ArticleImmunology2016
Patency of Litomosoides sigmodontis infection depends on Toll-like receptor 4 whereas Toll-like receptor 2 signalling influences filarial-specific CD4(+) T-cell responses.
Article in Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Differences of in vitro immune responses between patent and pre-patent Litomosoides sigmodontis-infected mice are independent of the filarial antigenic stimulus used.Parasitology research · 2024Article
- Filariasis research - from basic research to drug development and novel diagnostics, over a decade of research at the Institute for Medical Microbiology, Immunology and Parasitology, Bonn, Germany.Frontiers in tropical diseases · 2023Article
- Human filariasis-contributions of the Litomosoides sigmodontis and Acanthocheilonema viteae animal model.Parasitology research · 2021Review
- The immune response of inbred laboratory mice to Litomosoides sigmodontis: A route to discovery in myeloid cell biology.Parasite immunology · 2020Review
- The central adaptor molecule TRIF influences L. sigmodontis worm development.Parasitology research · 2019Article
- Absence of IL-17A in Litomosoides sigmodontis-infected mice influences worm development and drives elevated filarial-specific IFN-γ.Parasitology research · 2018Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BALB/c mice develop a patent state [release of microfilariae (Mf), the transmission life-stage, into the periphery] when exposed to the rodent filariae Litomosoides sigmodontis. Interestingly, only a portion of the infected mice become patent, which reflects the situation in human individuals infected with Wuchereria bancrofti. Since those individuals had differing filarial-specific profiles, this study compared differences in immune responses between Mf(+) and Mf(-) infected BALB/c mice. We demonstrate that cultures of total spleen or mediastinal lymph node cells from Mf(+) mice produce significantly more interleukin-5 (IL-5) to filarial antigens but equal levels of IL-10 when compared with Mf(-) mice. However, isolated CD4(+) T cells from Mf(+) mice produced significantly higher amounts of all measured cytokines, including IL-10, when compared with CD4(+) T-cell responses from Mf(-) mice. Since adaptive immune responses are influenced by triggering the innate immune system we further studied the immune profiles and parasitology in infected Toll-like receptor-2-deficient (TLR2(-/-)) and TLR4(-/-) BALB/c mice. Ninety-three per cent of L. sigmodontis-exposed TLR4(-/-) BALB/c mice became patent (Mf(+)) although worm numbers remained comparable to those in Mf(+) wild-type controls. Lack of TLR2 had no influence on patency outcome or worm burden but infected Mf(+) mice had significantly lower numbers of Foxp3(+) regulatory T cells and dampened peripheral immune responses. Interestingly, in vitro culturing of CD4(+) T cells from infected wild-type mice with granulocyte-macrophage colony-stimulating factor-derived TLR2(-/-) dendritic cells resulted in an overall diminished cytokine profile to filarial antigens. Hence, triggering TLR4 or TLR2 during chronic filarial infection has a significant impact on patency and efficient CD4(+) T-cell responses, respectively.
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