T-Helper 17 Cells Are Associated With Pathology in Human Schistosomiasis

Mbow, Moustapha; Larkin, Bridget; Meurs, Lynn; Wammes, Linda J.; Jong, Sanne E. de; Labuda, Lucja A.; Camara, Makhtar; Smits, Hermelijn H.; Polman, Katja; Diéye, Tandakha Ndiaye; Mboup, Souleymane; Stadecker, Miguel J.; Yazdanbakhsh, Maria

doi:10.1093/infdis/jis654

Cited by 80 publications

(75 citation statements)

References 35 publications

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“…We subsequently showed in the same lung migration model that IL-17A deficient animals were protected from the peak of tissue damage [46 ]. In addition, IL-17 is associated with more severe pathology in both murine and human schistosomiasis [48,49] and human onchocerchiasis [50] These data are consistent with the proposal that IL-17 pushes the type 2 response into a more pathological state [51]. The ability of IL-17 to exacerbate type 2 pathology has recently become a central focus of asthma research [reviewed in [15]].…”

Section: Il-17 and Type 2 Cytokinesmentioning

confidence: 83%

IL-17 and neutrophils: unexpected players in the type 2 immune response

Allen¹,

Sutherland²,

Rückerl³

2015

Current Opinion in Immunology

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The study of immunity to helminth infection has been central to understanding the function of type 2 cytokines and their targets. Although type 2 cytokines are considered anti-inflammatory and promote tissue repair, they also contribute to allergy and fibrosis. Here, we utilise data from helminth infection models, to illustrate that IL-17 and neutrophils, typically associated with pro-inflammatory responses, are intimately linked with type 2 immunity. Neutrophils work with IL-4Rα-activated macrophages to control incoming larvae but this comes at a cost of enhanced tissue damage. Chitinase like proteins (CLPs) bridge these diverse outcomes, inducing both protective IL-17 and reparative Th2 responses. Dysregulation of CLPs, IL-17 and neutrophils likely contribute to disease severity and pathology associated with type 2 immunity.

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Section: Il-17 and Type 2 Cytokinesmentioning

confidence: 83%

IL-17 and neutrophils: unexpected players in the type 2 immune response

Allen¹,

Sutherland²,

Rückerl³

2015

Current Opinion in Immunology

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“…In addition, T cells from helminth-infected asymptomatic human subjects show skewed cytokine profiles, favoring IL-4 over IL-17 and IFN-γ 10 and with more conspicuous IL-10 and TGF-β components 12, 13. In contrast, in patients in whom symptomatic disease develops, there is a failure of tolerance, allowing T H 1 and T H 17 responses to surface and mediate significant pathology in infected tissues 14, 15…”

Section: Immunologic Tolerance In Human Helminth Infectionsmentioning

confidence: 99%

Regulation of the host immune system by helminth parasites

Maizels

McSorley

2016

Journal of Allergy and Clinical Immunology

418

380

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Helminth parasite infections are associated with a battery of immunomodulatory mechanisms that affect all facets of the host immune response to ensure their persistence within the host. This broad-spectrum modulation of host immunity has intended and unintended consequences, both advantageous and disadvantageous. Thus the host can benefit from suppression of collateral damage during parasite infection and from reduced allergic, autoimmune, and inflammatory reactions. However, helminth infection can also be detrimental in reducing vaccine responses, increasing susceptibility to coinfection and potentially reducing tumor immunosurveillance. In this review we will summarize the panoply of immunomodulatory mechanisms used by helminths, their potential utility in human disease, and prospective areas of future research.

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“…Both IL-23 and IL-6 are crucial cytokines for the induction and maintenance of T H 17 cells 45 . The induction of T H 17 responses is associated with severe forms of schistosomiasis with granulomatous inflammation in host tissues, both in mice and humans, although with relatively low incidence in humans 46,47 . S. mansoni SEA has been reported to suppress T H 17 differentiation 48 .…”

Section: Bcl3 Mediates Expression Of T H 2-attracting Chemokinesmentioning

confidence: 99%

Fucose-specific DC-SIGN signalling directs T helper cell type-2 responses via IKKε- and CYLD-dependent Bcl3 activation

et al. 2014

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Carbohydrate-specific signalling through DC-SIGN provides dendritic cells with plasticity to tailor immunity to the nature of invading microbes. Here we demonstrate that recognition of fucose-expressing extracellular pathogens like Schistosoma mansoni and Helicobacter pylori by DC-SIGN favors T helper cell type-2 (T H 2) responses via activation of atypical NF-kB family member Bcl3. Crosstalk between TLR and DC-SIGN signalling results in TLR-induced MK2-mediated phosphorylation of LSP1, associated with DC-SIGN, upon fucose binding. Subsequently, IKKe and CYLD are recruited to phosphorylated LSP1. IKKe activation is pivotal for suppression of CYLD deubiquitinase activity and subsequent nuclear translocation of ubiquitinated Bcl3. Bcl3 activation represses TLR-induced proinflammatory cytokine expression,

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T-Helper 17 Cells Are Associated With Pathology in Human Schistosomiasis

Abstract: This is the first study to indicate that Th17 cells may be involved in the pathogenesis of human schistosomiasis.

Cited by 80 publications

References 35 publications

IL-17 and neutrophils: unexpected players in the type 2 immune response

IL-17 and neutrophils: unexpected players in the type 2 immune response

Regulation of the host immune system by helminth parasites

Fucose-specific DC-SIGN signalling directs T helper cell type-2 responses via IKKε- and CYLD-dependent Bcl3 activation

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