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The true potential of human-AI collaboration lies in exploiting the complementary capabilities of humans and AI to achieve a joint performance superior to that of the individual AI or human, i.e., to achieve complementary team performance (CTP). To realize this complementarity potential, humans need to exercise discretion in following AI's advice, i.e., appropriately relying on the AI's advice. While previous work has focused on building a mental model of the AI to assess AI recommendations, recent research has shown that the mental model alone cannot explain appropriate reliance. We hypothesize that, in addition to the mental model, human learning is a key mediator of appropriate reliance and, thus, CTP. In this study, we demonstrate the relationship between learning and appropriate reliance in an experiment with 100 participants. This work provides fundamental concepts for analyzing reliance and derives implications for the effective design of human-AI decision-making.

The cGAS‐STING (cyclic GMP‐AMP synthase‐stimulator of interferon genes) axis is the predominant DNA sensing system in cells of the innate immune system. However, human T cells also express high levels of STING, while its role and physiological trigger remain largely unknown. Here, we show that the cGAS‐STING pathway is indeed functional in human primary T cells. In the presence of a TCR‐engaging signal, both cGAS and STING activation switches T cells into type I interferon‐producing cells. However, T cell function is severely compromised following STING activation, as evidenced by increased cell death, decreased proliferation, and impaired metabolism. Interestingly, these different phenotypes bifurcate at the level of STING. While antiviral immunity and cell death require the transcription factor interferon regulatory factor 3 (IRF3), decreased proliferation is mediated by STING independently of IRF3. In summary, we demonstrate that human T cells possess a functional cGAS‐STING signaling pathway that can contribute to antiviral immunity. However, regardless of its potential antiviral role, the activation of the cGAS‐STING pathway negatively affects T cell function at multiple levels. Taken together, these results could help inform the future development of cGAS‐STING‐targeted immunotherapies.

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