Type I interferon signaling promotes early innate control of Borrelia burgdorferi infection.

IFN-I signaling via IFNAR1 restricts early Borrelia burgdorferi expansion in mice, with IFNAR1 deficiency causing markedly elevated spirochetal burdens at 5 days post-challenge.

• Why it matters: Although IFN-I is induced early and linked to chronic Lyme arthritis, its functional role during the initial control of B. burgdorferi infection is unclear.
• What they did: Mice lacking IFNAR1 were assessed at 5 and 10 days post-challenge for spirochetal burdens in skin, heart, and joints, alongside macrophage uptake, phagosomal processing, intracellular killing, cytokine responses, and recruitment; pharmacological IFN-I activation was also tested.
• The result: IFNAR1 deficiency increased bacterial loads in skin at 10 days and showed a trend in heart, while joint burdens were unaffected; IFN-I enhanced macrophage antimicrobial functions and improved bacterial clearance, supporting protective early host defense.