Protective Host Response to Parasite and Its Limitations

Truyens, Carine; Carlier, Yves; Tellería, Jenny; Tibayrenc, Michel

doi:10.1016/b978-0-12-384876-5.00024-1

Cited by 3 publications

(2 citation statements)

References 426 publications

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“…Our present and previous results [34] are in line with others showing that live parasites or selected parasitederived molecules are able to induce functional maturation of human and murine DCs, endowing them to favour a protective type 1 T cell response ( [9,10,18,24,27,28] and reviewed in [47]). However, another study indicates that the parasite does not up-regulate MHC class II and co-stimulatory molecules on DCs, which in turn do not trigger T cell activation [30].…”

Section: Discussionsupporting

confidence: 91%

Trypanosoma cruzi activates cord blood myeloid dendritic cells independently of cell infection

Rodríguez

Carlier

Truyens

2012

Med Microbiol Immunol

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We recently showed that T. cruzi parasites enhance expression of co-stimulatory surface molecules on cord blood myeloid dendritic cells (mDCs). This study aims to gain insight into the role of live parasites and intracellular infection in mDC activation using CSFE-labelled parasites. First, we observed that only a low proportion of mDCs was infected by T. cruzi after overnight culture of whole blood samples and trypomastigotes, as compared with monocytes and granulocytes. Cord blood mDCs were also less infected than their adult counterpart. Second, expression levels of HLA-DR and co-stimulatory molecules CD80, CD83 and CD86 were similar on infected and uninfected mDCs. Parasite lysate also triggered mDCs phenotypic maturation of both cord and adult blood cells, though in a lower extent than live parasites. These results strongly support a central role for extracellular trypomastigotes in activation of mDCs when parasites are incubated with whole blood cells. However, viability of trypomastigotes was not absolutely required for mDC activation.

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Section: Discussionsupporting

confidence: 91%

Trypanosoma cruzi activates cord blood myeloid dendritic cells independently of cell infection

Rodríguez

Carlier

Truyens

2012

Med Microbiol Immunol

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“…7 Resistance against infection could be regulated by the genetic characteristics of the host, but the persistence of the infection is due to additional factors depending on both the parasite and the host. 8 In most cases, the immune response of the host is not enough to eradicate the parasite. Therefore, a vaccine in order to reinforce immune response to the parasite has been proposed, but it is still in the early stages of development.…”

Section: Introduction: Biology and Epidemiology Of Chagas Diseasementioning

confidence: 99%

Chagas disease: from Latin America to the world

Gascón¹,

Pinazo²

2015

RIP

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Migratory flows have globalized Chagas disease and have contributed to change its epidemiology. Additionally, Chagas disease has a great impact on the affected people as well as on the economy of their countries. However, till now, this disease remains a neglected disease. Historically, very few resources have been invested to study Chagas disease or to provide care to the millions of affected people. In Latin America, the endemic countries still have several challenges ahead, which include care for the affected people, the effective control of vertical transmission, or the maintenance of vector control. In nonendemic countries where the disease is emerging, care for patients and the control programs for blood banks, organ transplant, and mother-to-child transmission should be the priorities.

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The Ly49E Receptor Inhibits the Immune Control of Acute Trypanosoma cruzi Infection

et al. 2016

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The protozoan parasite Trypanosoma cruzi circulates in the blood upon infection and invades various cells. Parasites intensively multiply during the acute phase of infection and persist lifelong at low levels in tissues and blood during the chronic phase. Natural killer (NK) and NKT cells play an important role in the immune control of T. cruzi infection, mainly by releasing the cytokine IFN-γ that activates the microbicidal action of macrophages and other cells and shapes a protective type 1 immune response. The mechanisms by which immune cells are regulated to produce IFN-γ during T. cruzi infection are still incompletely understood. Here, we show that urokinase plasminogen activator (uPA) is induced early upon T. cruzi infection and remains elevated until day 20 post-infection. We previously demonstrated that the inhibitory receptor Ly49E, which is expressed, among others, on NK and NKT cells, is triggered by uPA. Therefore, we compared wild type (WT) to Ly49E knockout (KO) mice for their control of experimental T. cruzi infection. Our results show that young, i.e., 4- and 6-week-old, Ly49E KO mice control the infection better than WT mice, indicated by a lower parasite load and less cachexia. The beneficial effect of Ly49E depletion is more obvious in 4-week-old male than in female mice and weakens in 8-week-old mice. In young mice, the lower T. cruzi parasitemia in Ly49E KO mice is paralleled by higher IFN-γ production compared to their WT controls. Our data indicate that Ly49E receptor expression inhibits the immune control of T. cruzi infection. This is the first demonstration that the inhibitory Ly49E receptor can interfere with the immune response to a pathogen in vivo.

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Protective Host Response to Parasite and Its Limitations

Cited by 3 publications

References 426 publications

Trypanosoma cruzi activates cord blood myeloid dendritic cells independently of cell infection

Trypanosoma cruzi activates cord blood myeloid dendritic cells independently of cell infection

Chagas disease: from Latin America to the world

The Ly49E Receptor Inhibits the Immune Control of Acute Trypanosoma cruzi Infection

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