Social sensing of infection reprograms peripheral immunity in healthy mice

preprint OA: closed
View at publisher

Abstract

In plants and insects, social immunity enables individuals to detect infection in neighbors and mount protective, community-level responses. Whether mammals possess analogous mechanisms remains unknown. Here, we asked how the presence of sick cage-mates influences the physiology of uninfected neighbors. We found that healthy mice co-housed with conspecifics infected with the non-communicable murine pathogen Toxoplasma gondii undergo a shift in peripheral immune responses that establishes a primed immune state. This exposure-induced priming conferred physiological resilience to a sublethal lipopolysaccharide (LPS)-inflammatory challenge and was mediated by increased myeloid-derived IL-10 production. Blocking IL-10 signaling abrogated exposure-induced protection against a subsequent immune challenge. Thus, our findings show that immune state in healthy mammals can be shaped by exposure to infected conspecifics, hinting at social immunity-based protective mechanisms in mammals. One sentence summary Immune responses in healthy mammals are shaped by exposure to infected conspecifics.

My notes (saved in your browser only)

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2026) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.

Source provenance

europepmc
last seen: 2026-05-20T01:45:00.602351+00:00