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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2006-11-30
pubmed:abstractText
Crosstalk between T cells and renal tubular epithelial cells (TECs) in the pathogenesis of tubular lesions, the most important sign of progressive renal diseases, has not been clarified. Previous work has shown that TECs harbor co-stimulatory signals that promote T-cell activation, which induces tubular lesions. Nevertheless, the expression and functional role of B7-H4, a recently identified co-stimulatory ligand of the B7 superfamily, in pathologic human kidneys is unclear. We investigated the expression of B7-H4 on cryostat renal biopsies from patients with idiopathic membranous nephropathy (n=20), immunoglobulin A nephropathy (n=19), lupus nephritis (n=16), and acute renal allograft rejection (n=15) using immunohistochemistry. In addition, we also analyzed TEC-associated B7-H4 in the regulation of T-cell activation. Immunohistological staining revealed that B7-H4 antigen is restricted to tubular epithelium and that the protein is prominent in sections with severe tubular lesions, although no correlation was observed between tubular B7-H4 expression and levels of serum creatinine, serum urea nitrogen concentration, and 24-h proteinuria in each type of nephropathy. In vitro, mixed lymphocyte reactions revealed that TEC-related B7-H4 promotes cytokine (interleukin-2 and interferon-gamma) production and proliferation of co-cultured T cells. Interestingly, the secretion of interleukin-2 by C10 T cell hybridomas also increased when C10 cells were co-cultured with the B7-H4-transgenic murine TEC line, 3M-1-secreting tubular epithelial cells (MCT) in the presence of the antigen hen egg lysozyme. Our results clearly show that TEC-associated B7-H4 induces T-cell activation and we propose that B7-H4 is a potential activator that promotes tubular lesion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0085-2538
pubmed:author
pubmed:issnType
Print
pubmed:volume
70
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2092-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:17051145-Animals, pubmed-meshheading:17051145-Antigen Presentation, pubmed-meshheading:17051145-Antigens, CD80, pubmed-meshheading:17051145-Biopsy, pubmed-meshheading:17051145-Cell Communication, pubmed-meshheading:17051145-Cell Division, pubmed-meshheading:17051145-Cell Line, pubmed-meshheading:17051145-Coculture Techniques, pubmed-meshheading:17051145-Epithelial Cells, pubmed-meshheading:17051145-Flow Cytometry, pubmed-meshheading:17051145-Gene Expression, pubmed-meshheading:17051145-Glomerulonephritis, Membranous, pubmed-meshheading:17051145-Humans, pubmed-meshheading:17051145-Kidney Tubules, pubmed-meshheading:17051145-Lymphocyte Culture Test, Mixed, pubmed-meshheading:17051145-Mice, pubmed-meshheading:17051145-RNA, Messenger, pubmed-meshheading:17051145-T-Lymphocytes, pubmed-meshheading:17051145-Transfection, pubmed-meshheading:17051145-V-Set Domain-Containing T-Cell Activation Inhibitor 1
pubmed:year
2006
pubmed:articleTitle
Expression of the novel co-stimulatory molecule B7-H4 by renal tubular epithelial cells.
pubmed:affiliation
Laboratory of Immunoregulation, Institute of Immunology, PLA, The Third Military Medical University, Chongqing, PR China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't