The involvement of NK cells in ankylosing spondylitis

被引:46
作者
Azuz-Lieberman, N
Markel, G
Mizrahi, S
Gazit, R
Hanna, J
Achdout, H
Gruda, R
Katz, G
Arnon, TI
Battat, S
Zamir, E
Adawi, M
Mader, R
Mandelboim, O [1 ]
机构
[1] Hebrew Univ Jerusalem, Hadassah Med Sch, Lautenberg Ctr Gen & Tumor Immunol, IL-91120 Jerusalem, Israel
[2] Hebrew Univ Jerusalem, Hadassah Med Org, Tissue Typing Unit, Jerusalem, Israel
[3] Hadassah Hebrew Univ, Dept Ophthalmol, Jerusalem, Israel
[4] HaEmek Med Ctr, Rheumat Dis Unit, Afula, Israel
[5] Technion Israel Inst Technol, Bruce Rappaport Fac Med, IL-31096 Haifa, Israel
基金
以色列科学基金会;
关键词
NK; natural killer; CEACAM ankylosing spondylitis;
D O I
10.1093/intimm/dxh270
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:837 / 845
页数:9
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