- Title Information
- Title
- A Novel Role for Programmed Cell Death Receptor Ligand 2 (PD-L2) in Sepsis-Induced Hepatic Dysfunction
- Type of Resource
- text
- Name:
Personal
- Name Part
- Le, Marilyn C
- Role
- Role Term:
Text
- creator
- Name:
Personal
- Name Part
- Zimmerman, Anita
- Role
- Role Term:
Text
- Reader
- Name:
Personal
- Name Part
- Bowen, Wayne
- Role
- Role Term:
Text
- Reader
- Name:
Personal
- Name Part
- Ayala, Alfred
- Role
- Role Term:
Text
- Advisor
- Name:
Corporate
- Name Part
- Brown University. Department of Molecular Pharmacology, Physiology and Biotechnology
- Role
- Role Term:
Text
- sponsor
- Origin Information
- Copyright Date
- 2017
- Physical Description
- Extent
- , 46 p.
- digitalOrigin
- born digital
- Note:
thesis
- Thesis (Sc. M.)--Brown University, 2017
- Genre (aat)
- theses
- Abstract
- Sepsis is defined as a state of life-threatening organ dysfunction due to dysregulated host response to infection. Because of its complex pathogenesis, sepsis is difficult to both diagnose and treat. In order to develop a viable therapeutic for sepsis, we must work to understanding its underlying mechanisms.
Programmed Cell Death Receptor 1 (PD-1) and its ligands, PD-L1 and PD-L2, have been studied in sepsis for their therapeutic effects. We have seen in our results that PD-L2 appears to be down-regulated in sepsis, and its expression was shown to change primarily in the liver. The liver is an organ whose dysfunction is strongly associated with mortality, as it plays a key role in metabolic and homeostatic activities. Understanding the pathophysiology of liver failure during sepsis will serve to develop a more efficient method of diagnosing liver dysfunction and encourage patient survival.
Therefore, our central hypothesis is that sepsis-induced change in PD-L2 expression in the liver should contribute to altered liver function and subsequently, altered general morbidity/mortality. In our study, we compared PD-L2-/-, PD-L1-/- and wild type mice to assess differences in survival, liver function, and overall impacts on septic outcomes. What we found was in support of our hypothesis; PD-L2 appeared to worsen liver function. Interestingly, we also saw some protective effects of PD-L2 knockout, namely in the case of bacterial clearance. PD-L2’s exact roles and underlying mechanisms of action are still unclear, but our study provided a strong foundation for us to answer these questions in the future.
- Subject (fast)
(authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/00968006")
- Topic
- Immunology
- Subject (fast)
(authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/01112835")
- Topic
- Septicemia
- Language
- Language Term (ISO639-2B)
- English
- Record Information
- Record Content Source (marcorg)
- RPB
- Record Creation Date
(encoding="iso8601")
- 20170616
- Identifier:
DOI
- 10.7301/Z05B00WQ
- Access Condition:
rights statement
(href="http://rightsstatements.org/vocab/InC/1.0/")
- In Copyright
- Access Condition:
restriction on access
- Collection is open for research.