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Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
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LPAR1 and ITGA4 regulate peripheral blood monocyte counts.

Narelle Maugeri1, Joseph E Powell, Peter A C 't Hoen

  • 1Queensland Institute of Medical Research, Brisbane, Australia.

Human Mutation
|May 21, 2011
PubMed
Summary

Genetic variants rs7023923 and rs6740847 influence monocyte counts by regulating LPAR1 and ITGA4 gene expression, respectively. These findings implicate specific genes in monocyte development and peripheral blood monocyte numbers.

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Published on: November 26, 2018

Area of Science:

  • Genetics
  • Immunology
  • Molecular Biology

Background:

  • Quantitative trait loci (QTL) for monocyte counts have been identified.
  • Understanding the genetic regulation of monocyte production is crucial for immune system research.

Purpose of the Study:

  • To investigate the functional role of genetic variants associated with monocyte counts.
  • To identify specific genes regulated by these variants and their impact on monocyte development.

Main Methods:

  • Utilized two independent approaches to demonstrate that rs7023923 regulates LPAR1 gene expression.
  • Replicated association of rs6740847 near ITGA4 with monocyte counts in 1,122 individuals.
  • Examined linkage disequilibrium between variants and expression quantitative trait loci (eQTLs).

Main Results:

  • rs7023923 was confirmed to regulate the expression of the nearby LPAR1 gene (P<0.0001).
  • rs6740847 near ITGA4 was replicated and associated with monocyte count variation (combined P=2.7×10(-10)).
  • rs7023923 upregulates LPAR1 and rs6740847 downregulates ITGA4, increasing circulating monocyte numbers.

Conclusions:

  • The genetic variants rs7023923 and rs6740847 play a role in regulating monocyte counts through LPAR1 and ITGA4.
  • These findings provide insights into the molecular mechanisms underlying monocyte development and regulation.
  • Further research is warranted to explore downstream mechanisms and immune function implications.