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. 2020 Jul 10;18(10):587–600. doi: 10.1038/s41579-020-0400-5

Fig. 3. Tick immune defences against Borrelia burgdorferi infection.

Fig. 3

a | Infection with Borrelia burgdorferi activates the immune deficiency (IMD) pathway in Ixodes scapularis. On activation, p47 is polyubiquitylated by X-linked inhibitor of apoptosis (XIAP) in complex with the Bendless–Uev1a heterodimer. Downstream signalling through Kenny results in phosphorylation of Relish and transcription of antimicrobial peptides (AMPs). b | Uninfected I. scapularis can ingest mouse interferon-γ (IFNγ) along with the bloodmeal when feeding on B. burgdorferi infected mice. Mouse IFNγ signals in the tick gut through an unknown receptor, resulting in STAT-mediated activation of a Rho-like GTPase (IGTPase) and production of the AMP Dae2. c | Certain microbiota compositions enable activation of the JAK–STAT pathway by an unknown molecular signal and in turn induce the expression of peritrophin genes. Peritrophins are crucial for the formation of a structurally intact peritrophic matrix. B. burgdorferi uses the peritrophic matrix as a shield or barrier protecting it from toxic contents during colonization of the gut epithelium. STAT-induced immune effectors, as well as environmental changes, can alter the microbiota composition. Certain changes in the microbiota composition impair JAK–STAT signalling, and this results in decreased expression of peritrophins, leading to a thinner and compromised peritrophic matrix. A compromised peritrophic matrix no longer functions as a protective shield and thus impairs B. burgdorferi colonization of the gut epithelium.