An intravascular immune response to Borrelia

Excerpt;

Here we investigate the dynamics of the hepatic intravascular
immune response to a pathogen relevant to invariant natural
killer T cells (iNKT cells).
Immobilized Kupffer cells with highly ramified extended processes
into multiple sinusoids could effectively capture blood-borne,
disseminating Borrelia burgdorferi, creating a highly efficient
surveillance and filtering system.
After ingesting B. burgdorferi, Kupffer cells induced chemokine
receptor CXCR3-dependent clustering of iNKT cells. Kupffer cells
and iNKT cells formed stable contacts via the antigen-presenting
molecule CD1d, which led to iNKT cell activation. An absence of
iNKT cells caused B. burgdorferi to leave the blood and enter the
joints more effectively. B. burgdorferi that escaped Kupffer
cells entered the liver parenchyma and survived despite Ito cell
responses. Kupffer cell-iNKT cell interactions induced a key
intravascular immune response that diminished the dissemination
of B. burgdorferi.