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Helminth Induced Immunoregulation and Novel Therapeutic Avenue of Allergy

Ayelign, Birhanu, Akalu, Yonas, Teferi, Banchamlak, Molla, Meseret Derbew, Shibabaw, Tewodros·2020·Journal of Asthma and Allergy
DOI 10.2147/jaa.s273556PMC PMC7548329
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Figure 1 The possible mechanism of the hygiene hypothesis and the effect of early helminthic infections on cytokine production. Improved hygiene, frequent use of antibiotics, and vaccination has led to reduced bacterial and viral infections in industrialized countries and therefore to insufficient stimulation of Th 1 responses, which in turn allows the expansion of Th2 cells. Th2 responses are characterized by increased IgE to allergens, mastocytosis, and eosinophilia. Mast cell degranulation and release of inflammatory mediators lead to mucus production and smooth muscle cell contraction, precipitating allergic diseases of the airways. Helminths are prevalent in developing countries and lead to strong Th2 responses. However, helminth-infected populations show little signs of allergic disorders. This difference may be explained by the differences in exposure to pathogens. A high prevalence of chronic infections in developing countries results in the persistent immunity challenge, with cycles of infection and inflammation, which is followed by the triggering of anti-inflammatory molecules such as IL-10, TGF-β, and arginase-1 (Arg-1) to restrict the immunopathology of allergic disease.
Figure 1 The possible mechanism of the hygiene hypothesis and the effect of early helminthic infections on cytokine production. Improved hygiene, frequent use of antibiotics, and vaccination has led to reduced bacterial and viral infections in industrialized countries and therefore to insufficient stimulation of Th 1 responses, which in turn allows the expansion of Th2 cells. Th2 responses are characterized by increased IgE to allergens, mastocytosis, and eosinophilia. Mast cell degranulation and release of inflammatory mediators lead to mucus production and smooth muscle cell contraction, precipitating allergic diseases of the airways. Helminths are prevalent in developing countries and lead to strong Th2 responses. However, helminth-infected populations show little signs of allergic disorders. This difference may be explained by the differences in exposure to pathogens. A high prevalence of chronic infections in developing countries results in the persistent immunity challenge, with cycles of infection and inflammation, which is followed by the triggering of anti-inflammatory molecules such as IL-10, TGF-β, and arginase-1 (Arg-1) to restrict the immunopathology of allergic disease.CC BY-NC · PubMed Central
Figure 2 Humans Immune response against helminthic infection. The entry of helminthic parasite into the intestine can initiate damage to the mucosa causing the release of alarmin cytokines and danger-associated molecular patterns (DAMPs). DAMPs released by dying cells, or signals resulting from apoptosis, might also influence either dendritic cells (DCs) or Th1 polarization towards Th2 or T regulatory cell (Treg) cell subset. Tuft cells are also stimulated and produce IL-33, IL-25, and TSLP. Alarmin cytokine, in turn, activates ILC2 which stimulates type 2 immunity. This canonical response is of the Th2 type and involves the cytokines interleukin‑3 (IL‑3), IL‑4, IL‑5, IL‑9, IL‑10, and IL‑13, the antibody isotypes IgG1, IgG4 and IgE, and expanded populations of eosinophil, basophils, and mast cells. After the epithelium insult with the parasite, DC is activated by alarmin cytokines or parasitic ES products; in turn, it acts as an APC (antigen-presenting cell) for T-cells of the nearby lymph node. Cytokine production by ILC2s and Th2 cells act locally to promote the expulsion of adult worms from the intestinal lumen by weeping and sweeping process. These processes are primarily mediated by IL-4 and IL-13 that increase smooth-muscle-cell motility, stimulates intestinal epithelial permeability, and elevates mucous secretion by goblet cells.
Figure 2 Humans Immune response against helminthic infection. The entry of helminthic parasite into the intestine can initiate damage to the mucosa causing the release of alarmin cytokines and danger-associated molecular patterns (DAMPs). DAMPs released by dying cells, or signals resulting from apoptosis, might also influence either dendritic cells (DCs) or Th1 polarization towards Th2 or T regulatory cell (Treg) cell subset. Tuft cells are also stimulated and produce IL-33, IL-25, and TSLP. Alarmin cytokine, in turn, activates ILC2 which stimulates type 2 immunity. This canonical response is of the Th2 type and involves the cytokines interleukin‑3 (IL‑3), IL‑4, IL‑5, IL‑9, IL‑10, and IL‑13, the antibody isotypes IgG1, IgG4 and IgE, and expanded populations of eosinophil, basophils, and mast cells. After the epithelium insult with the parasite, DC is activated by alarmin cytokines or parasitic ES products; in turn, it acts as an APC (antigen-presenting cell) for T-cells of the nearby lymph node. Cytokine production by ILC2s and Th2 cells act locally to promote the expulsion of adult worms from the intestinal lumen by weeping and sweeping process. These processes are primarily mediated by IL-4 and IL-13 that increase smooth-muscle-cell motility, stimulates intestinal epithelial permeability, and elevates mucous secretion by goblet cells.CC BY-NC · PubMed Central
Figure 3 Summarizes the main roles proposed for Treg as well as AAM. Helminthic modulation of allergy or inflammation. Helminth can modulate APC, type 2 immunity system, B-cell, eosinophil and induce Treg. The other regulatory cell is AAMs. The immunosuppressive role of Treg controlled by IL-10, TGF-β and CTLA-4. The differentiation of AAM, can inactivate the production of Th1, Th2, or Th17 cells, and in some cases, induce fibrosis in tissues mediated by regulatory cytokines mainly RELMα and arg-1. On the other hand, IL-10 controls untoward immune responses to minimize overall harm secondary to the parasite and then it acts as mediator of immune tolerance.
Figure 3 Summarizes the main roles proposed for Treg as well as AAM. Helminthic modulation of allergy or inflammation. Helminth can modulate APC, type 2 immunity system, B-cell, eosinophil and induce Treg. The other regulatory cell is AAMs. The immunosuppressive role of Treg controlled by IL-10, TGF-β and CTLA-4. The differentiation of AAM, can inactivate the production of Th1, Th2, or Th17 cells, and in some cases, induce fibrosis in tissues mediated by regulatory cytokines mainly RELMα and arg-1. On the other hand, IL-10 controls untoward immune responses to minimize overall harm secondary to the parasite and then it acts as mediator of immune tolerance.CC BY-NC · PubMed Central

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Metadata

Authors
Ayelign, B., Akalu, Y., Teferi, B., Molla, M. D., & Shibabaw, T.
Venue
Journal of Asthma and Allergy
Publisher
Informa UK Limited
Published
2020-10
Volume
Volume 13
Pages
439-451
ISSN
1178-6965
DOI
10.2147/jaa.s273556
PMC
PMC7548329
Cited by
32
References
6
Language
en
Licence
creativecommons.org/licenses/by-nc/3.0/ (unspecified)

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