ArticleImmunology2016
Characteristics of Schistosoma japonicum infection induced IFN-γ and IL-4 co-expressing plasticity Th cells.
Article in Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Synergistic interaction between the macrophage polarizing signals IL-4 and IFNγ is controlled by the STAT6/STAT1/IRF1 axis.Nucleic acids research · 2026Article
- IRF4 regulates myeloid-derived suppressor cells expansion and function in Schistosoma japonicum-infected mice.Parasites & vectors · 2024Article
- The Cytokine Profile in Different Stages of Schistosomiasis Japonica.Pathogens (Basel, Switzerland) · 2023Article
- TLR7 controls myeloid-derived suppressor cells expansion and function in the lung of C57BL6 mice infected with Schistosoma japonicum.PLoS neglected tropical diseases · 2022Article
- MULT1-Encoding DNA Alleviates Schistosomiasis-Associated Hepatic Fibrosis via Modulating Cellular Immune Response.Journal of inflammation research · 2022Article
- Ikzf2 Regulates the Development of ICOSFrontiers in immunology · 2021Article
- Therapeutic potential of fucoidan in the reduction of hepatic pathology in murine schistosomiasis japonica.Parasites & vectors · 2020Article
- Changes of CD103-expressing pulmonary CD4BMC infectious diseases · 2019Article
- TLR7 Modulated T Cell Response in the Mesenteric Lymph Node ofJournal of immunology research · 2019Article
- Article
- TLR3 Modulates the Response of NK Cells againstJournal of immunology research · 2018Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schistosoma japonicum infection can induce granulomatous inflammation and cause tissue damage in the mouse liver. The cytokine secretion profile of T helper (Th) cells depends on both the nature of the activating stimulus and the local microenvironment (e.g. cytokines and other soluble factors). In the present study, we found an accumulation of large numbers of IFN-γ(+) IL-4(+) CD4(+) T cells in mouse livers. This IFN-γ(+) IL-4(+) cell population increased from 0·68 ± 0·57% in uninfected mice to 7·05 ± 3·0% by week 4 following infection and to 9·6 ± 5·28% by week 6, before decreasing to 6·3 ± 5·9% by week 8 in CD4 T cells. Moreover, IFN-γ(+) IL-4(+) Th cells were also found in mouse spleen and mesenteric lymph nodes 6 weeks after infection. The majority of the IFN-γ(+) IL-4(+) Th cells were thought to be related to a state of immune activation, and some were memory T cells. Moreover, we found that these S. japonicum infection-induced IFN-γ(+) IL-4(+) cells could express interleukin-2 (IL-2), IL-9, IL-17 and high IL-10 levels at 6 weeks after S. japonicum infection. Taken together, our data suggest the existence of a population of IFN-γ(+) IL-4(+) plasticity effector/memory Th cells following S. japonicum infection in C57BL/6 mice.
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