CXCR3 controls T-cell accumulation in fat inflammation

Area of Science:

• Immunology
• Metabolic disease research
• Adipose tissue biology

Background:

• Obesity is linked to increased inflammatory cells in adipose tissue (AT).
• The precise mechanisms of T-cell recruitment to AT in obesity are not fully understood.
• Chemokine receptor CXCR3 is a potential mediator of immune cell trafficking.

Purpose of the Study:

• To investigate the role of CXCR3 in T-cell accumulation within adipose tissue of obese mice.
• To determine if CXCR3 influences local adipose tissue inflammation and systemic metabolic function in obesity.

Main Methods:

• Compared gene expression of CXCR3 in adipose tissue from lean and obese mice.
• Utilized CXCR3-deficient and wild-type mice fed a high-fat diet to assess in vivo function.
• Quantified T-cell infiltration in adipose tissue via flow cytometry.
• Assessed glucose tolerance and measured inflammatory gene expression in adipose tissue.

Main Results:

• Obese mice showed higher CXCR3 mRNA expression in AT stromal vascular cells.
• CXCR3-deficient obese mice had significantly fewer T cells in periepididymal AT compared to controls.
• Obese CXCR3-deficient mice exhibited improved glucose tolerance at 8 weeks but not 16 weeks.
• Reduced expression of pro-inflammatory mediators and altered expression of certain anti-inflammatory genes were observed in CXCR3-deficient mice's AT.

Conclusions:

• CXCR3 plays a critical role in the recruitment of T cells to adipose tissue in obese mice.
• CXCR3 influences the accumulation of specific T-cell subsets.
• The balance of T-cell subsets regulated by CXCR3 may impact adipose tissue inflammation and metabolic health over time.