ArticlePLoS pathogens2015
NK-, NKT- and CD8-Derived IFNγ Drives Myeloid Cell Activation and Erythrophagocytosis, Resulting in Trypanosomosis-Associated Acute Anemia.
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 41 papers.
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Who cites it
41 citing papers in PubMed, 58 citations in OpenAlex.
- Comparative Pathogenicity and Semi-quantitative Multi-organ Histopathology of Trypanosoma congolense and Trypanosoma brucei Infection in Mice.Acta parasitologica · 2026Article
- Pathogens of the Human Central Nervous System-the Major Protozoan Parasites and Helminths.Molecular neurobiology · 2026Review
- IL-10 Plays a Critical Role in Mitigating Acute Anaemia Development During African Trypanosome Infection.Pathogens (Basel, Switzerland) · 2025Article
- Roles of cytokines in modulatingFrontiers in parasitology · 2025Article
- Systemic inflammation impairs recovery from hookworm-associated anemia in a wild marine mammal host.Frontiers in immunology · 2025Article
- Advances in the Immunology of the Host-Parasite Interactions in African Trypanosomosis, including Single-Cell Transcriptomics.Pathogens (Basel, Switzerland) · 2024Review
- Altered Frequency, Activation, and Clinical Relevance of Circulating Innate and Innate-Like Lymphocytes in Patients With Alcoholic Liver Cirrhosis.Immune network · 2023Article
- Heme-deficient metabolism and impaired cellular differentiation as an evolutionary trade-off for human infectivity in Trypanosoma brucei gambiense.Nature communications · 2022Article
- The Role of MIF and IL-10 as Molecular Yin-Yang in the Modulation of the Host Immune Microenvironment During Infections: African Trypanosome Infections as a Paradigm.Frontiers in immunology · 2022Review
- Tipping the balance between erythroid cell differentiation and induction of anemia in response to the inflammatory pathology associated with chronic trypanosome infections.Frontiers in immunology · 2022Article
- Article
- CXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.PLoS pathogens · 2021Article
- Autoimmunity to phosphatidylserine and anemia in African Trypanosome infections.PLoS neglected tropical diseases · 2021Article
- Mouse experiments demonstrate differential pathogenicity and virulence of Trypanosoma brucei rhodesiense strains.Experimental parasitology · 2021Article
- Miltefosine enhances infectivity of a miltefosine-resistant Leishmania infantum strain by attenuating its innate immune recognition.PLoS neglected tropical diseases · 2021Article
- Occurrence of foamy macrophages during the innate response of zebrafish to trypanosome infections.eLife · 2021Article
- African Trypanosomosis Obliterates DTPa Vaccine-Induced Functional Memory So That Post-TreatmentVaccines · 2021Article
- Salivarian Trypanosomes Have Adopted Intricate Host-Pathogen Interaction Mechanisms That Ensure Survival in Plain Sight of the Adaptive Immune System.Pathogens (Basel, Switzerland) · 2021Review
- Article
- Computational Identification of Master Regulators Influencing Trypanotolerance in Cattle.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
African trypanosomes are the causative agents of Human African Trypanosomosis (HAT/Sleeping Sickness) and Animal African Trypanosomosis (AAT/Nagana). A common hallmark of African trypanosome infections is inflammation. In murine trypanosomosis, the onset of inflammation occurs rapidly after infection and is manifested by an influx of myeloid cells in both liver and spleen, accompanied by a burst of serum pro-inflammatory cytokines. Within 48 hours after reaching peak parasitemia, acute anemia develops and the percentage of red blood cells drops by 50%. Using a newly developed in vivo erythrophagocytosis assay, we recently demonstrated that activated cells of the myeloid phagocytic system display enhanced erythrophagocytosis causing acute anemia. Here, we aimed to elucidate the mechanism and immune pathway behind this phenomenon in a murine model for trypanosomosis. Results indicate that IFNγ plays a crucial role in the recruitment and activation of erythrophagocytic myeloid cells, as mice lacking the IFNγ receptor were partially protected against trypanosomosis-associated inflammation and acute anemia. NK and NKT cells were the earliest source of IFNγ during T. b. brucei infection. Later in infection, CD8+ and to a lesser extent CD4+ T cells become the main IFNγ producers. Cell depletion and transfer experiments indicated that during infection the absence of NK, NKT and CD8+ T cells, but not CD4+ T cells, resulted in a reduced anemic phenotype similar to trypanosome infected IFNγR-/- mice. Collectively, this study shows that NK, NKT and CD8+ T cell-derived IFNγ is a critical mediator in trypanosomosis-associated pathology, driving enhanced erythrophagocytosis by myeloid phagocytic cells and the induction of acute inflammation-associated anemia.
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