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Regulation of I-309 gene expression in human monocytes by endogenous interleukin-1

R S Selvan1, L J Zhou, M S Krangel

  • 1Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA. selva001@mc.duke.edu

European Journal of Immunology
|March 1, 1997
PubMed

Insights

Human monocytes produce the beta-chemokine I-309, with its gene expression strongly induced by immobilized immunoglobulin G (IgG) and lipopolysaccharide (LPS). Interleukin (IL)-1alpha is crucial for this I-309 induction.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cellular Biology

Background:

  • Activated human monocytes are known producers of various beta-chemokines.
  • The specific role and regulation of beta-chemokine I-309 production by monocytes require further elucidation.
  • Understanding chemokine regulation is vital for immune response modulation.

Purpose of the Study:

  • To investigate whether human monocytes produce the beta-chemokine I-309.
  • To compare the induction requirements for I-309 with those of other beta-chemokines.
  • To identify key regulatory factors, such as interleukin-1 (IL-1), involved in I-309 gene expression.

Main Methods:

  • Purification of human peripheral blood monocytes.
  • Stimulation of monocytes with immobilized immunoglobulin G (IgG) and lipopolysaccharide (LPS).
  • Analysis of I-309, monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-1alpha (MIP-1alpha) gene expression using transcript analysis.
  • Investigation of the role of endogenous and exogenous IL-1alpha and IL-1beta via neutralization and addition experiments.

Main Results:

  • Human monocytes express I-309 transcripts and secrete I-309 protein upon stimulation.
  • Immobilized IgG and LPS synergistically induce I-309 gene expression.
  • Endogenous IL-1alpha plays a critical role in I-309 induction; its neutralization inhibits induction, while exogenous IL-1alpha or IL-1beta can induce it.
  • MCP-1 and MIP-1alpha gene expression show distinct regulatory patterns compared to I-309, with differing responses to combined stimuli and IL-1.
  • Each beta-chemokine gene exhibits distinct regulatory control within human monocytes.

Conclusions:

  • Human monocytes are a source of I-309, a beta-chemokine.
  • I-309 gene expression in monocytes is significantly regulated by the synergistic action of immobilized IgG and LPS, with a crucial role for endogenous IL-1alpha.
  • The distinct regulatory mechanisms for I-309, MCP-1, and MIP-1alpha highlight the complex control of chemokine production by human monocytes.

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