A tick C1q protein alters infectivity of the Lyme disease agent by modulating interferon γ
Xiao‐Tian Tang, Gunjan Arora, Jaqueline Matias, Thomas Hart, Yingjun Cui, Erol Fikrig
Abstract
In North America, the Lyme disease agent, Borrelia burgdorferi , is commonly transmitted by the black-legged tick, Ixodes scapularis . Tick saliva facilitates blood feeding and enhances pathogen survival and transmission. Here, we demonstrate that I. scapularis complement C1q-like protein 3 (IsC1ql3), a tick salivary protein, directly interacts with B. burgdorferi and is important during the initial stage of spirochetal infection of mice. Mice fed upon by B. burgdorferi -infected IsC1ql3 -silenced ticks, or IsC1ql3-immunized mice fed upon by B. burgdorferi -infected ticks, have a lower spirochete burden during the early phase of infection compared with control animals. Mechanically, IsC1ql3 interacts with the globular C1q receptor present on the surface of CD4 + and CD8 + T cells, resulting in decreased production of interferon γ. IsC1ql3 is a C1q-domain-containing protein identified in arthropod vectors and has an important role in B. burgdorferi infectivity as the spirochete transitions from the tick to vertebrate host.