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Toxoplasma gondii ‐infected natural killer cells display a hypermotility phenotype in vivo
Author(s) -
Ueno Norikiyo,
Lodoen Melissa B,
Hickey Graeme L,
Robey Ellen A,
Coombes Janine L
Publication year - 2014
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2014.106
Subject(s) - toxoplasma gondii , biology , immune system , intracellular parasite , immunology , context (archaeology) , phenotype , in vivo , microbiology and biotechnology , antibody , genetics , paleontology , gene
Toxoplasma gondii is a highly prevalent intracellular protozoan parasite that causes severe disease in congenitally infected or immunocompromised hosts. T. gondii is capable of invading immune cells and it has been suggested that the parasite harnesses the migratory pathways of these cells to spread through the body. Although in vitro evidence suggests that the parasite further enhances its spread by inducing a hypermotility phenotype in parasitized immune cells, in vivo evidence for this phenomenon is scarce. Here we use a physiologically relevant oral model of T. gondii infection, in conjunction with two‐photon laser scanning microscopy, to address this issue. We found that a small proportion of natural killer (NK) cells in mesenteric lymph nodes contained parasites. Compared with uninfected ‘bystander’ NK cells, these infected NK cells showed faster, more directed and more persistent migratory behavior. Consistent with this, infected NK cells showed impaired spreading and clustering of the integrin, LFA‐1, when exposed to plated ligands. Our results provide the first evidence for a hypermigratory phenotype in T. gondii ‐infected NK cells in vivo , providing an anatomical context for understanding how the parasite manipulates immune cell motility to spread through the host.