Mediators of Inflammation

Mediators of Inflammation / 1999 / Article

Open Access

Volume 8 |Article ID 397534 | https://doi.org/10.1080/09629359990324

Toshiaki Kogure, Hiroshi Fujinaga, Atsushi Niizawa, Le Xuan Hai, Yutaka Shimada, Hiroshi Ochiai, Katsutoshi Terasawa, "Killer-Cell Inhibitory Receptors, CD158a/b, are Upregulated by Interleukin-2, but not Interferon-γ or Interleukin-4", Mediators of Inflammation, vol. 8, Article ID 397534, 6 pages, 1999. https://doi.org/10.1080/09629359990324

Killer-Cell Inhibitory Receptors, CD158a/b, are Upregulated by Interleukin-2, but not Interferon-γ or Interleukin-4

Abstract

Although it is now accepted that killer-cell inhibitory receptors (KIRs), which were molecularly cloned in 1995, deliver negative signals to natural killer (NK) cells regarding the recognition of target cells, it is still unclear how the expression of these receptors on lymphocytes is regulated. Therefore, we investigated the regulation of expression of representative KIRs, CD158a and CD158b, by cytokines such as interleukin-2 (IL-2), IL-4 and interferon-γ (IFN-γ). Neither IL-4 nor IFN-γ affected the expression of CD158a/b, but incubation for 48 h with IL-2, which enhances the killer activity of NK cells, upregulated the expression of the KIRs. This upregulation by IL-2 was also observed in CD16-positive cells sorted from total lymphocytes. In contrast, IL-4, which is a downregulator of IL-2-induced killer responses, did not change the level of CD158a/b expression when added after the IL-2 treatment. These findings suggest that IL-2 plays an important role in the regulation of CD158a/b expression, and might be involved in controlling NK activity via regulating expression of these molecules.

Copyright © 1999 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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