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Expression and Role of CD166 in the Chronic Kidney Disease
Yan Sun1, Yiping Wang2, Qi Cao2
1Department of Pediatrics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.
Insights
CD166 is upregulated in chronic kidney disease, aiding lymphocyte recruitment to inflamed kidneys. This study reveals CD166
Area of Science:
- Immunology
- Nephrology
- Cell Biology
Background:
- CD166, an immunoglobulin superfamily adhesion molecule, facilitates lymphocyte trafficking into tissues.
- The role and expression of CD166 in chronic kidney disease (CKD) remain largely uncharacterized.
Purpose of the Study:
- To investigate CD166 expression in the context of chronic kidney disease.
- To elucidate the functional role of CD166 in conjunction with CD4+ T cells during kidney inflammation.
Main Methods:
- CD166 expression analyzed via Flow Cytometry (FACS) on LPS-stimulated macrophages.
- In vivo analysis of CD166 and CD4 expression in adriamycin-induced nephropathy (AN) mouse kidneys using immunohistochemistry.
- Co-culture of macrophages and lymphocytes to assess CD166-CD4 interactions via immunofluorescent staining and evaluate T cell activation/proliferation.
Main Results:
- CD166 expression is upregulated on activated macrophages and glomerular endothelia in AN mice.
- Increased CD4+ T cells correlate with CD166 expression in AN mice.
- CD166 mediates the interaction between macrophages and CD4+ T cells, crucial for lymphocyte recruitment in CKD, without affecting T cell proliferation or activation.
Conclusions:
- CD166 is expressed on macrophages and endothelia within the inflamed kidneys of AN mice.
- CD166 facilitates CD4+ T cell recruitment into inflamed kidneys in CKD.
- CD166 presents a potential therapeutic target for mitigating inflammatory cell infiltration in chronic kidney disease.
Background:
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.
Objectives:
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.
Materials And Methods:
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.
Results:
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.
Conclusions:
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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