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T cell responses upon infection display a remarkably reproducible pattern of expansion, contraction, and memory formation. If the robustness of this pattern builds entirely on signals derived from other cell types or if activated T cells themselves contribute to the orchestration of these population dynamics-akin to bacterial quorum regulation-is unclear. Here, we examined this question using time-lapse microscopy, genetic perturbation, bioinformatic predictions, and mathematical modeling. We found that ICAM-1-mediated cell clustering enabled CD8+ T cells to collectively regulate the balance between proliferation and apoptosis. Mechanistically, T cell expressed CD80 and CD86 interacted with the receptors CD28 and CTLA-4 on neighboring T cells; these interactions fed two nested antagonistic feedback circuits that regulated interleukin 2 production in a manner dependent on T cell density as confirmed by in vivo modulation of this network. Thus, CD8+ T cell-population-intrinsic mechanisms regulate cellular behavior, thereby promoting robustness of population dynamics.

Learning of environmental features can influence both mating behaviour and the location where young are produced. This may lead to speciation in three steps: (i) colonization of a new habitat, (ii) genetic divergence of the two groups by adaptation to the habitats, and (iii) a decrease of genetic mixing between the lineages (similar to reinforcement). In a previous paper we showed that steps (i) and (ii) occur readily for a wide range of fixed mating and habitat preferences. Here, we study whether this can ultimately lead to speciation through selective changes in these preferences. We show that this indeed occurs, and, furthermore, it is very general: for a large class of models there is selection toward producing young more frequently in the natal habitat. Once habitat preference is strong, there is selection toward stronger assortative mating. Even when steps (i) and (ii) initially fail, genetic divergence may succeed at a later evolutionary stage, after which a decrease of genetic mixing completes speciation. Our results show that speciation by the learning of habitat features is an extremely effective mechanism.