Abstract
Pattern recognition receptors sense pathogens in arthropods and mammals through distinct immune processes. Whether these molecules share a similar function and recognize the same microbe in evolutionarily distant species remain ill-defined. Here, we establish that the CD36 superfamily is required for Borrelia burgdorferi resistance in both the arthropod vector and humans. Using the blacklegged tick Ixodes scapularis and an electronic health record-linked biobank, we demonstrate that CD36 members elicit immunity to the Lyme disease spirochete. In ticks, the CD36-like protein Croquemort recognizes lipids and initiates the immune deficiency and jun N-terminal kinase pathways against B. burgdorferi. In humans, exome sequencing and clinical information reveal that individuals with CD36 loss-of-function variants have increased prevalence of Lyme disease. Altogether, we discovered a conserved mechanism of anti-bacterial immunity.
One Sentence Summary Lipid receptors belonging to the CD36 superfamily exhibit a shared immune function in both ticks and humans.
Competing Interest Statement
Ron Do reported receiving grants from AstraZeneca, research grants and non-financial support from Goldfinch Bio. Ron Do is also a scientific co-founder, consultant and equity holder (pending) for Pensieve Health and a consultant for Variant Bio. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
