School of Optometry 眼科視光學院
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About us > Our People > Research Students > Ms Meng CHENG
Our People
Mr. Chunghim SO | Mr. Dong LIANG | Mr. Milan RAI | Ms. Jing ZHANG | Ms. Shuwen JIA | Ms. Wing Yan LAU | Ms. Yingkun CUI | Ms Jingfang Jennifer BIAN | Mr Shashi Kant CHAUDHARY | Ms Meng CHENG | Mr Ka Wai Jimmy CHEUNG | Ms Hang I Christie LAM | Ms Hoi Lam LI | Ms Sonal Aswin VYAS | Mr Kin Ken WAN | Ms Biyue GUO | Ms Li PAN | Ms Qi TAN | Mr Mezbah UDDIN | Ms Rong LI | Ms. Yuanyuan LIANG | Ms Anqi LYU | Mr Ying Hon SZE | Ms Qin WANG | Ms Hanyu ZHANG | Ms Wei YANG | Ms Mei ZHAO | Ms Yajing YANG | Ms Fangyu XU | Mr Sung Hei Jimmy TSE | Ms. Seen Hang CHAN | Mr. CHAN Kin Ho | Ms. AYERAKWAH Patience Ansomah | Mr. SO Ching | Mr. CATRAL Kirk Patrick Carreon | Mr. LIU Zhengji | Mr. LU Daqian | Ms. QIU Chunting | Mr. YANG Xiayin


PhD Student

ORCiD 0000-0001-7909-6719

Title of project:
The functional role of TREM2 in mouse models of human retinitis pigmentosa

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.