IGF1R Promotes Th17/Treg Cell Development in Experimental Autoimmune Prostatitis.

Area of Science:

• Urology
• Immunology
• Endocrinology

Background:

• Chronic prostatitis is a prevalent urological condition in men, marked by recurrent episodes and an unclear cause.
• The role of insulin-like growth factor 1 (IGF1) and its related ligands in chronic prostatitis pathogenesis remains largely unexplored.

Purpose of the Study:

• To investigate the involvement of the IGF1/IGF1R axis in the development and progression of experimental autoimmune prostatitis (EAP).
• To identify potential molecular targets for therapeutic intervention in chronic prostatitis.

Main Methods:

• Established a chronic experimental autoimmune prostatitis (EAP) mouse model.
• Utilized H&E staining, RT-qPCR, Western blot, immunofluorescence, and flow cytometry to analyze prostate tissue and immune cell infiltration.
• Employed adeno-associated virus (AAV) for gene knockdown and ELISA for cytokine measurement.

Main Results:

• IGF1R expression was significantly elevated in prostate tissue and CD4+ T cells of EAP mice.
• Stimulation with desIGF1 exacerbated prostate inflammation and pain, increasing Th17 cells and decreasing Treg cells.
• Knockdown of IGF1R alleviated inflammation and pain, implicating the IGF1/IGF1R axis in disease exacerbation.
• PKC-β pathway activation was linked to increased Th17 cell differentiation and prostate inflammation.

Conclusions:

• The IGF1/IGF1R axis, potentially through PKC-β signaling, plays a crucial role in Th17 cell differentiation and prostate inflammation in EAP.
• This axis represents a promising molecular target for developing novel therapeutic strategies for chronic prostatitis.