Chronic helminth infections induce immunomodulation: Consequences and mechanisms

Riet, Elly van; Hartgers, Franca C.; Yazdanbakhsh, Maria

doi:10.1016/j.imbio.2007.03.009

Cited by 335 publications

(304 citation statements)

References 109 publications

(72 reference statements)

Supporting

Mentioning

283

Contrasting

Unclassified

Order By: Relevance

“…In lymphatic filariasis, patients show decreased Th1 and Th2 cell frequencies, which might in part be explained by the upregulation of expression of Treg associated FOXP3, TGF-b and CTLA-4 in response to live Brugia malayi parasites [4]. Interestingly, it has also been shown that helminth infections can affect responses to unrelated Ag, such as those expressed in vaccines or by other pathogens [5]. Geohelminth infections have, for example, been associated with reduced immune responses to BCG vaccination [6] and to the cholera vaccine [7].…”

Section: Cd25mentioning

confidence: 99%

Regulatory T cells in human geohelminth infection suppress immune responses to BCG and Plasmodium falciparum

et al. 2010

Self Cite

View full text Add to dashboard Cite

Chronic helminth infections induce T-cell hyporesponsiveness, which may affect immune responses to other pathogens or to vaccines. This study investigates the influence of Treg activity on proliferation and cytokine responses to BCG and Plasmodium falciparum-parasitized RBC in Indonesian schoolchildren. Geohelminth-infected children's in vitro T-cell proliferation to either BCG or pRBC was reduced compared to that of uninfected children. Although the frequency of CD41 T cells was similar regardless of infection status, the suppressive activity differed between geohelminth-infected and geohelminthuninfected groups: Ag-specific proliferative responses increased upon CD4 1 CD25 hi T-cell depletion in geohelminth-infected subjects only. In addition, IFN-c production in response to both BCG and parasitized RBC was increased after removal of CD4These data demonstrate that geohelminth-associated Treg influence immune responses to bystander Ag of mycobacteria and plasmodia. Geohelminth-induced immune modulation may have important consequences for co-endemic infections and vaccine trials.

show abstract

Section: Cd25mentioning

confidence: 99%

Regulatory T cells in human geohelminth infection suppress immune responses to BCG and Plasmodium falciparum

et al. 2010

Self Cite

View full text Add to dashboard Cite

show abstract

“…Chronic infections favor immunosuppression, the so-called modulated Th2-response, associated with poor parasite-specific reactivity alongside with the strong production of anti-inflammatory cytokines, such as IL-10 and TGF-b [1]. This helminth-induced immunosuppression may spill over to bystander antigens [3], downmodulate reactivity against other pathogens [4] and impair vaccination efficacy [5]. However, such effects can be beneficial by downregulating inflammatory reactions to allergens and inflammatory disorders of the intestinal tract.…”

Section: Introductionmentioning

confidence: 99%

Establishment of nematode infection despite increased Th2 responses and immunopathology after selective depletion of Foxp3⁺ cells

et al. 2009

View full text Add to dashboard Cite

Here, we show that Treg limit intestinal pathology during nematode infection and that they control the onset and magnitude of the anti-parasitic Th Th2 response. Using mice expressing the diptheria toxin receptor under the control of the foxp3 locus, we removed Foxp3 1 Treg during the early phase of infection with Heligmosomoides polygyrus bakeri. Depletion of Treg in infected animals did not affect adult worm burden, but led to increased pathology at the site of infection. Infected, depleted mice displayed higher frequencies of activated CD4 1 T cells and increased levels of the Th2 cytokines IL-4 and IL-13. The stronger parasite-specific Th2 response was accompanied by higher levels of IL-10. Only a moderate change in Th1 (IFN-c) reactivity was detected in worm-infected, Treg-depleted mice. Furthermore, we detected an accelerated onset of parasite-specific Th2 and IL-10 responses in the transient absence of Foxp3 1 Treg. However, adult worm burdens were not affected by the increased Th2-reactivity in Treg-depleted mice. Hence, our data show that Treg restrict the onset and strength of Th2 responses during intestinal worm infection, while increasing primary Th2 responses does not necessarily lead to killing of larvae or accelerated expulsion of adult worms.Key words: Foxp3 . Nematode . Pathology . Th2 response . Treg IntroductionParasitic worms are the most potent inducers of highly polarized Th cell type 2 (Th2) responses. Helminth infections tend to be long lasting and are often associated with insufficient immunity to re-infection [1,2]. Chronic infections favor immunosuppression, the so-called modulated Th2-response, associated with poor parasite-specific reactivity alongside with the strong production of anti-inflammatory cytokines, such as . This helminth-induced immunosuppression may spill over to bystander antigens [3], downmodulate reactivity against other pathogens [4] and impair vaccination efficacy [5]. However, such effects can be beneficial by downregulating inflammatory reactions to allergens and inflammatory disorders of the intestinal tract. Studies in animal models showed that helminths can suppress airway hyperreactivity and colitis [6][7][8] and nematodes have been used to efficiently treat human inflammatory bowel disease in clinical trials [9,10]. 3066In animal models, the beneficial effects of nematode infections on inflammatory disorders were associated with the presence of Treg populations [6,11,12]. However, it is not yet clear whether such Treg suppress anti-parasite immune reactivity and thus contribute to survival and well-being of the worms, or whether they predominantly dampen immunopathology. Several studies investigated the role of Treg in infections with helminths or other parasites and yielded in diverging conclusions (reviewed in [1] and [13]). There is evidence that certain parasites depend on Treg action for their persistence [14][15][16][17]. Other species profit more indirectly from Treg circuits, which control infectioninduced pathology [18][19][20].In a previous study ...

show abstract

“…This was also confirmed in this paper by BOMA cell line for TNF-α secretion. In general helminths bias immune response towards Th 2 phenotype as well as induce overall down-regulation of immune system (van Riet et al 2007). TNF-α is rather associated with proinflammatory Th 17 response (Weaver et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Fasciola hepatica — the pilot study of in vitro assessing immune response against native and recombinant antigens of the fluke

Bąska

Zawistowska-Deniziak

Zdziarska

et al. 2013

Acta Parasitologica

View full text Add to dashboard Cite

Fasciola hepatica is a liver fluke that infects 2.4 million of people and causes great economical loss in animal production. To date a 100% effective vaccine has not been developed and the disease is controlled by drug therapy. Great efforts are put into development of effective vaccine against parasite what is difficult since Fasciola spp. (like other helmints) during evolutionary process has developed sophisticated and efficient methods to evade immune response. During preliminary experiments it is convenient to use cell lines which are relatively cheap and allow for reproducible comparison of results between laboratories. We stimulated BOMA (bovine monocyte/macrophage cell line) and BOMAC (bovine macrophage cell line) with native or recombinant antigens of Fasciola hepatica and assessed IFN-γ, IL-4 and TNF-α level upon stimulation. We observed diminished secretion of proinflammatory TNF-α in LPS activated BOMA cells stimulated with Excretory/Secretory products of adult fluke (Fh-ES). We also observed greater changes in gene expression in LPS activated BOMA cells than in non activated BOMA cells upon stimulation using Fh-ES. The results show possibility of using cell lines for in vitro research of bovine immune response against liver fluke, although this model still requires validation and further characterization.

show abstract

Chronic helminth infections induce immunomodulation: Consequences and mechanisms

Cited by 335 publications

References 109 publications

Regulatory T cells in human geohelminth infection suppress immune responses to BCG and Plasmodium falciparum

Regulatory T cells in human geohelminth infection suppress immune responses to BCG and Plasmodium falciparum

Establishment of nematode infection despite increased Th2 responses and immunopathology after selective depletion of Foxp3⁺ cells

Fasciola hepatica — the pilot study of in vitro assessing immune response against native and recombinant antigens of the fluke

Contact Info

Product

Resources

About

Chronic helminth infections induce immunomodulation: Consequences and mechanisms

Cited by 335 publications

References 109 publications

Regulatory T cells in human geohelminth infection suppress immune responses to BCG and Plasmodium falciparum

Regulatory T cells in human geohelminth infection suppress immune responses to BCG and Plasmodium falciparum

Establishment of nematode infection despite increased Th2 responses and immunopathology after selective depletion of Foxp3+ cells

Fasciola hepatica — the pilot study of in vitro assessing immune response against native and recombinant antigens of the fluke

Contact Info

Product

Resources

About

Establishment of nematode infection despite increased Th2 responses and immunopathology after selective depletion of Foxp3⁺ cells