ArticleThe Journal of infectious diseases2011
Intradermal infections of mice by low numbers of african trypanosomes are controlled by innate resistance but enhance susceptibility to reinfection.
Article in The Journal of infectious diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Roles of cytokines in modulatingFrontiers in parasitology · 2025Article
- Advances in the Immunology of the Host-Parasite Interactions in African Trypanosomosis, including Single-Cell Transcriptomics.Pathogens (Basel, Switzerland) · 2024Review
- Infections With Extracellular Trypanosomes Require Control by Efficient Innate Immune Mechanisms and Can Result in the Destruction of the Mammalian Humoral Immune System.Frontiers in immunology · 2020Review
- To the Skin and Beyond: The Immune Response to African Trypanosomes as They Enter and Exit the Vertebrate Host.Frontiers in immunology · 2020Review
- Influence of the Draining Lymph Nodes and Organized Lymphoid Tissue Microarchitecture on Susceptibility to IntradermalFrontiers in immunology · 2020Article
- Route of inoculation influences Trypanosoma congolense and Trypanosoma brucei brucei virulence in Swiss white mice.PloS one · 2019Article
- Host Immune Responses and Immune Evasion Strategies in African Trypanosomiasis.Frontiers in immunology · 2019Review
- Neutrophils enhance early Trypanosoma brucei infection onset.Scientific reports · 2018Article
- Adenylate Cyclases ofPathogens (Basel, Switzerland) · 2018Review
- Trypanosoma brucei growth control by TNF in mammalian host is independent of the soluble form of the cytokine.Scientific reports · 2017Article
- Modeling Rabbit Responses to Single and Multiple Aerosol Exposures of Bacillus anthracis Spores.Risk analysis : an official publication of the Society for Risk Analysis · 2017Article
- Trypanosoma brucei Invasion and T-Cell Infiltration of the Brain Parenchyma in Experimental Sleeping Sickness: Timing and Correlation with Functional Changes.PLoS neglected tropical diseases · 2016Article
- The Dermis as a Delivery Site of Trypanosoma brucei for Tsetse Flies.PLoS pathogens · 2016Article
- Nitric Oxide Protects against Infection-Induced Neuroinflammation by Preserving the Stability of the Blood-Brain Barrier.PLoS pathogens · 2016Article
- Distinct Contributions of CD4+ and CD8+ T Cells to Pathogenesis of Trypanosoma brucei Infection in the Context of Gamma Interferon and Interleukin-10.Infection and immunity · 2015Article
- Low-dose intradermal infection with trypanosoma congolense leads to expansion of regulatory T cells and enhanced susceptibility to reinfection.Infection and immunity · 2014Article
- Isolation, cloning, and pathologic analysis of Trypanosoma evansi field isolates.Parasitology research · 2013Article
- Immunosuppression: cause for failures of vaccines against African Trypanosomiases.PLoS neglected tropical diseases · 2013Article
- Non-invasive in vivo study of the Trypanosoma vivax infectious process consolidates the brain commitment in late infections.PLoS neglected tropical diseases · 2013Article
- Distinct Toll-like receptor signals regulate cerebral parasite load and interferon α/β and tumor necrosis factor α-dependent T-cell infiltration in the brains of Trypanosoma brucei-infected mice.The Journal of infectious diseases · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Antibodies are required to control blood-stage forms of African trypanosomes in humans and animals. Here, we report that intradermal infections by low numbers of African trypanosomes are controlled by innate resistance but prime the adaptive immune response to increase susceptibility to a subsequent challenge. Mice were found 100 times more resistant to intradermal infections by Trypanosoma congolense or Trypanosoma brucei than to intraperitoneal infections. B cell-deficient and RAG2(-/-) mice are as resistant as wild-type mice to intradermal infections, whereas inducible nitric oxide synthase (iNOS)(-/-) mice and wild-type mice treated with antibody to tumor necrosis factor (TNF) α are more susceptible. We conclude that primary intradermal infections with low numbers of parasites are controlled by innate defense mediated by induced nitric oxide (NO). CD1d(-/-) and major histocompatibility complex (MHC) class II(-/-) mice are more resistant than wild-type mice to primary intradermal infections. Trypanosome-specific spleen cells, as shown by cytokine production, are primed as early as 24 h after intradermal infection. Infecting mice intradermally with low numbers of parasites, or injecting them intradermally with a trypanosomal lysate, makes mice more susceptible to an intradermal challenge. We suggest that intradermal infections with low numbers of trypanosomes or injections with trypanosomal lysates prime the adaptive immune system to suppress protective immunity to an intradermal challenge.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.