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Examining the Role of Non-Canonical NOD-like Receptors and Inflammasomes in Inflammation and Disease

Download
ucalgary_2018_platnich_jaye.pdf (11.38Mb) Embargoed until: 9999-09-09
Advisor
Muruve, Daniel A.
Author
Platnich, Jaye Matthew
Committee Member
MacDonald, Justin Anthony
Power, Christopher
Duff, Henry J.
Peters, Nathan C.
Accessioned
2018-04-04T14:16:43Z
Available
2018-04-04T14:16:43Z
Issued
2018-03-21
Classification
Biology
Microbiology
Physiology
Immunology
Medicine and Surgery
Subject
Inflammasome
NLRP6
Inflammation
Kidney disease
Shiga toxin
NLRP3
Macrophage
NLR
Cell death
Pyroptosis
Caspase
ATPase
Type
doctoral thesis
Metadata
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Abstract
The NOD-like Receptors (NLRs) are a family of pattern recognition receptors known to regulate a variety of immune signaling pathways. A substantial portion of NLR research focuses on the pyrin domain-containing NLRP subfamily. The canonical NLRPs are inflammasome-forming proteins responsible for the activation of caspase-1 and the maturation and secretion of the pro-inflammatory cytokines IL-1β and IL-18. In contrast, the non-canonical inflammasome-independent NLRPs regulate a variety of other pathways, including MAPK and NF-κB, through the formation of non-inflammasome complexes. Interestingly, not all inflammasomes are nucleated by NLRPs. The recently characterized non-canonical caspase-4 (caspase-11 in mice) inflammasome is known to be a key driver of the innate immune response to intracellular pathogens (and the molecules associated with them), by triggering both inflammatory cell death and the activation of canonical inflammasomes. At the outset of this PhD work, the understanding of both non-inflammasome-forming NLRPs and the non-canonical caspase-4 inflammasome was poor and the studies were sparse. It was the goal of this thesis to characterize the expression, gene regulation, and function of the non-inflammasome-forming NLR protein NLRP6, both at the cellular and biochemical level. Furthermore, using a pathogen-associated molecular pattern (PAMP)-driven model of inflammation, we sought to elucidate the function of the non-canonical caspase-4 inflammasome, particularly as it pertains to the regulation of the canonical inflammasome and cell death. By studying the fundamental biology underlying these lesser-known mediators of the innate immune system, we hoped to better understand their contribution to the early immune response and their role in driving inflammatory disease with a view to, one day, ameliorating the condition of patients suffering from these afflictions through the development of targeted therapeutics.
Faculty
Cumming School of Medicine
Institution
University of Calgary
Doi
http://dx.doi.org/10.5072/PRISM/31757
Uri
http://hdl.handle.net/1880/106465
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