Death of retinal ganglion cells (RGC) in conditions like glaucoma leads to permanent visual loss. RGC death can be due to the initial stress such as raised intraocular pressure or secondary to mechanism such as oxidative stress. Programmed cell death-1 (PD-1) is a receptor which is known to regulate T lymphocytes and is important in immune responses. PD-1 provides inhibitory signals that suppress such responses via pathways such as PI3 kinase and Akt signalling. A receptor for PD-1, PD-L1 is found on tumour cells and inhibits immune responses against the tumour, and blockade of this pathway has been effective in treating patients with cancer. Previous work by the authors has shown that PD-1 is constitutively expressed on RGC and that interaction with its receptor is involved during retinal development. In this paper, PD-1 expression, mRNA and protein, was increased in murine retina following optic nerve crush injury, particularly in a subset of large RGC. These PD-1 positive cells did not express cleaved caspase-3, a marker of apotosis, suggesting that PD-1 may be involved in RGC survival. The relevance of the increase in large RGC and PD-1 expression requires further study, but offers a potential pathway to influence RGC death is sight-threatening conditions.