Abstract
Abstract The role of T-bet, a hallmark transcription factor of Type 1 immune responses, has been examined in a variety of infection models. The results of these studies have been contradictory in that the immune response to some pathogens (e.g. Salmonella, TB) requires T-bet while its expression is dispensable for resistance to other pathogens (e.g. LCMV, Listeria monocytogenes). The intracellular parasite Toxoplasma gondii induces a rapid Type 1 response in mice, characterized by production of the cytokine interferon-γ, which is required for controlling the parasite. In the absence of T-bet, mice challenged with T. gondii develop normal NK responses and have largely intact T cell activity, including production of IFN-γ. However, despite production of IFN-γ by NK and T cells, T-bet deficient mice succumb to acute infection; this increased susceptibility is characterized by control of parasite replication in the liver and peritoneum, but higher parasite burden in other sites. These data suggest local differences in the requirement for T-bet to control parasite replication and reveal an essential function of T-bet in the regional vs. systemic immune response necessary for control of T. gondii.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
