Misinformation interventions decay rapidly without an immediate posttest

In recent years, many kinds of interventions have been developed that seek to reduce susceptibility to misinformation. In two preregistered longitudinal studies (N1 = 503, N2 = 673), we leverage two previously validated “inoculation” interventions (a video and a game) to address two important questions in misinformation interventions research: (1) whether displaying additional stimuli (such as videos unrelated to misinformation) alongside an intervention interferes with its effectiveness, and (2) whether administering an immediate posttest (in the form of a social media post evaluation task after the intervention) plays a role in the longevity of the intervention. We find no evidence that other stimuli interfere with intervention efficacy, but strong evidence that immediate posttests strengthen the learnings from the intervention. In study 1, we find that 48 h after watching a video, participants who received an immediate posttest continued to be significantly better at discerning untrustworthy social media posts from neutral ones than the control group (d = 0.416, p = .007), whereas participants who only received a posttest 48 h later showed no differences with a control (d = 0.010, p = .854). In study 2, we observe highly similar results for a gamified intervention, and provide evidence for a causal mechanism: immediate posttests help strengthen people's memory of the lessons learned in the intervention. We argue that the active rehearsal and application of relevant information are therefore requirements for the longevity of learning‐based misinformation interventions, which has substantial implications for their scalability

Publisher Correction: IL-17 signalling is critical for controlling subcutaneous adipose tissue dynamics and parasite burden during chronic murine Trypanosoma brucei infection.

Correction to: Nature Communications https://doi.org/10.1038/s41467-023-42918-8, published online 03 November 2023

Misinformation interventions decay rapidly without an immediate post-test

In recent years, many kinds of interventions have been developed that seek to reduce susceptibility to misinformation. In two preregistered longitudinal studies (N1 = 503, N2 = 673), we leverage two previously validated “inoculation” interventions (a video and a game) to address two important questions in misinformation interventions research: 1) whether displaying additional stimuli (such as videos unrelated to misinformation) alongside an intervention interferes with its effectiveness, and 2) whether administering an immediate post-test (in the form of a social media post evaluation task after the intervention) plays a role in the longevity of the intervention. We find no evidence that other stimuli interfere with intervention efficacy, but strong evidence that immediate post-tests strengthen the learnings from the intervention. In Study 1, we find that 48 hours after watching a video, participants who received an immediate post-test continued to be significantly better at discerning untrustworthy social media posts from neutral ones than the control group (d = .416, p = .007), whereas participants who only received a post-test 48 hours later showed no differences with a control (d = .010, p = .854). In Study 2, we observe highly similar results for a gamified intervention, and provide evidence for a causal mechanism: immediate post-tests help strengthen people’s memory of the lessons learned in the intervention. We argue that the active rehearsal and application of relevant information are therefore requirements for the longevity of learning-based misinformation interventions, which has substantial implications for their scalability

IL-17 signalling is critical for controlling subcutaneous adipose tissue dynamics and parasite burden during chronic Trypanosoma brucei infection

In the skin, Trypanosoma brucei colonises the subcutaneous white adipose tissue, and is proposed to be competent for forward transmission. The interaction between parasites, adipose tissue, and the local immune system is likely to drive the adipose tissue wasting and weight loss observed in cattle and humans infected with T. brucei. However, mechanistically, events leading to subcutaneous white adipose tissue wasting are not fully understood. Here, using several complementary approaches, including mass cytometry by time of flight, bulk and single cell transcriptomics, and in vivo genetic models, we show that T. brucei infection drives local expansion of several IL-17A-producing cells in the murine WAT, including T H17 and Vγ6 + cells. We also show that global IL-17 deficiency, or deletion of the adipocyte IL-17 receptor protect from infection-induced WAT wasting and weight loss. Unexpectedly, we find that abrogation of adipocyte IL-17 signalling results in a significant accumulation of Dpp4 + Pi16 + interstitial preadipocytes and increased extravascular parasites in the WAT, highlighting a critical role for IL-17 signalling in controlling preadipocyte fate, subcutaneous WAT dynamics, and local parasite burden. Taken together, our study highlights the central role of adipocyte IL-17 signalling in controlling WAT responses to infection, suggesting that adipocytes are critical coordinators of tissue dynamics and immune responses to T. brucei infection.</p

IL-17 signalling is critical for controlling subcutaneous adipose tissue dynamics and parasite burden during chronic murine Trypanosoma brucei infection

In the skin, Trypanosoma brucei colonises the subcutaneous white adipose tissue, and is proposed to be competent for forward transmission. The interaction between parasites, adipose tissue, and the local immune system is likely to drive the adipose tissue wasting and weight loss observed in cattle and humans infected with T. brucei. However, mechanistically, events leading to subcutaneous white adipose tissue wasting are not fully understood. Here, using several complementary approaches, including mass cytometry by time of flight, bulk and single cell transcriptomics, and in vivo genetic models, we show that T. brucei infection drives local expansion of several IL-17A-producing cells in the murine WAT, including TH17 and Vγ6+ cells. We also show that global IL-17 deficiency, or deletion of the adipocyte IL-17 receptor protect from infection-induced WAT wasting and weight loss. Unexpectedly, we find that abrogation of adipocyte IL-17 signalling results in a significant accumulation of Dpp4+ Pi16+ interstitial preadipocytes and increased extravascular parasites in the WAT, highlighting a critical role for IL-17 signalling in controlling preadipocyte fate, subcutaneous WAT dynamics, and local parasite burden. Taken together, our study highlights the central role of adipocyte IL-17 signalling in controlling WAT responses to infection, suggesting that adipocytes are critical coordinators of tissue dynamics and immune responses to T. brucei infection