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IL-27 and the Regulation of Innate and Adaptive Immunity During Toxoplasmosis
IL-27 and the Regulation of Innate and Adaptive Immunity During Toxoplasmosis
상세정보
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20260202103043
- ISBN
- 9798280760868
- DDC
- 616.079
- 서명/저자
- IL-27 and the Regulation of Innate and Adaptive Immunity During Toxoplasmosis
- 발행사항
- [Sl] : University of Pennsylvania, 2025
- 발행사항
- Ann Arbor : ProQuest Dissertations & Theses, 2025
- 형태사항
- 177 p
- 주기사항
- Source: Dissertations Abstracts International, Volume: 86-12, Section: B.
- 주기사항
- Advisor: Hunter, Christopher A.
- 학위논문주기
- Thesis (Ph.D.)--University of Pennsylvania, 2025.
- 초록/해제
- 요약The 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.
- 일반주제명
- Immunology
- 일반주제명
- Microbiology
- 일반주제명
- Cellular biology
- 일반주제명
- Pathology
- 기타저자
- University of Pennsylvania Immunology
- 기본자료저록
- Dissertations Abstracts International. 86-12B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
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■020 ▼a9798280760868
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■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a616.079
■1001 ▼aAldridge, Daniel L.
■24510▼aIL-27 and the Regulation of Innate and Adaptive Immunity During Toxoplasmosis
■260 ▼a[Sl]▼bUniversity of Pennsylvania▼c2025
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2025
■300 ▼a177 p
■500 ▼aSource: Dissertations Abstracts International, Volume: 86-12, Section: B.
■500 ▼aAdvisor: Hunter, Christopher A.
■5021 ▼aThesis (Ph.D.)--University of Pennsylvania, 2025.
■520 ▼aThe 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.
■590 ▼aSchool code: 0175.
■650 4▼aImmunology
■650 4▼aMicrobiology
■650 4▼aCellular biology
■650 4▼aPathology
■653 ▼aToxoplasma gondii
■653 ▼aInfection-induced pathology
■653 ▼aChronic infection
■653 ▼aT cell expression
■690 ▼a0982
■690 ▼a0379
■690 ▼a0410
■690 ▼a0571
■71020▼aUniversity of Pennsylvania▼bImmunology.
■7730 ▼tDissertations Abstracts International▼g86-12B.
■790 ▼a0175
■791 ▼aPh.D.
■792 ▼a2025
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17356823▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
