptions about dormancy affect some, but not all predictions, about plant population dynamics. In the studies of species with unobservable stages, assumptions about dormancy should be carefully defined and possible consequences of these assumptions for the predictions of the population model should be evaluated. Nonetheless, if we are only interested in overall population viability, ad hoc models of prolonged dormancy are sufficient as a first step.