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Flow Cytometry Analysis of Immune Cells Within Murine Aortas
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T Cell CX3CR1 Mediates Excess Atherosclerotic Inflammation in Renal Impairment

Lei Dong1, Johannes Nordlohne2, Shuwang Ge1

  • 1Division of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany; Department of Nephrology, Tongji Hospital, Huazhong University of Science and Technology, China; and.

Journal of the American Society of Nephrology : JASN
|October 10, 2015
PubMed

Insights

Fractalkine receptor CX3CR1 deficiency protects against atherosclerosis in mice with impaired kidney function. T cell CX3CR1 expression, induced by TGF-beta, drives this enhanced cardiovascular risk.

Area of Science:

  • Cardiovascular Research
  • Renal Medicine
  • Immunology

Background:

  • Reduced kidney function elevates atherosclerosis and cardiovascular mortality risk.
  • Leukocyte infiltration in arterial walls promotes atherosclerotic plaque development.
  • The role of fractalkine receptor CX3CR1 in renal impairment-associated atherosclerosis requires elucidation.

Purpose of the Study:

  • To investigate the function of fractalkine receptor CX3CR1 in atherosclerotic inflammation within the context of renal impairment.
  • To determine the specific contribution of T cell CX3CR1 expression to atherosclerosis progression during kidney dysfunction.

Main Methods:

  • Utilized apolipoprotein E-deficient (Apoe(-/-)) and LDL receptor-deficient (LDLr(-/-)) mouse models with induced renal impairment.
  • Employed bone marrow chimeras and genetic deficiency models (CX3CR1(-/-), Il17a(-/-)) to dissect cellular contributions.
  • Analyzed atherosclerotic lesion size, macrophage accumulation, and inflammatory leukocyte profiles (T cells, myeloid cells) via flow cytometry and gene expression analysis.
  • Investigated in vitro T cell polarization and cytokine-induced CX3CR1 expression.

Main Results:

  • CX3CR1 deficiency in mice with renal impairment significantly reduced aortic atherosclerotic lesion size and macrophage accumulation.
  • CX3CR1 intrinsically promoted T cell accumulation in atherosclerotic aortas and increased IL-17-producing T cell counts.
  • Transforming growth factor-beta (TGF-β) was identified as an inducer of T cell CX3CR1 expression and IL-17A production, exacerbating atherosclerosis in renal impairment.

Conclusions:

  • T cell-intrinsic fractalkine receptor CX3CR1 expression plays a critical role in promoting atherosclerosis during renal impairment.
  • TGF-β-induced CX3CR1 upregulation on T cells contributes to enhanced cardiovascular risk in kidney disease.
  • Targeting T cell CX3CR1 or its induction pathways may offer therapeutic strategies for atherosclerosis in patients with renal impairment.

Keywords:
arteriosclerosischemokine receptorlymphocytes

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