Inflammation and Diabetic Kidney Disease.

Area of Science:

• Nephrology
• Immunology
• Diabetology

Background:

• Diabetes is a primary cause of end-stage kidney disease.
• Despite new treatments, diabetic kidney disease (DKD) still poses high residual risks.
• Immune activation is an under-explored factor in DKD pathogenesis.

Purpose of the Study:

• To review novel insights into immune cell contributions to DKD development.
• To focus on the innate immune system's role in DKD.
• To examine cellular crosstalk between immune and kidney cells in DKD.

Main Methods:

• Review of current literature on immune cell involvement in DKD.
• Focus on innate immunity and cellular interactions.
• Analysis of mouse models and specific cell types like macrophages and podocytes.

Main Results:

• Immune cells, including macrophages, T-cells, B-cells, dendritic cells, and neutrophils, infiltrate kidneys during DKD.
• Bidirectional crosstalk exists between immune cells (e.g., macrophages) and intrinsic kidney cells (e.g., podocytes).
• Macrophages can induce podocyte injury via TNF-α, while podocytes can recruit more macrophages.

Conclusions:

• Immune-mediated injury is a critical factor in DKD.
• Understanding immune cell and kidney cell interactions is vital for reducing residual DKD risk.
• Targeting immune pathways may offer new therapeutic strategies for DKD.