Immunity to gastrointestinal nematodes in ruminants: Effector cell mechanisms and cytokines
Open accessAbstract
Gastrointestinal nematodes (GINs) of ruminants are prevalent and have major economic impacts worldwide. The insight studies of immune responses triggered against GINs are of great concern to understand interaction between host's immune system and parasite. T-helper 2 cytokines drive the effector cell mechanisms which include eosinophils and mast cells. The immune responses are controlled by Th2 secreted interleukins (IL); IL3, IL-4, IL-5, IL-9, IL-10 and IL-13. B-Cell immune response is incorporated in defense mechanisms developed against GINs specially immunoglobulins (Ig); IgA, IgE and IgG. The immune resistance of the infected host is presented by failure of larval establishment or hypobiosis, low worm burden and decreased female fecundity. The host-parasite interaction is a complex series that affected by host's genetic constitution, nutrition, age and physiological status. The GINs have different immune evasion mechanisms to improve their survival within the host. Also, management of the host influences GINs parasitism. Thus, the aim of this review is to highlight the hallmarks of immune responses that endorse GINs parasitism. The insights studies of the triggered immune responses developed against GINs will improve the appropriate protective immune strategy.
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Immunomodulatory mediators such as ES-62, cystatins, legumains and cathepsin L and S have an immunomodulatory effect to enhance production of anti-inflammatory IL10.
“They have an immunomodulatory effect to enhance the production of anti-inflammatory IL10 [17,22].”
From Emergent and Neglected Equine Filariosis in Egypt: Species Diversity and Host Immune Response (2022) · cites this paper as [17]
The “Parasitic immune evasion strategies” section says cystatins have an immunomodulatory effect and enhance anti-inflammatory IL10 production. It describes legumains and cathepsins L and S as enzymes inhibited by cystatins, and attributes other immune effects—not IL10 enhancement—to ES-62. The cited passage has no page number in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredHost-parasite interaction relies on the expressed cytokine profile which is modulated by the parasite itself.
“Host–parasite interaction relies on the expressed cytokine profile which is modulated by the parasite itself [15,16,17].”
From Emergent and Neglected Equine Filariosis in Egypt: Species Diversity and Host Immune Response (2022) · cites this paper as [17]
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Emergent and Neglected Equine Filariosis in Egypt: Species Diversity and Host Immune Response
Abo-Aziza, F. A. M., Hendawy, S. H. M., Abdullah, H. H. A. M., El Namaky, A., Laidoudi, Y., & Mediannikov, O. (2022) · Pathogens · doi:10.3390/pathogens11090979 · Cited by 4 · see citing works
“They have an immunomodulatory effect to enhance the production of anti-inflammatory IL10 [17,22].”
BackgroundSelf-citation
- Authors
- Hendawy, S. H. M.
- Affiliations
- National Research Centre (EG)
- Corresponding author
- Hendawy, Seham H. M.
- ORCID
- Hendawy, Seham H. M.
- Venue
- Journal of Parasitic Diseases
- Published
- 2018-08-09
- Volume
- 42
- Issue
- 4
- Pages
- 471-482
- ISSN
- 0971-7196 (ISSN-L)
- 0975-0703
- PMC
- PMC6261135
- OpenAlex
- W2886301595
- Cited by
- 56
- References
- 78
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 8 · 2023: 7 · 2022: 15 · 2021: 4 · 2020: 5 · 2019: 2
- FWCI
- 0.58
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Parasitic Diseases (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Veterinary › Small Animals › Helminth infection and control
- Life Sciences › Immunology and Microbiology › Parasitology › Parasites and Host Interactions
- Life Sciences › Agricultural and Biological Sciences › Insect Science › Mollusks and Parasites Studies
- Keywords
- gastrointestinal nematodes, ruminants, host-parasite interactions, Th2 cytokines, eosinophils, mast cells, interleukins, immunoglobulins, IgA, IgE, IgG, immune evasion, host resistance, protective immunity
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