Ms Meng CHENG
PhD Student
➲ ORCiD 0000-0001-7909-6719
Title of project:
The functional role of TREM2 in mouse models of human retinitis pigmentosa
Synopsis:
Retinitis pigmentosa (RP) is a progressive neural degenerative disease and
commonly caused by gene mutations. It can cause the functional or morphological damage
of photoreceptors and eventually leads to the death of photoreceptors and the loss of visual function. These damages are currently irreversible and there is no effective therapeutic approach to slow down the degenerative process of RP. Recently new therapeutic strategies are emerging, including gene therapy, neuroprotection, retinal prothesis, although underlying mechanisms are still poorly understood.
The retina is protected from external and internal insults by its blood-retina barriers, immune suppressive microenvironment and its own defense system, i.e., microglia and the complement system. As we all know, microglia is the primary resident immune cell type and participates in potential neurodegeneration by producing proinflammatory neurotoxic cytokines and removing living neurons via phagocytosis under pathological conditions. Triggering receptor expressed on myeloid cells 2 (TREM2) is specifically expressed by microglia and interacts with signal transduction partners to initiate signal transduction pathways that promote microglial cell phagocytosis.
This project aims to investigate the functional role of TREM2 in neuroinflammation in the rd10 mouse model of RP, highlight the role of microglia and establish the translational potential of TREM2- directed therapies for RP patients.
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