Impaired pro-inflammatory cytokine production and increased Th2-biasing ability of dendritic cells exposed to Taenia excreted/secreted antigens: A critical role for carbohydrates but not for STAT6 signaling

Terrazas, César; Gómez-García, Lorena; Terrazas, Luis I.

doi:10.1016/j.ijpara.2010.02.016

Cited by 51 publications

(54 citation statements)

References 57 publications

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“…These DCs significantly decreased levels of proinflammatory cytokines, including IL-12p40 and IL-12p70, as well as TNF- α and IL-15. IL-10 was, however not affected in this study [127]. Thus, downregulation of proinflammatory cytokines seems to be a frequent mechanism in immune modulation by helminths.…”

Section: Host Cells Targeted By Helminth Infectionsmentioning

confidence: 58%

Modulation of Specific and Allergy‐Related Immune Responses by Helminths

Daniłowicz-Luebert

O’Regan

Steinfelder

et al. 2011

BioMed Research International

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Helminths are master regulators of host immune responses utilising complex mechanisms to dampen host protective Th2-type responses and favour long-term persistence. Such evasion mechanisms ensure mutual survival of both the parasite and the host. In this paper, we present recent findings on the cells that are targeted by helminths and the molecules and mechanisms that are induced during infection. We discuss the impact of these factors on the host response as well as their effect in preventing the development of aberrant allergic inflammation. We also examine recent findings on helminth-derived molecules that can be used as tools to pinpoint the underlying mechanisms of immune regulation or to determine new anti-inflammatory therapeutics.

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Section: Host Cells Targeted By Helminth Infectionsmentioning

confidence: 58%

Modulation of Specific and Allergy‐Related Immune Responses by Helminths

Daniłowicz-Luebert

O’Regan

Steinfelder

et al. 2011

BioMed Research International

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“…Compared to nematode and trematode infections, immunomodulatory functions of DC in cestode infections have drawn significantly less attention, although this is clearly an emerging field since several studies concerning the influence of parasite products on DC maturation and cytokine secretion profiles have been conducted very recently. In two of these recent reports, Reyes et al [45] and Terrazas et al [46] investigated the effects of E/S-products of Taenia crassiceps cysticerci, representing the metacestode larval stage of this Taenia infection model, on the activation of murine DC. These authors observed impaired DC maturation in response to TLR dependent stimuli, particularly when DC of infection susceptible mouse strains were pre-incubated with parasite E/S-products [45].…”

Section: Discussionmentioning

confidence: 99%

Excretory/Secretory-Products of Echinococcus multilocularis Larvae Induce Apoptosis and Tolerogenic Properties in Dendritic Cells In Vitro

et al. 2012

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BackgroundAlveolar echinococcosis, caused by Echinococcus multilocularis larvae, is a chronic disease associated with considerable modulation of the host immune response. Dendritic cells (DC) are key effectors in shaping the immune response and among the first cells encountered by the parasite during an infection. Although it is assumed that E.multilocularis, by excretory/secretory (E/S)-products, specifically affects DC to deviate immune responses, little information is available on the molecular nature of respective E/S-products and their mode of action.Methodology/Principal FindingsWe established cultivation systems for exposing DC to live material from early (oncosphere), chronic (metacestode) and late (protoscolex) infectious stages. When co-incubated with Echinococcus primary cells, representing the invading oncosphere, or metacestode vesicles, a significant proportion of DC underwent apoptosis and the surviving DC failed to mature. In contrast, DC exposed to protoscoleces upregulated maturation markers and did not undergo apoptosis. After pre-incubation with primary cells and metacestode vesicles, DC showed a strongly impaired ability to be activated by the TLR ligand LPS, which was not observed in DC pre-treated with protoscolex E/S-products. While none of the larvae induced the secretion of pro-inflammatory IL-12p70, the production of immunosuppressive IL-10 was elevated in response to primary cell E/S-products. Finally, upon incubation with DC and naïve T-cells, E/S-products from metacestode vesicles led to a significant expansion of Foxp3+ T cells in vitro.ConclusionsThis is the first report on the induction of apoptosis in DC by cestode E/S-products. Our data indicate that the early infective stage of E. multilocularis is a strong inducer of tolerance in DC, which is most probably important for generating an immunosuppressive environment at an infection phase in which the parasite is highly vulnerable to host attacks. The induction of CD4+CD25+Foxp3+ T cells through metacestode E/S-products suggests that these cells fulfill an important role for parasite persistence during chronic echinococcosis.

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“…On the other hand, B regulatory cells (Breg) also contribute to immune modulation and can release IL-10 and restrict proinflammatory responses [93]. Helminths also induce the differentiation of anti-inflammatory M φ , called alternatively activated M φ (AAM φ ) [94, 95], as well as regulatory dendritic cells (DCreg), which are characterized by the expression of the regulatory cytokines IL-10 and TGF- β [96, 97] (Figure 2). …”

Section: Helminthsmentioning

confidence: 99%

Helminth Parasites Alter Protection againstPlasmodiumInfection

Salazar-Castañón

Legorreta-Herrera

Rodrı́guez-Sosa

2014

BioMed Research International

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More than one-third of the world's population is infected with one or more helminthic parasites. Helminth infections are prevalent throughout tropical and subtropical regions where malaria pathogens are transmitted. Malaria is the most widespread and deadliest parasitic disease. The severity of the disease is strongly related to parasite density and the host's immune responses. Furthermore, coinfections between both parasites occur frequently. However, little is known regarding how concomitant infection with helminths and Plasmodium affects the host's immune response. Helminthic infections are frequently massive, chronic, and strong inductors of a Th2-type response. This implies that infection by such parasites could alter the host's susceptibility to subsequent infections by Plasmodium. There are a number of reports on the interactions between helminths and Plasmodium; in some, the burden of Plasmodium parasites increased, but others reported a reduction in the parasite. This review focuses on explaining many of these discrepancies regarding helminth-Plasmodium coinfections in terms of the effects that helminths have on the immune system. In particular, it focuses on helminth-induced immunosuppression and the effects of cytokines controlling polarization toward the Th1 or Th2 arms of the immune response.

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Impaired pro-inflammatory cytokine production and increased Th2-biasing ability of dendritic cells exposed to Taenia excreted/secreted antigens: A critical role for carbohydrates but not for STAT6 signaling

Cited by 51 publications

References 57 publications

Modulation of Specific and Allergy‐Related Immune Responses by Helminths

Modulation of Specific and Allergy‐Related Immune Responses by Helminths

Excretory/Secretory-Products of Echinococcus multilocularis Larvae Induce Apoptosis and Tolerogenic Properties in Dendritic Cells In Vitro

Helminth Parasites Alter Protection againstPlasmodiumInfection

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