Eosinophils and mast cells in leishmaniasis

Rodríguez, Nilda E.; Wilson, Mary E.

doi:10.1007/s12026-014-8536-x

Cited by 42 publications

(39 citation statements)

References 116 publications

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“…mexicana and L . donovani [ 63 ]. Therefore, induction of this cytokine, observed here by immunization with NGP5B, could be beneficial for the control of L .…”

Section: Discussionmentioning

confidence: 99%

An α-Gal-containing neoglycoprotein-based vaccine partially protects against murine cutaneous leishmaniasis caused by Leishmania major

et al. 2017

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BackgroundProtozoan parasites from the genus Leishmania cause broad clinical manifestations known as leishmaniases, which affect millions of people worldwide. Cutaneous leishmaniasis (CL), caused by L. major, is one the most common forms of the disease in the Old World. There is no preventive or therapeutic human vaccine available for L. major CL, and existing drug treatments are expensive, have toxic side effects, and resistant parasite strains have been reported. Hence, further therapeutic interventions against the disease are necessary. Terminal, non-reducing, and linear α-galactopyranosyl (α-Gal) epitopes are abundantly found on the plasma membrane glycolipids of L. major known as glycoinositolphospholipids. The absence of these α-Gal epitopes in human cells makes these glycans highly immunogenic and thus potential targets for vaccine development against CL.Methodology/Principal findingsHere, we evaluated three neoglycoproteins (NGPs), containing synthetic α-Gal epitopes covalently attached to bovine serum albumin (BSA), as vaccine candidates against L. major, using α1,3-galactosyltransferase-knockout (α1,3GalT-KO) mice. These transgenic mice, similarly to humans, do not express nonreducing, linear α-Gal epitopes in their cells and are, therefore, capable of producing high levels of anti-α-Gal antibodies. We observed that Galα(1,6)Galβ-BSA (NGP5B), but not Galα(1,4)Galβ-BSA (NGP12B) or Galα(1,3)Galα-BSA (NGP17B), was able to significantly reduce the size of footpad lesions by 96% in comparison to control groups. Furthermore, we observed a robust humoral and cellular immune response with production of high levels of protective lytic anti-α-Gal antibodies and induction of Th1 cytokines.Conclusions/SignificanceWe propose that NGP5B is an attractive candidate for the study of potential synthetic α-Gal-neoglycoprotein-based vaccines against L. major infection.

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“…mexicana and L . donovani [ 63 ]. Therefore, induction of this cytokine, observed here by immunization with NGP5B, could be beneficial for the control of L .…”

Section: Discussionmentioning

confidence: 99%

An α-Gal-containing neoglycoprotein-based vaccine partially protects against murine cutaneous leishmaniasis caused by Leishmania major

et al. 2017

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“…More importantly, activation of TLR2, TLR4, or TLR9 by their respective antigens results in significant protection from Leishmania pathogenesis and parasite burden [77]. Additionally, the results of recent studies show a surprising role for eosinophils and mast cells in inducing proper immune responses against Leishmania and in providing protection, mostly through the regulation of DCs and adaptive immunity [78,79]. …”

Section: Leishmaniasismentioning

confidence: 99%

Immune responses against protozoan parasites: a focus on the emerging role of Nod-like receptors

Gurung

Kanneganti

2016

Cell. Mol. Life Sci.

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Nod-like receptors (NLRs) have gained attention in recent years because of the ability of some family members to assemble into a multimeric protein complex known as the inflammasome. The role of NLRs and the inflammasome in regulating innate immunity against bacterial pathogens has been well studied. However, recent studies show that NLRs and inflammasomes also play a role during infections caused by protozoan parasites, which pose a significant global health burden. Herein, we review the diseases caused by the most common protozoan parasites in the world and discuss the roles of NLRs and inflammasomes in host immunity against these parasites.

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“…In contrast, IL-4 induces the differentiation of CD4+ T cells to a Th2 profile, which produces IL-4, IL-5, and IL-13. This profile suppresses NO production and leads to an increase in eosinophils [ 32 ].…”

Section: Inflammatory Response To Leishmania Inmentioning

confidence: 99%

Natural Products: Insights into Leishmaniasis Inflammatory Response

Rodrigues

Mazotto

Cardoso

et al. 2015

Mediators of Inflammation

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Leishmaniasis is a vector-borne disease that affects several populations worldwide, against which there are no vaccines available and the chemotherapy is highly toxic. Depending on the species causing the infection, the disease is characterized by commitment of tissues, including the skin, mucous membranes, and internal organs. Despite the relevance of host inflammatory mediators on parasite burden control, Leishmania and host immune cells interaction may generate an exacerbated proinflammatory response that plays an important role in the development of leishmaniasis clinical manifestations. Plant-derived natural products have been recognized as bioactive agents with several properties, including anti-protozoal and anti-inflammatory activities. The present review focuses on the antileishmanial activity of plant-derived natural products that are able to modulate the inflammatory response in vitro and in vivo. The capability of crude extracts and some isolated substances in promoting an anti-inflammatory response during Leishmania infection may be used as part of an effective strategy to fight the disease.

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Eosinophils and mast cells in leishmaniasis

Cited by 42 publications

References 116 publications

An α-Gal-containing neoglycoprotein-based vaccine partially protects against murine cutaneous leishmaniasis caused by Leishmania major

An α-Gal-containing neoglycoprotein-based vaccine partially protects against murine cutaneous leishmaniasis caused by Leishmania major

Immune responses against protozoan parasites: a focus on the emerging role of Nod-like receptors

Natural Products: Insights into Leishmaniasis Inflammatory Response

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