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International Immunology Advance Access published online on June 3, 2005
International Immunology, doi:10.1093/intimm/dxh270
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© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org
Received December 5, 2004
Accepted April 6, 2005

Article

The involvement of NK cells in ankylosing spondylitis

Niva Azuz-Lieberman 1 *, Gal Markel 1 *, Sa'ar Mizrahi 1, Roi Gazit 1, Jacob Hanna 1, Hagit Achdout 1, Raizy Gruda 1, Gil Katz 1, Tal I. Arnon 1, Shosh Battat 2, Ehud Zamir 3, Muhammed Adawi 4, Reuven Mader 4, and Ofer Mandelboim 1*

1 The Lautenberg Center for General and Tumor Immunology, The Hebrew University, Hadassah Medical School, Jerusalem, 91120, Israel
2 Tissue Typing Unit, Hebrew University-Hadassah Medical Organization, Jerusalem, Israel
3 Department of Ophthalmology, Hadassah-Hebrew University, Jerusalem, Israel
4 Rheumatic Disease Unit, Ha'Emek Medical Center, Afula and the B. Rappaport Faculty of Medicine, Technion Institute for Technology, Haifa, Israel

* To whom correspondence should be addressed.
Ofer Mandelboim, E-mail: oferman{at}md2.huji.ac.il


  Abstract

A role for NK cells in the regulation of autoimmunity has been demonstrated. Since there is a strong association between Ankylosing Spondylitis (AS) and HLA-B27, which is specifically recognized by the NK-inhibitory receptor KIR3DL1, this study evaluated the potential involvement of NK cells in AS. We studied 19 AS patients and 22 healthy volunteer donors and assessed the percentage, activity and receptor expression of peripheral blood NK cells. We also evaluated candidate-inflammatory mediators in sera. We found that AS patients have significantly higher percentages of NK cells. However, we found no differences between the ability of NK cells derived from AS and healthy controls to recognize target cells expressing HLA-B27. Remarkably, we observed that the NK-inhibitory receptor CEACAM1 (carcino-embryonic antigen-cell adhesion molecule) is highly expressed among AS-derived NK cells. Furthermore, engagement of CEACAM1 inhibited NK activity in these patients. Finally, we demonstrated that CEACAM1 expression is induced by IL-8 and SDF-1 (stromal cell derived factor), both of which are present in high levels in the sera of AS patients. These results may indicate that NK cells and CEACAM1 play a role in AS pathogenesis and implicate chemokines in the mechanism of CEACAM1 expression.

Keywords: NK; natural killer; CEACAM ankylosing spondylitis.

*These authors contributed equally to the work presented here.


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