From 24 – 27 February, the EMBO | EMBL Symposium ‘Collectivity in living systems‘ brought together 105 on-site and 33 virtual participants to explore how interactions between biological components give rise to complex behaviours across living systems. Alongside the talks and discussions, 46 posters were presented, showcasing new research and offering early-career scientists the opportunity to share their work with the community. Eight fellowships were provided by the EMBL Corporate Partnership Programme and EMBO.

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!

Continuous turnover of regulatory T cells enables rapid immune morphogenesis

Presenter: Max Brambach

Authors: Max Brambach, Alon Oyler-Yaniv, Jennifer Oyler-Yaniv

Abstract:

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.

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.

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 ‘bursts’ 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.

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–driven expansion, but through antigen-driven cycling combined with survival gating.

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.

View poster

Tracking the growth vs. defense trade off of bacterial collectives under protistan predation

Presenter: Laura Sanchis

Authors: Laura Sanchis, Jordi van Gestel

Abstract:

Bacteria display an astonishing diversity of collectives: from fruiting bodies carrying spores, to biofilms and motile swarms. These multicellular aggregates have a very different lifestyle from planktonic single cells and have complex structures that usually reflect their essential ecological roles, such as dispersal or protection. We recently showed that some Bacillus subtilis collectives, filaments and biofilms, also serve as a defense against protistan predators, by outgrowing their phagocytic pocket. However, they also come with significant costs, creating a trade off between growth and protection, and making it difficult to predict the fate of individual collectives as predation dynamics fluctuate. Here, we explore how collective defense strategies impact the fate of bacterial lineages across the whole population – under protistan predation. To this end, we have constructed a barcoded library of Bacillus mutants, building on the genes responsible for collective defenses identified in our previous study. We then tag them by introducing a short DNA barcode into the bacterial genome which gets passed on to their offspring, allowing us to track lineages with single cell resolution. By competing different barcoded mutants in predation assays together with the protist D. discoideum, we expect that our analysis will allow us to quantify the fitness landscape of different defense strategies as they compete against each other and their predator. The changes in barcode relative abundance over time reveals which collective behaviors provide the most lasting benefit within the population and long term survival. In the future, we aim to bring in more of the soil’s natural microbial diversity, by introducing our barcoded mutants in more complex bacterial communities, allowing us to test the impact of this trade off in increasingly realistic ecological contexts.

Due to the confidentiality of the unpublished data, we cannot show the poster.

The EMBO | EMBL Symposium ‘Collectivity in living systems: emergence, function, and evolution‘ took place from 24 – 27 February 2026 at EMBL Heidelberg and virtually.