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Published online before print August 1, 2006

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(Journal of Leukocyte Biology. 2006;80:922-928.)
© 2006 by Society for Leukocyte Biology

Z39Ig is expressed on macrophages and may mediate inflammatory reactions in arthritis and atherosclerosis

Min-Young Lee^*,, Won-Jung Kim^*, Yoon-Joong Kang^*, Young-Mi Jung^*,, Young-Mo Kang, Kyoungho Suk, Jeong-Euy Park^¶, Eun-Mi Choi^||, Beom-Kyu Choi^||, Byoung S. Kwon^|| and Won-Ha Lee^*,1

^* Department of Genetic Engineering, College of Natural Sciences,
Agro-Biotechnology Education Center, and Departments of
Rheumatology and
Pharmacology, School of Medicine, Kyungpook National University, Taegu, Korea;
^¶ Cardiology Division, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; and
^|| Immunomodulation Research Center, University of Ulsan, Ulsan, Korea

¹ Correspondence: Department of Genetic Engineering, Kyungpook National University, Taegu 702-701, Korea. E-mail: whl{at}knu.ac.kr

Z39Ig is a transmembrane protein containing two Ig homology domains with unknown functions. Immunohistochemical analyses of human carotid atherosclerotic plaques detected Z39Ig staining in areas rich in foamy macrophages. Z39Ig staining was also observed in macrophages in the lining layers and sublining areas of rheumatoid arthritis synovium. Z39Ig staining in the osteoarthritis synovium was restricted to macrophages in the lining layers. To identify the role(s) of Z39Ig in the function of macrophages, we used human monocytic cell lines TF-1A (Z39Ig-negative) and THP-1 (Z39Ig-positive). The expression of Z39Ig was induced in TF-1A cells ,when they were differentiated into macrophages by treatment with PMA. The stimulation of PMA-treated TF-1A or THP-1 cells with immobilized anti-Z39Ig mAb induced the secretion of IL-8 and matrix metalloproteinase (MMP)-9, which was dependent on NF-B activation. These data indicate that the macrophage Z39Ig is involved in the pathogenesis of inflammatory diseases through chemokine induction, which will promote the migration of inflammatory cells into the lesion area, and MMP-9 induction, which will contribute to cartilage destruction or extracellular matrix degradation.

Key Words: matrix metalloproteinase • extracellular matrix • rheumatoid arthritis

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