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Parkinson's disease (PD) is driven in part by neuroinflammation. We investigated whether the transcription factor BCL11B contributes to dopaminergic neurodegeneration in this context. Transcriptome sequencing of MPTP-induced PD mice revealed BCL11B upregulation, which was confirmed in MPP+-treated MN9D cells, MPTP-lesioned mice, and dopaminergic neurons exposed to inflammatory conditioned medium. BCL11B knockdown attenuated dopaminergic neuron loss, reduced apoptosis, improved motor deficits, and partially blocked JAK2/STAT3 pathway activation in both inflammatory and MPTP-induced PD models. Mechanistically, BCL11B mediated neurotoxicity through the JAK2/STAT3 pathway, with acetylation modifications potentially modulating its activity. These findings establish BCL11B as a key regulator of neuroinflammation and dopaminergic survival in PD, and suggest that targeting BCL11B may offer a therapeutic approach for this neurodegenerative disease.
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