| First Author | He T | Year | 2017 |
| Journal | PLoS One | Volume | 12 |
| Issue | 4 | Pages | e0175522 |
| PubMed ID | 28441398 | Mgi Jnum | J:246980 |
| Mgi Id | MGI:5917724 | Doi | 10.1371/journal.pone.0175522 |
| Citation | He T, et al. (2017) The effects of immune protein CD3zeta development and degeneration of retinal neurons after optic nerve injury. PLoS One 12(4):e0175522 |
| abstractText | 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, CD3zeta, are expressed by mouse retinal ganglion cells (RGCs) and displaced amacrine cells. Mutation of these molecules compromises the development of RGCs. We investigated whether CD3zeta regulates the development and degeneration of amacrine cells after RGC death. Surprisingly, mutation of CD3zeta not only impairs the proper development of amacrine cells expressing CD3zeta but also those not expressing CD3zeta. In contrast to effects of MHCI and its receptor, PirB, on other neurons, mutation of CD3zeta has no effect on RGC death and starburst amacrine cells degeneration after optic nerve crush. Thus, unlike MHCI and PirB, CD3zeta regulates the development of RGCs and amacrine cells but not their degeneration after optic nerve crush. |
