ArticlePLoS pathogens2015
Helminth Infection and Commensal Microbiota Drive Early IL-10 Production in the Skin by CD4+ T Cells That Are Functionally Suppressive.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed.
- Pathogenic type-2 immunity beyond allergy: the role of Th2 cell heterogeneity in helminth infections.Infection and immunity · 2026Review
- TRPV1+ neurons promote cutaneous immunity against Schistosoma mansoni.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- From cercariae to chronic inflammation: understanding schistosome infection and host immune responses.Frontiers in immunology · 2025Review
- Getting into host's skin: initial immune response toFrontiers in immunology · 2025Review
- MrgprA3 neurons drive cutaneous immunity against helminths through selective control of myeloid-derived IL-33.Nature immunology · 2024Article
- Th2 single-cell heterogeneity and clonal distribution at distant sites in helminth-infected mice.eLife · 2022Article
- Tissue-specific immunity in helminth infections.Mucosal immunology · 2022Review
- Molecular switches for regulating the differentiation of inflammatory and IL-10-producing anti-inflammatory T-helper cells.Cellular and molecular life sciences : CMLS · 2020Review
- Article
- Early Induction of Human Regulatory Dermal Antigen Presenting Cells by Skin-PenetratingFrontiers in immunology · 2018Article
- Alternatively Activated Mononuclear Phagocytes from the Skin Site of Infection and the Impact of IL-4Rα Signalling on CD4+T Cell Survival in Draining Lymph Nodes after Repeated Exposure to Schistosoma mansoni Cercariae.PLoS neglected tropical diseases · 2016Article
- CD4 T-cell hyporesponsiveness induced by schistosome larvae is not dependent upon eosinophils but may involve connective tissue mast cells.Parasite immunology · 2016Article
- IL-10 Production in Macrophages Is Regulated by a TLR-Driven CREB-Mediated Mechanism That Is Linked to Genes Involved in Cell Metabolism.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The skin provides an important first line of defence and immunological barrier to invasive pathogens, but immune responses must also be regulated to maintain barrier function and ensure tolerance of skin surface commensal organisms. In schistosomiasis-endemic regions, populations can experience repeated percutaneous exposure to schistosome larvae, however little is known about how repeated exposure to pathogens affects immune regulation in the skin. Here, using a murine model of repeated infection with Schistosoma mansoni larvae, we show that the skin infection site becomes rich in regulatory IL-10, whilst in its absence, inflammation, neutrophil recruitment, and local lymphocyte proliferation is increased. Whilst CD4+ T cells are the primary cellular source of regulatory IL-10, they expressed none of the markers conventionally associated with T regulatory (Treg) cells (i.e. FoxP3, Helios, Nrp1, CD223, or CD49b). Nevertheless, these IL-10+ CD4+ T cells in the skin from repeatedly infected mice are functionally suppressive as they reduced proliferation of responsive CD4+ T cells from the skin draining lymph node. Moreover, the skin of infected Rag-/- mice had impaired IL-10 production and increased neutrophil recruitment. Finally, we show that the mechanism behind IL-10 production by CD4+ T cells in the skin is due to a combination of an initial (day 1) response specific to skin commensal bacteria, and then over the following days schistosome-specific CD4+ T cell responses, which together contribute towards limiting inflammation and tissue damage following schistosome infection. We propose CD4+ T cells in the skin that do not express markers of conventional T regulatory cell populations have a significant role in immune regulation after repeated pathogen exposure and speculate that these cells may also help to maintain skin barrier function in the context of repeated percutaneous insult by other skin pathogens.
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