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Updated: Jun 7, 2025

T Cells Capture Bacteria by Transinfection from Dendritic Cells
Published on: January 13, 2016
A model of proximate protection against pathogenic infection through shared immunity
Douglas F Nixon1, Margarita Kyza-Karavioti2, Sreeradha Mallick2
1Institute of Translational Research, The Feinstein Institutes for Medical Research, Manhasset, New York, USA.
Abstract:
Drosophila melanogaster exhibits innate immune priming, a mechanism leading to protection upon repeated challenge with a given pathogen. However, whether immunological priming can be propagated from a challenged host to naive bystanders is unknown. Here, we show that priming half a vial of D. melanogaster adult flies with non-pathogenic Escherichia coli bacteria leads to protection of the whole vial from a lethal dose of the insect pathogen, Photorhabdus luminescens. The protective effect observed in these bystander flies was similar in magnitude to that of the E. coli primed hosts themselves but did not require transfer of E. coli to occur. This work broadens the scope of how immunological priming can occur and suggests that infected hosts can produce signals that influence immunity in their neighbors, leading to a shared immune collective.IMPORTANCEHere, we have introduced the new concept of shared immunity and priming by proximity. These findings are of particular significance because they indicate that the presence of compromised hosts can increase the response to the pathogenic challenge of healthy individuals that cohabitate within close distance. This shared immunity may involve proximate boosting of the host's immune defenses via the sensing of specific chemical, behavioral, or microbial signals. Determining the breadth, mechanistic basis, and translatability of these findings has the potential to transform biomedical research and public health.
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