We previously reported that specific neural activations involving sensory and sympathetic neurons trigger neuro-inflammation in the CNS via blood-brain barrier breaching at specific vessels. We demonstrated that gravity-, electric stimulation- or pain-mediated specific sensory inputs activate specific sympathetic pathways to release norepinephrine, which in turn enhances expression of chemokines through activation of NF-κB in the specific blood vessels to open a gateway for immune cells toward the CNS. We termed the phenomena as the gateway reflex. Because light is a common neuronal stimulus to the retina, we examined the effect of light on local retinal inflammation. While the photoperiod length affects immune responses, whether light intensity can impact the course of autoimmune diseases remains unknown. Here, we showed that exposure to photopic light suppresses subsequent ocular inflammation, including chemokine and cytokine expressions, immune cell infiltration, and the clinical scores in a mouse model of autoimmune posterior uveitis. Mechanistic analysis showed that photopic light exposure increases norepinephrine concentration in eyes and down-regulates retinal expression of α1A-adrenoreceptor (α1AAR), which is known to enhance NF-κB activity most likely via their desensitization. Consistently, blockade of α1AAR signaling under mesopic light condition recapitulated the protective effect of the photopic light stimulation. These results reveal that photopic light can inhibit ocular inflammation via regulating local noradrenergic system. Thus, we revealed a previously unrecognized role for light intensity in the control of ocular inflammation, which can be called “light-gateway reflex”. Our study also suggests that photopic light treatment or targeting of retinal α1AAR pathway might represent a novel therapeutic strategy for autoimmune uveitis.