2. Academic Validation
  3. IFN-λ is protective against lethal oral Toxoplasma gondii infection

IFN-λ is protective against lethal oral Toxoplasma gondii infection

  • bioRxiv. 2023 Feb 24:2023.02.24.529861. doi: 10.1101/2023.02.24.529861.
Mateo Murillo-León 1 2 3,  Aura M Bastidas-Quintero 1 2 3,  Niklas S Endres 1 2 3 4,  Daniel Schnepf 1 5,  Estefanía Delgado-Betancourt 6,  Annette Ohnemus 1 2,  Gregory A Taylor 7 8,  Martin Schwemmle 1 2,  Peter Staeheli 1 2,  Tobias Steinfeldt 1 2
Affiliations

Affiliations

  • 1 Institute of Virology, Medical Center University of Freiburg, 79104 Freiburg, Germany.
  • 2 Faculty of Medicine, University of Freiburg, 79104 Freiburg, Germany.
  • 3 Faculty of Biology, University of Freiburg, 79104 Freiburg, Germany.
  • 4 Current address:Institute of Virology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
  • 5 Current address: Immunoregulation Laboratory, The Francis Crick Institute, London, UK.
  • 6 FG 16: Mycotic and Parasitic Agents and Mycobacteria, Robert Koch-Institute, Berlin, Germany.
  • 7 Departments of Medicine; Molecular Genetics and Microbiology; and Immunology; and Center for the Study of Aging and Human Development, Duke University Medical Center, NC 27710 Durham, North Carolina, United States of America.
  • 8 Geriatric Research, Education, and Clinical Center, Durham VA Health Care System, NC 27705 Durham, North Carolina, United States of America.
PMID: 36865100 DOI: 10.1101/2023.02.24.529861
Abstract

Interferons are essential for innate and adaptive immune responses against a wide variety of pathogens. Interferon lambda (IFN-λ) protects mucosal barriers during pathogen exposure. The intestinal epithelium is the first contact site for Toxoplasma gondii (T. gondii) with its hosts and the first defense line that limits parasite Infection. Knowledge of very early T. gondii Infection events in the gut tissue is limited and a possible contribution of IFN-λ has not been investigated so far. Here, we demonstrate with systemic interferon lambda receptor (IFNLR1) and conditional (Villin-Cre) knockout mouse models and bone marrow chimeras of oral T. gondii Infection and mouse intestinal organoids a significant impact of IFN-λ signaling in intestinal epithelial cells and neutrophils to T. gondii control in the gastrointestinal tract. Our results expand the repertoire of interferons that contribute to the control of T. gondii and may lead to novel therapeutic approaches against this world-wide zoonotic pathogen.

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