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Expression and Role of CD166 in the Chronic Kidney Disease
Author(s) -
Yan Sun,
Yiping Wang,
Qi Cao,
Hong Yu,
Zheng Dong,
Wang Ya,
David C.H. Harris
Publication year - 2015
Publication title -
iranian journal of pediatrics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.168
H-Index - 25
eISSN - 2008-2150
pISSN - 2008-2142
DOI - 10.5812/ijp.543
Subject(s) - flow cytometry , kidney , medicine , kidney disease , immunology , downregulation and upregulation , cancer research , microbiology and biotechnology , pathology , biology , biochemistry , gene
CD166, an adhesion molecule of the immunoglobulin superfamily, is one of the crucial effectors that traffic lymphocytes into tissues. Till now, the expression and role of CD166 in the chronic kidney disease remains unknown.In the present study, we are to examine the expression of CD166 in the chronic kidney disease, and to explore its function with CD4+ T cells.CD166 expression was tested by Flow Cytometry (FACS) in the primary macrophages stimulated with LPS. In vivo, the expression of CD166 and CD4 were examined in the kidney tissues of adriamycin-induced nephropathy (AN) mice by immnohistochemistry. Macrophages and lymphocytes were co-cultured, the interaction between CD166 and CD4 was tested by immunofluorescent staining. Furthermore, the effects of CD166 on the activation and proliferation of T cells were explored.In this study, CD166 expression was found to be upregulated on activated macrophages and glomerular endothelia in the adriamycin-induced nephropathy (AN) mice and CD4+ T cells were increased with CD166 expression in the AN mice. The interaction between macrophages and CD4+ T cells indicated that CD166 played a key role in the recruitment of lymphocytes in the chronic kidney disease, and neither proliferation nor activation of T cells was affected by CD166.CD166 expressed on macrophages and endothelia in AN kidney, and the function was related to the recruitment of CD4+ T cells into inflamed kidney, indicating that CD166 may be a potential target for reducing the inflammatory infiltrates in the chronic kidney disease.

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