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Defining the role of a novel NLR protein in stomach B cell lymphoma associated with chronic Helicobacter infection

Description 
Our laboratory has for the first time identified a new NOD-like receptor (NLR) protein in the regulation of inflammation in response to chronic Helicobacter pylori infection. Specifically, we have shown that conditional knockout mice lacking this NLR exhibit an accelerated formation of gastric B cell mucosa-associated lymphoid tissue (MALT), consistent with the early stages of MALT lymphoma, in response to chronic Helicobacter infection. The overall aims of the project are to investigate how this novel NLR prevents B cell lymphomagenesis induced by chronic infection and whether this protein may play much broader functions in the host immune system. These questions will be addressed in both in vitro and in vivo models, including conditional knockout mice. The project will involve various techniques, such as primary cell culture, mouse infection, immunohistochemistry, flow cytometry, cytokine ELISA and qPCR.
Essential criteria: 
Minimum entry requirements can be found here: https://www.monash.edu/admissions/entry-requirements/minimum
Keywords 
Innate immunity, infection, signal transduction, gastrointestinal disease, cancer, MALT lymphoma
School 
School of Clinical Sciences at Monash Health / Hudson Institute of Medical Research
Available options 
PhD/Doctorate
Masters by research
Honours
BMedSc(Hons)
Time commitment 
Full-time
Top-up scholarship funding available 
No
Physical location 
Monash Health Translation Precinct (Monash Medical Centre)
Co-supervisors 
Dr 
Dongmei Tong

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