Objective: We propose that IGF2 induces a distinct inflammatory phenotype in macrophages or microglia derived from Parkinson’s disease (PD) patients.

Background: Microglia are the resident immune cells of the central nervous system, responsible for sensing and responding to pathological stimuli, thereby promoting an inflammatory response known as neuroinflammation. Recent studies indicate that insulin-like growth factor II (IGF2) exerts immunomodulatory effects on peripheral macrophages through epigenetic remodeling via the IGF2/IGF2 receptor (IGF2R)/GSK3β axis. However, the role of IGF2 in microglial immune regulation in PD remains poorly understood.

Method: Primary microglial cultures or microglia derived from peripheral blood mononuclear cells (PBMCs) of PD patients were treated with IGF2. The inflammatory profile of microglia was assessed via quantitative PCR (qPCR) to evaluate the gene expression of pro-inflammatory markers, including TNF-α, and anti-inflammatory markers, including IL-10 and Nurr1. Additionally, immunofluorescence analysis was performed to assess the nuclear translocation of IGF2Rand GSK3β.

Results: Our findings indicate that IGF2 modulates microglial migration and promotes an anti-inflammatory phenotype in a time- and dose-dependent manner. This suggests that IGF2 plays a critical role in shaping the microglial inflammatory response.

Conclusion: IGF2 regulates the inflammatory response of microglia by upregulating the expression of anti-inflammatory markers. These findings highlight the potential of IGF2 as an immunomodulatory molecule in the neuroinflammatory processes associated with PD.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/targeting-igf2-signaling-for-immune-modulation-of-microglia-in-parkinsons-disease/