Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add more filters










Database
Language
Publication year range
1.
Int Immunol ; 17(7): 837-45, 2005 Jul.
Article in English | MEDLINE | ID: mdl-15937057

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.


Subject(s)
Autoimmunity/immunology , HLA-B27 Antigen/immunology , Killer Cells, Natural/immunology , Receptors, Immunologic/immunology , Spondylitis, Ankylosing/immunology , Adult , Antigens, CD/immunology , Cell Adhesion Molecules/immunology , Cells, Cultured , Gene Expression Regulation/immunology , Humans , Interleukin-8/immunology , Killer Cells, Natural/pathology , Male , Middle Aged , Receptors, KIR , Receptors, KIR3DL1 , Spondylitis, Ankylosing/pathology
SELECTION OF CITATIONS
SEARCH DETAIL
...