Rapid induction of intercellular adhesion molecule-1 on monocytes and myelomonocytic cell lines after interferon

P Hutchinson1, N Kraft, R C Atkins

  • 1Nephrology Department, Monash Medical Centre, Clayton, Victoria, Australia.

Transplantation
|October 1, 1992
PubMed

Insights

Interferon gamma increases intercellular adhesion molecule-1 (ICAM-1) on human monocytes and related cell lines. This enhanced ICAM-1 expression boosts accessory cell activity, though other factors also contribute to immune cell function.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Intercellular Adhesion Molecule-1 (ICAM-1) is crucial for lymphocyte activation and migration into tissues.
  • ICAM-1 is typically low on monocytes but can increase with certain activation factors.
  • Previous research highlighted interferon gamma's (IFNγ) role in ICAM-1 induction on non-leukocytic cells.

Purpose of the Study:

  • To investigate the effect of IFNγ on ICAM-1 expression in human monocytes and myelomonocytic cell lines.
  • To determine the functional consequences of IFNγ-induced ICAM-1 upregulation on accessory cell activity.
  • To explore the contribution of ICAM-1 to the overall increase in cell activity.

Main Methods:

  • Treatment of human monocytes and Rc2A/U937 cell lines with IFNγ.
  • Quantification of ICAM-1 expression using flow cytometry or similar techniques.
  • Assessment of accessory cell activity via mitogen and allogeneic responses.
  • Inhibition studies using specific antibodies against ICAM-1.
  • Measurement of Class II MHC and IL-1 production.

Main Results:

  • IFNγ induced time- and dose-dependent increases in ICAM-1 on human monocytes and Rc2A/U937 cells.
  • Enhanced ICAM-1 on Rc2A cells correlated with increased accessory cell activity (mitogen/allogeneic response).
  • Specific antibody inhibition showed ICAM-1 accounted for up to 50% of the increased activity.
  • IFNγ did not elevate Class II MHC expression or IL-1 production in these cells.

Conclusions:

  • IFNγ effectively upregulates ICAM-1 on human monocytes and related cell lines.
  • Increased ICAM-1 contributes significantly, but not exclusively, to enhanced monocyte accessory function.
  • Other unidentified factors are involved in IFNγ-mediated increases in monocyte activity.