YY1 lactylation exacerbates autoimmune uveitis by enhancing microglial functions through inflammatory genes. In experimental autoimmune uveitis (EAU), increased YY1 lactylation in retinal microglia is associated with enhanced microglial activation, proliferation, and migration. Inhibition of YY1 lactylation reduces microglial activation and inflammation in EAU. Mechanistically, YY1 lactylation promotes microglial activation by regulating the transcription of inflammatory genes such as STAT3, CCL5, IRF1, IDO1, and SEMA4D. p300 is identified as the writer of YY1 lactylation, and its inhibition reduces YY1 lactylation and suppresses microglial inflammation. These findings suggest that YY1 lactylation promotes microglial dysfunction in autoimmune uveitis by upregulating inflammatory cytokine secretion and enhancing cell migration and proliferation. Targeting the lactate/p300/YY1 lactylation/inflammatory genes axis may provide therapeutic benefits for autoimmune uveitis. The study highlights the role of YY1 lactylation in microglial activation and its contribution to the progression of autoimmune uveitis. The results indicate that YY1 lactylation is a potential therapeutic target for autoimmune uveitis. The study also identifies five inflammatory genes (IRF1, IDO1, SEMA4D, CCL5, and STAT3) as downstream targets of YY1 lactylation. These findings provide insights into the molecular mechanisms underlying autoimmune uveitis and suggest potential therapeutic strategies. The study demonstrates that YY1 lactylation is involved in microglial activation and inflammatory responses in autoimmune uveitis. The results suggest that targeting YY1 lactylation could be a promising approach for treating autoimmune uveitis. The study also highlights the importance of lactate in regulating YY1 lactylation and microglial function. The findings indicate that YY1 lactylation plays a crucial role in the pathogenesis of autoimmune uveitis. The study provides a novel understanding of the molecular mechanisms underlying autoimmune uveitis and suggests potential therapeutic targets. The results suggest that YY1 lactylation is a key factor in the progression of autoimmune uveitis. The study also highlights the potential of targeting the lactate/p300/YY1 lactylation/inflammatory genes axis for the treatment of autoimmune uveitis. The findings indicate that YY1 lactylation is a potential therapeutic target for autoimmune uveitis. The study provides a comprehensive understanding of the role of YY1 lactylation in microglial activation and inflammatory responses in autoimmune uveitis. The results suggest that targeting YY1 lactylation could be a promising approach for treating autoimmune uveitis. The study also highlights the importance of lactate in regulating YY1 lactylation and microglial function. The findings indicate that YY1 lactylation is a key factor in the progression of autoimmune uveitis. The study provides a novel understanding of the molecular mechanisms underlying autoimmune uYY1 lactylation exacerbates autoimmune uveitis by enhancing microglial functions through inflammatory genes. In experimental autoimmune uveitis (EAU), increased YY1 lactylation in retinal microglia is associated with enhanced microglial activation, proliferation, and migration. Inhibition of YY1 lactylation reduces microglial activation and inflammation in EAU. Mechanistically, YY1 lactylation promotes microglial activation by regulating the transcription of inflammatory genes such as STAT3, CCL5, IRF1, IDO1, and SEMA4D. p300 is identified as the writer of YY1 lactylation, and its inhibition reduces YY1 lactylation and suppresses microglial inflammation. These findings suggest that YY1 lactylation promotes microglial dysfunction in autoimmune uveitis by upregulating inflammatory cytokine secretion and enhancing cell migration and proliferation. Targeting the lactate/p300/YY1 lactylation/inflammatory genes axis may provide therapeutic benefits for autoimmune uveitis. The study highlights the role of YY1 lactylation in microglial activation and its contribution to the progression of autoimmune uveitis. The results indicate that YY1 lactylation is a potential therapeutic target for autoimmune uveitis. The study also identifies five inflammatory genes (IRF1, IDO1, SEMA4D, CCL5, and STAT3) as downstream targets of YY1 lactylation. These findings provide insights into the molecular mechanisms underlying autoimmune uveitis and suggest potential therapeutic strategies. The study demonstrates that YY1 lactylation is involved in microglial activation and inflammatory responses in autoimmune uveitis. The results suggest that targeting YY1 lactylation could be a promising approach for treating autoimmune uveitis. The study also highlights the importance of lactate in regulating YY1 lactylation and microglial function. The findings indicate that YY1 lactylation plays a crucial role in the pathogenesis of autoimmune uveitis. The study provides a novel understanding of the molecular mechanisms underlying autoimmune uveitis and suggests potential therapeutic targets. The results suggest that YY1 lactylation is a key factor in the progression of autoimmune uveitis. The study also highlights the potential of targeting the lactate/p300/YY1 lactylation/inflammatory genes axis for the treatment of autoimmune uveitis. The findings indicate that YY1 lactylation is a potential therapeutic target for autoimmune uveitis. The study provides a comprehensive understanding of the role of YY1 lactylation in microglial activation and inflammatory responses in autoimmune uveitis. The results suggest that targeting YY1 lactylation could be a promising approach for treating autoimmune uveitis. The study also highlights the importance of lactate in regulating YY1 lactylation and microglial function. The findings indicate that YY1 lactylation is a key factor in the progression of autoimmune uveitis. The study provides a novel understanding of the molecular mechanisms underlying autoimmune u