Functional aspects of Toll-like receptor/MyD88 signalling during protozoan infection: focus on <i>Toxoplasma gondii</i>

Egan, Charlotte E.; Sukhumavasi, Woraporn; Butcher, Barbara A.; Denkers, Eric

doi:10.1111/j.1365-2249.2009.03876.x

Cited by 50 publications

(39 citation statements)

References 93 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study we evaluated the expression of only two PRR involved in recognition of parasitic molecules, namely the TLR2 and the TLR4 [31,42,43]. The expression of TLRs by T lymphocytes usually is induced and/or amplified by TCR-activation; neverthless we could observe significant differences in the expression of TLR4 by activated T lymphocytes following stimulus with T. gondii and with P. falciparum extracts.…”

Section: Discussionmentioning

confidence: 99%

Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-β mediated pathways in activated CD4+ T lymphocytes

Clemente

Severini

Castronovo

et al. 2014

Microbes and Infection

View full text Add to dashboard Cite

Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-breceptor activated pathways. We explored the properties of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites, Trichinella spiralis muscle larvae to expand the pool of T-regulatory cells in a population of polyclonally activated T cells in the absence of accessory cells, and compared their effects to those induced by Plasmodium falciparum extracts. Similarly to P. falciparum, L. infantum extracts activate the latent soluble form of transforming growth factor-b and that bound to the membrane of activated T lymphocytes. The interaction of the active cytokine with transforming growth factor-b receptor induces Foxp3 expression by activated lymphocytes, favoring their conversion through the T-regulatory phenotype. Both Toxoplasma gondii and L. infantum extracts are able to induce transforming growth factor-b production by activated T cells in the absence of accessory cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-β mediated pathways in activated CD4+ T lymphocytes

Clemente

Severini

Castronovo

et al. 2014

Microbes and Infection

View full text Add to dashboard Cite

show abstract

“…GM-CSF, M-CSF and IL-3) during many of these infections, as discussed in the previous paragraph, this perhaps formulates an ideal cytokine composition for the expansion and activation of MDSC. As a matter of fact, a sepsis-like situation often occurs during the acute phase of protozoan parasite infection, including infection with Trypanosoma, Toxoplasma, Plasmodium and Leishmania species, given the overwhelming presence of parasites/TLR ligands and the ensuing massive inflammatory/Th1 (IFN-g) responses [37,38]. It should be noted that helminth parasites, such as S. mansoni, also trigger TLR/MyD88 signaling to induce an early Th1 response, which is subsequently converted to a dominant Th2 response [39,40].…”

mentioning

confidence: 99%

Myeloid‐derived suppressor cells in parasitic infections

et al. 2010

View full text Add to dashboard Cite

BelgiumMyeloid-derived suppressor cells (MDSC) are a heterogeneous population of immature myeloid cells that share a common property of suppressing immune responses. Several helminth and protozoan parasite species have developed efficient strategies to increase the rate of medullary or extramedullary myelopoiesis and to induce the expansion and accumulation of immature myeloid cells such as MDSC. In this review, we examine current knowledge on the factors mediating enhanced myelopoiesis and MDSC induction and recruitment during parasitic infections and how the MDSC phenotype and mechanism of immune modulation and suppression depends on the factors they encounter within the host. Finally, we place MDSC expansion in the context of the critical balance between parasite elimination and pathogenicity to the host and suggest attractive avenues for future research.Key words: Myeloid-derived suppressor cells . Myelopoiesis . Parasitic infection .T-cell suppression IntroductionParasitic infections are notoriously associated with suppression of immune responses. Populations of mature myeloid cells, such as macrophages in various activation states, are capable of displaying immunosuppressive features, and as a result play important roles in the critical balance between parasite elimination and pathogenicity to host tissues [1][2][3]. Heterogeneous populations of immature myeloid cells, characterized by the surface expression of both Gr-1 and CD11b molecules in mice and a shared potent immune-suppressing activity in vitro and in vivo, have been recognized to arise as a conserved response to various insults, including cancer, bacterial and parasitic infections. Collectively, these cells have been termed myeloid-derived suppressor cells (MDSC) [4]. A number of factors complicate the analysis of MDSC biology. First, MDSC are a heterogeneous mixture of immature myeloid cells that are in various intermediate stages of myeloid cell differentiation (reflected by expression of various levels of macrophage and DC markers such as F4/80 and CD11c, respectively, as well as MHC class II, CD80/86) and murine MDSC consist of different subpopulations with varying levels of reactivity with the Gr-1 monoclonal antibody. This Gr-1 antibody binds a common epitope on the Ly6G and Ly6C antigens [5]. Using antibodies specifically recognizing Ly6C or Ly6G, MDSC have been shown to contain at least two main subfractions: the CD11b suppressive capacity in all tumor models [7,16]. The heterogeneity and plasticity of MDSC and the lack of markers to optimally distinguish MDSC from other, more mature myeloid cell types, render T-cell anti-proliferative activity to be the ultimate defining characteristic of MDSC. Despite the above-mentioned limitations, the impact of MDSC on immune responses has made MDSC the topic of intense research. To date, most of the attention has been focused on cancer-associated MDSC, whereas relatively few studies have reported the activation, phenotype and especially the role of MDSC during parasitic infections (Table 1). In thi...

show abstract

“…T. gondii profilin induces IL-12 via toll-like receptor 11 (TLR11)/myeloid differentiation factor 88 (MyD88), promotes parasite actin assembly, and contributes to gliding motility and invasion and egress (21,32). Glycosylphosphatidylinositol-anchored proteins on the surface of T. gondii trigger tumor necrosis factor alpha (TNF-␣) production from macrophages in a TLR2/TLR4/MyD88-dependent manner (14).…”

mentioning

confidence: 99%

Toxoplasma gondiiCyclophilin 18 Regulates the Proliferation and Migration of Murine Macrophages and Spleen Cells

Ibrahim

Xuan

Nishikawa

2010

Clin Vaccine Immunol

View full text Add to dashboard Cite

Functional aspects of Toll-like receptor/MyD88 signalling during protozoan infection: focus on Toxoplasma gondii

Cited by 50 publications

References 93 publications

Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-β mediated pathways in activated CD4+ T lymphocytes

Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-β mediated pathways in activated CD4+ T lymphocytes

Myeloid‐derived suppressor cells in parasitic infections

Toxoplasma gondiiCyclophilin 18 Regulates the Proliferation and Migration of Murine Macrophages and Spleen Cells

Contact Info

Product

Resources

About