Killer-Cell Inhibitory Receptors, CD158a/b, are Upregulated by Interleukin-2, but not Interferon-γ or Interleukin-4
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. The...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
1999-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1080/09629359990324 |
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| _version_ | 1832566604551946240 |
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| author | Toshiaki Kogure Hiroshi Fujinaga Atsushi Niizawa Le Xuan Hai Yutaka Shimada Hiroshi Ochiai Katsutoshi Terasawa |
| author_facet | Toshiaki Kogure Hiroshi Fujinaga Atsushi Niizawa Le Xuan Hai Yutaka Shimada Hiroshi Ochiai Katsutoshi Terasawa |
| author_sort | Toshiaki Kogure |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-3dbe2a4a03f9417cb969b57f2cf9e61c |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 1999-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-3dbe2a4a03f9417cb969b57f2cf9e61c2025-02-03T01:03:37ZengWileyMediators of Inflammation0962-93511466-18611999-01-018631331810.1080/09629359990324Killer-Cell Inhibitory Receptors, CD158a/b, are Upregulated by Interleukin-2, but not Interferon-γ or Interleukin-4Toshiaki Kogure0Hiroshi Fujinaga1Atsushi Niizawa2Le Xuan Hai3Yutaka Shimada4Hiroshi Ochiai5Katsutoshi Terasawa6Department of Japanese Oriental Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930–0194, JapanDepartment of Japanese Oriental Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930–0194, JapanDepartment of Japanese Oriental Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930–0194, JapanDepartment of Japanese Oriental Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930–0194, JapanDepartment of Japanese Oriental Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930–0194, JapanDepartment of Human Science, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930–0194, JapanDepartment of Japanese Oriental Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930–0194, JapanAlthough 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.http://dx.doi.org/10.1080/09629359990324 |
| spellingShingle | 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 |
| title | Killer-Cell Inhibitory Receptors, CD158a/b, are Upregulated by Interleukin-2, but not Interferon-γ or Interleukin-4 |
| title_full | Killer-Cell Inhibitory Receptors, CD158a/b, are Upregulated by Interleukin-2, but not Interferon-γ or Interleukin-4 |
| title_fullStr | Killer-Cell Inhibitory Receptors, CD158a/b, are Upregulated by Interleukin-2, but not Interferon-γ or Interleukin-4 |
| title_full_unstemmed | Killer-Cell Inhibitory Receptors, CD158a/b, are Upregulated by Interleukin-2, but not Interferon-γ or Interleukin-4 |
| title_short | Killer-Cell Inhibitory Receptors, CD158a/b, are Upregulated by Interleukin-2, but not Interferon-γ or Interleukin-4 |
| title_sort | killer cell inhibitory receptors cd158a b are upregulated by interleukin 2 but not interferon γ or interleukin 4 |
| url | http://dx.doi.org/10.1080/09629359990324 |
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