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The Effects of Immune Protein CD3ζ Development and Degeneration of Retinal Neurons After Optic Nerve Injury

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Journal PLoS One
Date 2017 Apr 26
PMID 28441398
Citations 4
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Abstract

Major histocompatibility complex (MHC) class I molecules and their receptors play fundamental roles in neuronal death during diseases. T-cell receptors (TCR) function as MHCI receptor on T-cells and both MHCI and a key component of TCR, CD3ζ, are expressed by mouse retinal ganglion cells (RGCs) and displaced amacrine cells. Mutation of these molecules compromises the development of RGCs. We investigated whether CD3ζ regulates the development and degeneration of amacrine cells after RGC death. Surprisingly, mutation of CD3ζ not only impairs the proper development of amacrine cells expressing CD3ζ but also those not expressing CD3ζ. In contrast to effects of MHCI and its receptor, PirB, on other neurons, mutation of CD3ζ has no effect on RGC death and starburst amacrine cells degeneration after optic nerve crush. Thus, unlike MHCI and PirB, CD3ζ regulates the development of RGCs and amacrine cells but not their degeneration after optic nerve crush.

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The Susceptibility of Retinal Ganglion Cells to Optic Nerve Injury is Type Specific.

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Correction: The effects of immune protein CD3ζ development and degeneration of retinal neurons after optic nerve injury.

He T, Mortensen X, Wang P, Tian N PLoS One. 2018; 13(6):e0198770.

PMID: 29856870 PMC: 5983475. DOI: 10.1371/journal.pone.0198770.


Microglial dynamics after axotomy-induced retinal ganglion cell death.

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