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Background  Microglia cells represent the resident innate immune cells of the retina and are important for retinal development and tissue homeostasis. However, dysfunctional microglia can have a negative impact on the structural and functional integrity of the retina under native and pathological conditions.    Methods  In this study, we examined interferon-regulatory factor 8 ( Irf8 )–deficient mice to determine the transcriptional profile, morphology, and temporospatial distribution of microglia lacking  Irf8  and to explore the effects on retinal development, tissue homeostasis, and formation of choroidal neovascularisation (CNV).    Results  Our study shows that  Irf8 -deficient MG exhibit a considerable loss of microglial signature genes accompanied by a severely altered MG morphology. An in-depth characterisation by fundus photography, fluorescein angiography, optical coherence tomography and electroretinography revealed no major retinal abnormalities during steady state. However, in the laser-induced CNV model,  Irf8 -deficient microglia showed an increased activity of biological processes critical for inflammation and cell adhesion and a reduced MG cell density near the lesions, which was associated with significantly increased CNV lesion size.    Conclusions  Our results suggest that loss of  Irf8  in microglia has negligible effects on retinal homeostasis in the steady state. However, under pathological conditions,  Irf8  is crucial for the transformation of resident microglia into a reactive phenotype and thus for the suppression of retinal inflammation and CNV formation.    Supplementary Information  The online version contains supplementary material available at 10.1186/s12974-021-02230-y.

The role of interferon regulatory factor 8 for retinal tissue homeostasis and development of choroidal neovascularisation