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IL-27 and the Regulation of Innate and Adaptive Immunity During Toxoplasmosis Daniel L Aldridge
- Format:
- Book
- Thesis/Dissertation
- Author/Creator:
- Aldridge, Daniel L., author.
- Language:
- English
- Subjects (All):
- Immunology.
- Microbiology.
- Cellular biology.
- Pathology.
- 0982.
- 0379.
- 0410.
- 0571.
- Local Subjects:
- Immunology.
- Microbiology.
- Cellular biology.
- Pathology.
- 0982.
- 0379.
- 0410.
- 0571.
- Physical Description:
- 1 electronic resource (177 pages)
- Contained In:
- Dissertations Abstracts International 86-12B
- Place of Publication:
- Ann Arbor : ProQuest Dissertations and Theses, 2025
- Language Note:
- English
- Summary:
- The cytokine IL-27 is a potent negative regulator of the inflammatory response to the pathogen Toxoplasma gondii, and the majority of the studies on IL-27 during this infection have focused on its ability to limit T cell responses. The basis for this suppressive activity is unclear, but it was proposed that the ability of IL-27 to promote T cell expression of inhibitory receptors (such as TIGIT and PD-L1) contributed to this activity. In chapter 2, the role of TIGIT during infection was assessed and indicated it was not a critical mediator of the suppressive effects of IL-27. In chapter 3, the impact of IL-27 neutralization on acute and chronic infection was examined and these data sets highlighted that in the absence of IL-27 there were enhanced monocyte responses, a cell type that does not express the IL-27R. During the later phase of infection, the overactive CD4+ T cell responses observed in the absence of IL-27 contributed to the increased monocyte response. However, analysis in chapter 4 of the most proximal events during infection-induced emergency myelopoiesis revealed that haemopoietic stem cells in the bone marrow express high levels of the IL-27R and that during infection IL-27 is a negative regulator of their differentiation into monocytes. Additionally, these studies revealed that IL-27 protected these stem cells from infection induced exhaustion. Thus, these studies highlight that IL-27 acts at multiple points during infection to limit key innate and adaptive events that contribute to infection-induced pathology
- Notes:
- Source: Dissertations Abstracts International, Volume: 86-12, Section: B.
- Advisors: Hunter, Christopher A. Committee members: Haldar, Malay; Punt, Jennifer A.; Laufer, Terri M.; Bailis, Will
- Ph.D. University of Pennsylvania 2025
- Local Notes:
- School code: 0175
- ISBN:
- 9798280760868
- Access Restriction:
- Restricted for use by site license
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