Transmission of
            <i>Toxoplasma gondii</i>
            from 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.00693-09

Cited by 20 publications

(41 citation statements)

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“…As plaques are areas where replicating T. gondii and host cells are in close association, these sites are the likely source of cellular infection. This idea is consistent with the observation of increased percentages of infected neutrophils and monocytes in the lamina propria, where LysM ϩ cells were visualized within plaques (3,6,8,9,39,40).…”

Section: Discussionsupporting

confidence: 75%

Replication and Distribution of Toxoplasma gondii in the Small Intestine after Oral Infection with Tissue Cysts

Gregg¹,

Taylor

John

et al. 2013

Infect Immun

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Natural infection by Toxoplasma gondii occurs via oral ingestion of tissue cysts that rupture in the small intestine, releasing zoites that infect locally before disseminating throughout the host. The studies presented here used fluorescent parasites combined with flow cytometry and multiphoton microscopy techniques to understand the events associated with parasite replication in the mucosa. At 3 days postinfection with tissue cysts, parasites were localized in small foci and flow cytometry revealed parasites present in macrophages, neutrophils, and monocytes in the lamina propria. By day 6 postinfection, there were large foci of replicating parasites; however, foci unexpectedly varied in the number of villi involved and were associated with the presence of viable tachyzoites within the intestinal lumen. Consistent with the flow cytometry data, neutrophils and monocytes in the lamina propria were preferentially associated with parasite plaques. In contrast, dendritic cells comprised a small fraction of the infected immune cell population and were localized at the periphery of parasite plaques. Together, these findings reveal the formation of localized sites of parasite replication and inflammation early during infection and suggest that sustained replication of T. gondii in the gut may be a function of pathogen luminal spread.

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Section: Discussionsupporting

confidence: 75%

Replication and Distribution of Toxoplasma gondii in the Small Intestine after Oral Infection with Tissue Cysts

Gregg¹,

Taylor

John

et al. 2013

Infect Immun

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“…Although not essential for egress, a drop in the host cell cytosolic K ϩ concentration is sufficient to trigger egress through the activation of a parasite PI-PLC, which in turn leads to an increase in the intraparasitic Ca 2ϩ concentration (59,88,100). In accordance with this, PFPs secreted by cytotoxic T or NK cells were shown to induce egress (106,107). Alternatively, an insufficient maintenance of the K ϩ gradient across the host plasma membrane due to an energy exhaustion of the host cell could cause a decrease in the concentration of host cell cytosolic K ϩ and thus trigger egress.…”

Section: Stimuli and Signaling Leading To Egresssupporting

confidence: 53%

Prison Break: Pathogens' Strategies To Egress from Host Cells

Friedrich

Hagedorn

Soldati‐Favre

et al. 2012

Microbiol Mol Biol Rev

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SUMMARYA wide spectrum of pathogenic bacteria and protozoa has adapted to an intracellular life-style, which presents several advantages, including accessibility to host cell metabolites and protection from the host immune system. Intracellular pathogens have developed strategies to enter and exit their host cells while optimizing survival and replication, progression through the life cycle, and transmission. Over the last decades, research has focused primarily on entry, while the exit process has suffered from neglect. However, pathogen exit is of fundamental importance because of its intimate association with dissemination, transmission, and inflammation. Hence, to fully understand virulence mechanisms of intracellular pathogens at cellular and systemic levels, it is essential to consider exit mechanisms to be a key step in infection. Exit from the host cell was initially viewed as a passive process, driven mainly by physical stress as a consequence of the explosive replication of the pathogen. It is now recognized as a complex, strategic process termed “egress,” which is just as well orchestrated and temporally defined as entry into the host and relies on a dynamic interplay between host and pathogen factors. This review compares egress strategies of bacteria, pathogenic yeast, and kinetoplastid and apicomplexan parasites. Emphasis is given to recent advances in the biology of egress in mycobacteria and apicomplexans.

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“…5C and D). In line with our previous observation that targeting of infected cells by T cells or NK cells (28,29) leads to parasite egress, effector T cells were readily infected by the egressing parasites after cytotoxic attack of the infected microglia or astrocytes (Fig. 5E).…”

Section: Downloaded Fromsupporting

confidence: 71%

“…However, already activated CD8 T cells would still be able to recognize infected cells, since the downmodulation of MHC class I expression is less pronounced. By not markedly downmodulating MHC class I levels, CD8 T cells could still target infected cells, allowing egress from infected cells to antigen-specific CD8 T cells, as we have reported previously (28,29). Further experimentation is needed to determine if Toxoplasma enhances its ability to avoid immuno-eradication by (i) maintaining low expression levels of MHC class II and CD86 molecules that would reduce the chances of abundant T cell activation and (ii) infecting T cells upon their lysis of infected glial cells in vivo.…”

Section: Discussionsupporting

confidence: 48%

Migratory Activation of Primary Cortical Microglia upon Infection with Toxoplasma gondii

et al. 2011

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Disseminated toxoplasmosis in the central nervous system (CNS) is often accompanied by a lethal outcome.Studies with murine models of infection have focused on the role of systemic immunity in control of toxoplasmic encephalitis, while knowledge remains limited on the contributions of resident cells with immune functions in the CNS. In this study, the role of glial cells was addressed in the setting of recrudescent Toxoplasma infection in mice. Activated astrocytes and microglia were observed in the close vicinity of foci with replicating parasites in situ in the brain parenchyma. Toxoplasma gondii tachyzoites were allowed to infect primary microglia and astrocytes in vitro. Microglia were permissive to parasite replication, and infected microglia readily transmigrated across transwell membranes and cell monolayers. Thus, infected microglia, but not astrocytes, exhibited a hypermotility phenotype reminiscent of that recently described for infected dendritic cells. In contrast to gamma interferon-activated microglia, Toxoplasma-infected microglia did not upregulate major histocompatibility complex (MHC) class II molecules and the costimulatory molecule CD86. Yet Toxoplasma-infected microglia and astrocytes exhibited increased sensitivity to T cell-mediated killing, leading to rapid parasite transfer to effector T cells in vitro. We hypothesize that glial cells and T cells, besides their role in triggering antiparasite immunity, may also act as "Trojan horses," paradoxically facilitating dissemination of Toxoplasma within the CNS. To our knowledge, this constitutes the first report of migratory activation of a resident CNS cell by an intracellular parasite.

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Transmission of Toxoplasma gondii from Infected Dendritic Cells to Natural Killer Cells

Cited by 20 publications

References 0 publications

Replication and Distribution of Toxoplasma gondii in the Small Intestine after Oral Infection with Tissue Cysts

Replication and Distribution of Toxoplasma gondii in the Small Intestine after Oral Infection with Tissue Cysts

Prison Break: Pathogens' Strategies To Egress from Host Cells

Migratory Activation of Primary Cortical Microglia upon Infection with Toxoplasma gondii

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