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Killer-cell inhibitory receptors, CD158a/b, are upregulated by interleukin-2, but not interferon-gamma or

T Kogure1, H Fujinaga, A Niizawa

  • 1Department of Japanese Oriental Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University. kogu2737@ms.toyama-mpu.ac.jp

Mediators of Inflammation
|May 18, 2000
PubMed

Insights

Interleukin-2 (IL-2) upregulates killer-cell inhibitory receptors (KIRs) on natural killer (NK) cells. This IL-2 effect on KIR expression may control NK cell activity.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Killer-cell inhibitory receptors (KIRs) mediate negative signals to natural killer (NK) cells.
  • The regulation of KIR expression on lymphocytes remains largely unknown.

Purpose of the Study:

  • To investigate the regulation of CD158a and CD158b (KIRs) expression by cytokines.
  • To determine the role of IL-2, IL-4, and IFN-gamma in KIR expression.

Main Methods:

  • Incubation of lymphocytes with IL-2, IL-4, and IFN-gamma.
  • Analysis of CD158a/b expression levels.
  • Sorting of CD16-positive cells for further analysis.

Main Results:

  • IL-2 upregulated CD158a/b expression on NK cells after 48 hours.
  • IL-4 and IFN-gamma did not affect CD158a/b expression.
  • IL-2-induced upregulation of KIRs was confirmed in CD16-positive cells.

Conclusions:

  • IL-2 plays a significant role in regulating CD158a/b expression.
  • IL-2 may control NK cell activity by modulating KIR expression.

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