Helminth parasites and immune regulation

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Helminth parasites are complex metazoans that belong to different taxonomic families but that collectively share the capacity to downregulate the host immune response directed toward themselves (parasite-specific immunoregulation). During long-standing chronic infection, these helminths appear able to suppress immune responses to bystander pathogens/antigens and atopic, autoimmune, and metabolic disorders. Helminth-induced immunoregulation occurs through the induction of regulatory T cells or Th2-type cells (or both). However, secreted or excreted parasite metabolites, proteins, or extracellular vesicles (or a combination of these) may also directly induce signaling pathways in host cells. Therefore, the focus of this review will be to highlight recent advances in understanding the immune responses to helminth infection, emphasizing the strategies/molecules and some of the mechanisms used by helminth parasites to modulate the immune response of their hosts.

Related collections

Most cited references 101

Record: found
Abstract: found
Article: not found

Tuft-cell-derived IL-25 regulates an intestinal ILC2-epithelial response circuit.

Jakob von Moltke, Ming Fei Ji, Hong-Erh Liang … (2016)

Parasitic helminths and allergens induce a type 2 immune response leading to profound changes in tissue physiology, including hyperplasia of mucus-secreting goblet cells and smooth muscle hypercontractility. This response, known as 'weep and sweep', requires interleukin (IL)-13 production by tissue-resident group 2 innate lymphoid cells (ILC2s) and recruited type 2 helper T cells (TH2 cells). Experiments in mice and humans have demonstrated requirements for the epithelial cytokines IL-33, thymic stromal lymphopoietin (TSLP) and IL-25 in the activation of ILC2s, but the sources and regulation of these signals remain poorly defined. In the small intestine, the epithelium consists of at least five distinct cellular lineages, including the tuft cell, whose function is unclear. Here we show that tuft cells constitutively express IL-25 to sustain ILC2 homeostasis in the resting lamina propria in mice. After helminth infection, tuft-cell-derived IL-25 further activates ILC2s to secrete IL-13, which acts on epithelial crypt progenitors to promote differentiation of tuft and goblet cells, leading to increased frequencies of both. Tuft cells, ILC2s and epithelial progenitors therefore comprise a response circuit that mediates epithelial remodelling associated with type 2 immunity in the small intestine, and perhaps at other mucosal barriers populated by these cells.

0 comments Cited 553 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

Immune regulation by helminth parasites: cellular and molecular mechanisms.

Rick Maizels, Maria Yazdanbakhsh (2003)

Immunology was founded by studying the body's response to infectious microorganisms, and yet microbial prokaryotes only tell half the story of the immune system. Eukaryotic pathogens--protozoa, helminths, fungi and ectoparasites--have all been powerful selective forces for immune evolution. Often, as with lethal protozoal parasites, the focus has been on acute infections and the inflammatory responses they evoke. Long-lived parasites such as the helminths, however, are more remarkable for their ability to downregulate host immunity, protecting themselves from elimination and minimizing severe pathology in the host.

0 comments Cited 345 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: found

Is Open Access

The Intestinal Microbiota Contributes to the Ability of Helminths to Modulate Allergic Inflammation

Mario Zaiss, Alexis Rapin, Luc Lebon … (2015)

Summary Intestinal helminths are potent regulators of their host’s immune system and can ameliorate inflammatory diseases such as allergic asthma. In the present study we have assessed whether this anti-inflammatory activity was purely intrinsic to helminths, or whether it also involved crosstalk with the local microbiota. We report that chronic infection with the murine helminth Heligmosomoides polygyrus bakeri (Hpb) altered the intestinal habitat, allowing increased short chain fatty acid (SCFA) production. Transfer of the Hpb-modified microbiota alone was sufficient to mediate protection against allergic asthma. The helminth-induced anti-inflammatory cytokine secretion and regulatory T cell suppressor activity that mediated the protection required the G protein-coupled receptor (GPR)-41. A similar alteration in the metabolic potential of intestinal bacterial communities was observed with diverse parasitic and host species, suggesting that this represents an evolutionary conserved mechanism of host-microbe-helminth interactions.

0 comments Cited 209 times – based on 0 reviews      Review now

All references

Author and article information

Contributors

Pedro H. Gazzinelli-Guimaraes: Role: ConceptualizationRole: Data CurationRole: MethodologyRole: SupervisionRole: Writing – Original Draft PreparationRole: Writing – Review & Editing

ORCID: https://orcid.org/0000-0003-4932-2206

Thomas B. Nutman: Role: ConceptualizationRole: Data CurationRole: MethodologyRole: SupervisionRole: Writing – Original Draft PreparationRole: Writing – Review & Editing

Journal

Journal ID (nlm-ta): F1000Res

Journal ID (iso-abbrev): F1000Res

Journal ID (pmc): F1000Research

Title: F1000Research

Publisher: F1000 Research Limited (London, UK )

ISSN (Electronic): 2046-1402

Publication date (Electronic): 23 October 2018

Publication date Collection: 2018

Volume: 7

Electronic Location Identifier: F1000 Faculty Rev-1685

Affiliations

[1 ]Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 4 Center Drive, Building 4, Room 211, Bethesda, MD, 20892, USA

Author notes

[a ] pedro.gazzinelliguimaraes@ 123456nih.gov

No competing interests were disclosed.

Author information

Pedro H. Gazzinelli-Guimaraes https://orcid.org/0000-0003-4932-2206

Article

DOI: 10.12688/f1000research.15596.1

PMC ID: 6206608

PubMed ID: 30416709

SO-VID: e04675bd-38af-4283-9d2b-4255c9609fb0

License:

This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

The author(s) is/are employees of the US Government and therefore domestic copyright protection in USA does not apply to this work. The work may be protected under the copyright laws of other jurisdictions when used in those jurisdictions.

History

Date accepted : 17 October 2018

Funding

Funded by: Division of Intramural Research of the National Institutes of Health

This work was supported by the Division of Intramural Research of the National Institutes of Health. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Helminth parasites and immune regulation

Read this article at

Abstract

Related collections

HLA-G and immune tolerance in pregnancy

Most cited references 101

Tuft-cell-derived IL-25 regulates an intestinal ILC2-epithelial response circuit.

Immune regulation by helminth parasites: cellular and molecular mechanisms.

The Intestinal Microbiota Contributes to the Ability of Helminths to Modulate Allergic Inflammation

Author and article information

Contributors

Journal

Affiliations

Author notes

Author information

Article

History

Funding

Categories

Comments

Comment on this article

Similar content 479

Cited by 56

Most referenced authors 1,293