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CD74 in Kidney Disease

Lara Valiño-Rivas1, Ciro Baeza-Bermejillo2, Laura Gonzalez-Lafuente1

  • 1Instituto de Investigación Sanitaria de la Fundación Jiménez Díaz, Universidad Autónoma de Madrid , Madrid , Spain.

Frontiers in Immunology
|October 7, 2015
PubMed

Insights

The CD74 protein, a receptor for MIF, is elevated in various kidney diseases. Its role in kidney cell function and disease progression requires further investigation for therapeutic development.

Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • CD74 (invariant MHC class II) is a key regulator of protein trafficking and a receptor for macrophage migration inhibitory factor (MIF).
  • Elevated CD74 expression is observed in kidney tubular cells, glomerular podocytes, and parietal cells across diverse human nephropathies, including metabolic disorders, polycystic kidney disease, graft rejection, and kidney cancer.
  • Kidney cell CD74 expression is upregulated by metabolic stressors (e.g., glucose, lyso-Gb3) and inflammatory cytokines.

Purpose of the Study:

  • To elucidate the multifaceted role of CD74 in kidney cell biology and its implications in various kidney diseases.
  • To investigate the functional consequences of MIF-mediated CD74 activation in kidney cells.
  • To assess the therapeutic potential and risks associated with targeting the MIF/CD74 pathway in kidney disease.

Main Methods:

  • Analysis of CD74 expression in human kidney diseases and experimental models.
  • Investigation of MIF-induced signaling pathways in kidney cells (podocytes, tubular cells, parietal cells).
  • Evaluation of the effects of MIF/CD74 pathway modulation on kidney injury, cystogenesis, and fibrosis.

Main Results:

  • MIF activation of CD74 promotes inflammatory cytokine production in podocytes and tubular cells, and proliferation in glomerular parietal epithelial and cyst cells.
  • MIF overexpression exacerbates experimental glomerular injury and cyst formation, while MIF targeting or CD74 deficiency confers protection against crescentic glomerulonephritis.
  • CD74 may offer protection against interstitial kidney fibrosis, but its expression on stressed kidney cells raises concerns for targeted cancer immunotherapies.

Conclusions:

  • CD74 plays a complex role in kidney pathophysiology, mediating both detrimental inflammatory responses and potentially protective mechanisms.
  • Understanding the intricate CD74 biology in kidney cells is crucial for developing effective and safe therapeutic strategies for kidney diseases.
  • Targeting the MIF/CD74 axis presents a potential therapeutic avenue, but careful consideration of CD74's dual roles and expression in stressed cells is warranted.
Keywords:
CD74Fabryd-dopachrome tautomerase (d-DT/MIF-2)diabetesinflammationkidneymacrophage inhibitory factorpolycystic kidney disease

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