The symposium highlighted the principles underlying the emergence of collective properties in biology, taking a look at themes such as coordination, cooperation, interaction, and decision-making. Discussions spanned a wide range of systems, from bacterial biofilms and cytoskeletal networks to cell migration, tissue formation, disease models, and animal behaviour. Among the many excellent poster presentations, two stood out and were recognised with poster prizes. Congratulations, Max and Laura!<\/p>\n\n\n\n
Continuous turnover of regulatory T cells enables rapid immune morphogenesis<\/h2>\n\n\n\n
<\/p>\n\n\n\n
Presenter: Max Brambach<\/strong><\/p>\n\n\n\n Authors: Max Brambach, Alon Oyler-Yaniv, Jennifer Oyler-Yaniv<\/p>\n\n\n\n <\/p>\n\n\n\n Abstract:<\/strong><\/p>\n\n\n\n Effective immune responses must act rapidly to control pathogens. Immune tolerance mechanisms must act even faster to intercept inappropriate activations. An established model of immune tolerance is that self-activated T cells (Tconv) produce interleukin-2 (IL-2) upon antigen recognition, which drives the proliferation of local regulatory T cells (Tregs) that suppresses Tconv expansion. In this view, IL-2 acts as the central mitogenic signal. However, in this model Treg expansion necessarily acts on the same time scale as Tconv proliferation raising the question of how suppression can be deployed rapidly enough to pre-empt inappropriate responses.<\/p>\n\n\n\n Here, we use a quantitative in vitro suppression assay, mathematical modelling and in vivo analyses to disentangle the signals that control Treg survival, proliferation and suppressive function. We find that IL-2 is not a mitogen for Tregs but instead acts as a survival signal. Restricting IL-2 leads to rapid Treg loss, while adding IL-2 sustains Tregs long-term. By contrast, we found that T cell receptor (TCR) signaling regulates Treg proliferation and suppressive capacity, consistent with recognition of self-antigens.<\/p>\n\n\n\n These findings imply a revised logic of Treg homeostasis. Self-antigens are abundantly presented to Tregs in vivo, driving them into the cell cycle and their survival depends on stochastic \u2018bursts\u2019 of IL-2 produced by self-activated Tconvs. This model predicts rapid Treg turnover sustained by transient, localized IL-2 availability, consistent with prior observations of high Treg proliferation and apoptosis in vivo.<\/p>\n\n\n\n Why maintain such energetically costly dynamics? Using mathematical modelling, we show that continuous cycling confers a kinetic advantage by enabling Tregs to rapidly accumulate and form suppressive microenvironments immediately following antigen encounter, outpacing the activation and expansion of Tconvs. In this revised model, tolerance is enforced not through IL-2\u2013driven expansion, but through antigen-driven cycling combined with survival gating.<\/p>\n\n\n\n Together, these findings highlight Treg turnover as a design feature of immune regulation and suggest that selective modulation of Treg survival, rather than global inhibition of suppressive function, may provide a route to tune local tolerance, including in contexts such as tumor immunity.<\/p>\n\n\n\n <\/p>\n\n\n\n View poster<\/a><\/p>\n\n\n\n <\/p>\n\n\n\n![\"\"](\"https:\/\/www.embl.org\/about\/info\/course-and-conference-office\/wp-content\/uploads\/Max-Brambach-819x1024.jpg\")
Harvard Medical School, USA
<\/figcaption><\/figure>\n\n\n\n
\n\n\n\nTracking the growth vs. defense trade off of bacterial collectives under protistan predation<\/strong><\/h2>\n\n\n\n
![\"\"](\"https:\/\/www.embl.org\/about\/info\/course-and-conference-office\/wp-content\/uploads\/Laura-Sanchis-819x1024.jpg\")