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CD11b is protective in complement-mediated immune complex glomerulonephritis

Jessy J Alexander1, Lee D Chaves1, Anthony Chang2

  • 1Division of Nephrology, Department of Medicine, Clinical and Translational Research Center, University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, New York, USA.

Kidney International
|January 8, 2015
PubMed

Insights

Complement factor H absence exacerbates immune complex glomerulonephritis. Mononuclear cell CD11b is crucial for anti-inflammatory responses in inflamed kidneys, mitigating disease severity.

Area of Science:

  • Immunology
  • Nephrology
  • Molecular Biology

Background:

  • Immune complex deposition in glomeruli can cause kidney disease.
  • Complement factor H (CfH) plays a role in regulating complement activation and preventing glomerulonephritis.
  • Leukocyte receptors like complement receptor 3 (CD11b) and Fcγ receptors can interact with immune complexes.

Purpose of the Study:

  • To investigate the role of complement factor H and leukocyte receptors in immune complex-mediated glomerulonephritis.
  • To determine the specific contribution of CD11b on mononuclear cells in the development of kidney inflammation.
  • To understand the cellular mechanisms underlying renal functional insufficiency in this disease model.

Main Methods:

  • Induction of immune complex-mediated glomerulonephritis in complement factor H-deficient mice.
  • Generation of chimeric mice with bone marrow stem cells lacking specific genes (wild-type, CfH(-/-), CD11b(-/-), FcRγ(-/-)).
  • Assessment of glomerulonephritis severity, immune responses, glomerular deposits, interstitial inflammation, macrophage polarization, T cell infiltration, and renal function.

Main Results:

  • Glomerulonephritis was significantly worse in CD11b(-/-) bone marrow chimeras compared to other groups.
  • Disease severity correlated with humoral immune responses and interstitial inflammation, particularly M1 macrophage accumulation.
  • CD11b(-/-) chimeras exhibited increased M1 macrophages and CD4(+) T cells in the kidneys.
  • CD11b(+) cells expressing colony-stimulating factor 1 receptor showed a negative correlation with glomerulonephritis scores.

Conclusions:

  • CD11b on mononuclear cells is essential for an anti-inflammatory response within the inflamed kidney.
  • The absence of CD11b exacerbates immune complex-mediated glomerulonephritis by promoting M1 macrophage and CD4(+) T cell accumulation.
  • These findings highlight CD11b as a potential therapeutic target for inflammatory kidney diseases.

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