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Retraction of “Cooperative Fe/Co-Catalyzed Remote Desaturation for the Synthesis of Unsaturated Amide Derivatives”
Measurement of interfacial thermal resistance in high-energy-density matter
Comfort, consistency, and efficiency of garments with textile electrodes versus hydrogel electrodes for neuromuscular electrical stimulation in a randomized crossover trial
Magneto-ionic vortices: voltage-reconfigurable swirling-spin analog-memory nanomagnets
Assessing the influence of olive waste on the filtration properties, elasticity, porosity, and strength of oil well cement
Author Correction: Isotopic evidence for initial coastal colonization and subsequent diversification in the human occupation of Wallacea
Early prediction of CKD from time series data using adaptive PSO optimized echo state networks
Author Correction: Atypical function of a centrosomal module in WNT signalling drives contextual cancer cell motility
Development of hypoeutectic SnBi alloy solder reinforced with WO3 nanoparticles for connecting Cu substrates via thermal bonding
CD301b+ dendritic cell-derived IL-2 dictates CD4+ T helper cell differentiation
Abstract T helper (Th) cell differentiation is fundamental to functional adaptive immunity. Different subsets of dendritic cells (DC) preferentially induce different types of Th cells, but the DC-derived mechanism for Th type 2 (Th2) differentiation is not fully understood. Here, we show that in mice, CD301b+ DCs, a major Th2-inducing DC subset, drive Th2 differentiation through cognate interaction by rapidly inducing IL-2 receptor signalling in CD4+ T cells. Mechanistically, CD40 engagement prompts IL-2 production selectively from CD301b+ DCs to maximize CD25 expression in CD4+ T cells, which instructs the Th2 fate decision, while simultaneously skewing CD4+ T cells away from the T follicular helper fate. Moreover, CD301b+ DCs utilize their own CD25 to facilitate directed action of IL-2 toward cognate CD4+ T cells, as genetic deletion of CD25 in CD301b+ DCs results in reduced IL-2-mediated signalling in antigen-specific CD4+ T cells and hence their Th2 differentiation. These results highlight the critical role of DC-intrinsic CD40–IL-2 axis in Th cell fate decision.
Research on a hybrid model for flood probability prediction based on time convolutional network and particle swarm optimization algorithm
Dual-function regulator MexL as a target to control phenazines production and pathogenesis of Pseudomonas aeruginosa
Ivermectin causes adverse effects on the metabolic rate and thermoregulatory capacity of Dung beetles
Expectation violations signal goals in novel human communication
Abstract Communication, often grounded in shared expectations, faces challenges when a Sender and Receiver lack a common linguistic background. Our study explores how people instinctively turn to the fundamental principles of the physical world to overcome such barriers. Specifically, through an experimental game in which Senders convey messages via trajectories, we investigate how they develop novel strategies without relying on common linguistic cues. We build a computational model based on the principle of expectancy violations and a set of common universal priors derived from movement kinetics. The model replicates participant-designed messages with high accuracy and shows how its core variable—surprise—predicts the Receiver’s physiological and neuronal responses in brain areas processing expectation violations. This work highlights the adaptability of human communication, showing how surprise can be a powerful tool in forming new communicative strategies without relying on common language.
Advanced synthesis, comprehensive characterization, and potent cytotoxicity of 2,6-Bis(2-aminophenylimino)methyl)-4-methoxyphenol and its binuclear copper(II) complex
Structure, motion, and multiscale search of traveling networks
Nutritional and qualitative comparison of temperate fruits from conventional and organic orchards
Unused housing in urban China and its carbon emission impact
MultiObjective optimization of the design of a protective components to chassis protection module for unmanned armored vehicles
Migration arrest and transendothelial trafficking of human pathogenic-like Th17 cells are mediated by differentially positioned chemokines
Abstract Human Th17/type 17 cells express the chemokine receptor CCR6, but the functions of CCR6 and other chemokine receptors in human type 17 Th cell extravasation have not been fully delineated. Here we show that human peripheral blood CD4+CCR6+ T cells co-expressing CCR2 have a pathogenic Th17 signature, can produce inflammatory cytokines without T cell receptor activation, and show enhanced expression of pathogenicity-associated and activation-associated genes in the cerebrospinal fluid of patients with multiple sclerosis as compared to controls. In flow chambers with activated endothelial cell (EC) monolayers, CD4+CCR6+CCR2+ T cells are efficient at transendothelial migration (TEM). Ligands for CCR5, CCR6 and CXCR3 localize to EC surfaces and mediate only arrest, whereas CCR2 ligands fail to bind well to ECs and mediate only TEM. Conversely, expressing a chimeric CCR2 ligand engineered to bind glycosaminoglycans on ECs results in CCR2-mediated arrest but blocks TEM induction. Our results from human pathogenic-like type 17 cells thus suggest that T cell migration arrest requires chemokine bound to EC surfaces, whereas TEM requires a transendothelial chemokine gradient.