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Sabrina Reinehr, Armin Safaei, Pia Grotegut, Annika Guntermann, Teresa Tsai, Stephan Hahn, Steffen Kösters, Carsten Theiß, Katrin Marcus-Alic, Burkhard Dick, Caroline May, Stephanie Christine Joachim

• Glaucomatous optic neuropathy is a common cause for blindness. An elevated intraocular pressure is the main risk factor, but also a contribution of the immune system seems likely. In the experimental autoimmune glaucoma model used here, systemic immunization with an optic nerve homogenate antigen (ONA) leads to retinal ganglion cell (RGC) and optic nerve degeneration. We processed retinae for quantitative real-time PCR and immunohistology 28 days after immunization. Furthermore, we performed mRNA profiling in this model for the first time. We detected a significant RGC loss in the ONA retinae. This was accompanied by an upregulation of mRNA expression of genes belonging to the heat shock protein family. Furthermore, mRNA expression levels of the genes of the immune system, such as \(\textit {C1qa, C1qb, Il18,}\) and \(\it Nfkb1\), were upregulated in ONA animals. After laser microdissection, inner retinal layers were used for mRNA microarrays. Nine of these probes were significantly upregulated in ONA animals (\(\it p\) < 0.05), including \(\it Hba-a1\) and \(\it Cxcl10\), while fifteen probes were significantly downregulated in ONA animals (\(\it p\) < 0.05), such as \(\it Gdf15\) and \(\it Wwox\). Taken together, these findings provide further insights into the pivotal role of the immune response in glaucomatous optic neuropathy and could help to identify novel diagnostic or therapeutic strategies.