Transmission ofToxoplasma gondiifrom Infected Dendritic Cells to Natural Killer Cells

Persson, Catrine M.; Lambert, Henrik; Vutova, Polya P.; Dellacasa-Lindberg, Isabel; Nederby, Joanna; Yagita, Hideo; Ljunggren, Hans‐Gustaf; Grandien, Alf; Barragán, Antonio; Chambers, Benedict J.

doi:10.1128/iai.00833-08

Cited by 59 publications

(50 citation statements)

References 44 publications

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“…and Toxoplasma gondii , have been reported to infect DCs (Prina et al, 2004; Persson et al, 2009). Some of these pathogens, such as T. gondii , which can initiate infection through intestinal mucosa, can also colonize distant tissues after being transported by DCs (Bierly et al, 2008; Courret et al, 2006).…”

Section: Resultsmentioning

confidence: 99%

Interaction ofCryptosporidium parvumwith mouse dendritic cells leads to their activation and parasite transportation to mesenteric lymph nodes

Pérez-Cordón

Yang²,

Zhou³

et al. 2013

Pathogens Disease

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Dendritic cells (DCs) are the antigen presenting cells capable of activating naïve T cells. Although CD4+ T cells are crucial for Cryptosporidium parvum clearance, little is known about the role of DCs in the immune response to this parasite. In this study the interaction between mouse DCs and C. parvum was investigated both in vitro and in vivo. For in vitro experiments, mouse bone marrow-derived dendritic cells (BMDCs) derived from wild type C57B1/6 or MyD88−/− or C3H/HeJ mice and DC cell line DC2.4 were pulsed with C. parvum. Active invasion of parasites was demonstrated by parasite co-localization with host cell membranes and actin-plaque formation at the site of attachment. DC activation induced by the parasite invasion was demonstrated by upregulation of costimulatory molecules CD40, CD80, and CD86, as well as inflammatory cytokines IL-12, TNF-α, and IL-6. BMDCs derived from MyD88−/− and C3H/HeJ mice failed to produce IL-12 in response to C. parvum, suggesting the importance of TLR-dependent signaling pathway specially presence of a functional TLR4 pathway, for C. parvum-induced cytokine production. In vivo experiments showed that both parasite antigens and live parasites were transported to mice mesenteric lymph nodes. All together, these data suggest that DCs play a key role in host immune responses to C. parvum and pathogenesis of the disease.

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Section: Resultsmentioning

confidence: 99%

Interaction ofCryptosporidium parvumwith mouse dendritic cells leads to their activation and parasite transportation to mesenteric lymph nodes

Pérez-Cordón

Yang²,

Zhou³

et al. 2013

Pathogens Disease

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“…The alteration in NK/DC cooperation was proposed by different authors as a common mechanism elicited by tumors and pathogens to escape from immune surveillance [7,42]. Perhaps to avoid immune recognition, the intracellular protozoan T. gondii exploits direct contact of these cells in vitro via its transfer from infected DCs to effector NK cells [43]. …”

Section: Discussionmentioning

confidence: 99%

Impairment in Natural Killer Cells Editing of Immature Dendritic Cells by Infection with a Virulent Trypanosoma cruzi Population

Batalla

Martínez

Poncini³

et al. 2013

J Innate Immun

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Early interactions between natural killer (NK) and dendritic cells (DC) shape the immune response at the frontier of innate and adaptive immunity. Activated NK cells participate in maturation or deletion of DCs that remain immature. We previously demonstrated that infection with a high virulence (HV) population of the protozoan parasite Trypanosoma cruzi downmodulates DC maturation and T-cell activation capacity. Here, we evaluated the role of NK cells in regulating the maturation level of DCs. Shortly after infection with HV T. cruzi, DCs in poor maturation status begin to accumulate in mouse spleen. Although infection induces NK cell cytotoxicity and cytokine production, NK cells from mice infected with HV T. cruzi exhibit reduced ability to lyse and fail to induce maturation of bone marrow-derived immature DCs (iDCs). NK-mediated lysis of iDCs is restored by in vitro blockade of the IL-10 receptor during NK-DC interaction or when NK cells are obtained from T. cruzi-infected IL-10 knockout mice. These results suggest that infection with a virulent T. cruzi strain alters NK cell-mediated regulation of the adaptive immune response induced by DCs. This regulatory circuit where IL-10 appears to participate might lead to parasite persistence but can also limit the induction of a vigorous tissue-damaging T-cell response.

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“…Despite their protective role during parasitic infections, recent evidence indicates that NK cells can be directly invaded by T. gondii 19, 2019, 20.…”

Section: Discussionmentioning

confidence: 99%

“…T. gondii ‐invaded NK cell are not efficiently targeted for destruction by other NK cells and are hypermotile 19, 20. This may allow the parasite to use NK cells to protect themselves from immune mediated destruction, while transiting successfully from the site of infection to muscles or brain.…”

Section: Discussionmentioning

confidence: 99%

“…More recently, the complexity of the ILC family has been better appreciated, and it is possible that some of the protective function attributed to NK cells may actually derive from ILC1 cells 18. Despite their protective role in the immune response against T. gondii , NK cells can themselves be parasitized via transmission of T. gondii from infected DCs 19. Consistent with this, small numbers of T. gondii ‐invaded NK cells are present in the lymph nodes of infected animals 20.…”

Section: Introductionmentioning

confidence: 99%

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Parasitized Natural Killer cells do not facilitate the spread of Toxoplasma gondii to the brain

Petit-Jentreau

Glover

Coombes

2018

Parasite Immunology

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Summary Toxoplasma gondii is a protozoan parasite capable of invading immune cells and co‐opting their migratory pathways to disseminate through the host. Natural Killer (NK) cells can be directly invaded by the parasite and this invasion alters NK cell migration, producing a hypermotile phenotype. However, the consequences of this hypermotile phenotype for the dissemination of T. gondii to the brain remain unknown. To address this, C57BL6/J mice were infected with freshly egressed tachyzoites (type II Prugniaud strain) or with parasitized NK cells. Under both conditions, parasite loads in the brain were comparable, indicating that parasitized NK cells were not able to facilitate spread of T. gondii to the brain. Consistent with this, we found no evidence for the recruitment of endogenous NK cells to the brain at early time points post‐infection, nor any changes in the expression of α4β1 integrin, involved in recruitment of NK cells to the brain. We therefore found no evidence for a role for hypermotile NK cells in delivery of parasites to the brain during acute infection with T. gondii.

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Transmission ofToxoplasma gondiifrom Infected Dendritic Cells to Natural Killer Cells

Cited by 59 publications

References 44 publications

Interaction ofCryptosporidium parvumwith mouse dendritic cells leads to their activation and parasite transportation to mesenteric lymph nodes

Interaction ofCryptosporidium parvumwith mouse dendritic cells leads to their activation and parasite transportation to mesenteric lymph nodes

Impairment in Natural Killer Cells Editing of Immature Dendritic Cells by Infection with a Virulent <b><i>Trypanosoma cruzi</i></b> Population

Parasitized Natural Killer cells do not facilitate the spread of Toxoplasma gondii to the brain

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