Tsuchiya, A. | bioRxiv Science

bioRxiv2026

Theta Dual-Brain Stimulation of rTPJ Shapes Joint Agency

Joint agency, the shared feeling of "we are doing this together", has been linked to inter-brain synchrony, but its causal role in shaping this experience remains unclear. We applied dual transcranial alternating current stimulation (dual-tACS) over the right temporo-parietal junction (rTPJ) to 13 dyads performing an alternating tapping task (target ITI = 0.5 s; 180 deg. relative phase), manipulating in- and anti-phase coupling at theta (6 Hz), alpha (10 Hz), and beta (20 Hz). As a result, tapping in the theta anti-phase condition was significantly slower than the memorized reference tempo, whereas the other stimulation conditions did not influence the inter-tap interval. Meanwhile, the relative phase remained close to 180 deg. across all conditions. In the theta condition, anti-phase stimulation produced significantly lower joint agency than in-phase stimulation. Furthermore, mediation analysis suggested that the inter-tap interval may partially account for the effect of theta dual-brain stimulation on joint agency, although this indirect pathway did not reach statistical significance. These findings suggest that anti-phase theta stimulation over the rTPJ lowers joint agency, possibly by reducing coordination efficiency while preserving the overall 180 deg. alternation structure.

neuroscience↗

bioRxiv2025

Regulatory T cell stability determines the efficiency of bile duct regeneration during cholangitis.

Background and AimsCholangiopathies such as Primary Sclerosing Cholangitis (PSC) cause damage to the bile ducts and fibrosis with no effective cure. A reduction and impairment in the function of regulatory T cells (Tregs) occurs in PSC. Yet, it is currently unknown what consequence this has on bile duct regeneration. We investigate whether Tregs regulate bile duct regeneration and the dynamics of Tregs turnover during bile duct injury. Approach and ResultsWe used the transgenic Foxp3GFPDTR model to mimic reduced Tregs infiltration to the liver during bile duct injury and showed that reduced intrahepatic Tregs limits bile duct regeneration. Fate mapping of Tregs (Foxp3CreERTAi14) showed that Tregs acquire a pro-inflammatory phenotype within the inflammatory microenvironment, even after IL2 mediated Tregs expansion. Ox40L expression correlates with fibrosis in PSC patients. In the 3,5-Diethoxycarbonyl-1,4-Dihydrocollidine (DDC)-diet mouse model of experimental cholangiopathy, combining IL2-complex administration and blocking Ox40L decreases periportal fibrosis level, increases Treg number and reduces the pro-inflammatory phenotype of Tregs. ConclusionsThese results indicate that Tregs mediate cholangiocyte response to biliary injury, and Tregs downregulate Foxp3 and acquire an inflammatory phenotype in an inflammatory microenvironment. Enhancing Treg numbers through IL2 complex administration and blocking Ox40 signalling simultaneously suppress the inflammatory phenotype of Tregs and reduces bile duct damage and fibrosis.

immunology↗