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SDF‐1 expression is elevated in chronic human renal allograft rejection
Author(s) -
Hoffmann U.,
Banas B.,
Krüger B.,
Banas M.,
Bergler T.,
Böger C.,
Kammerl M.,
Obed A.,
Rümmele P.,
Segerer S.,
Riegger G. A. J.,
Krämer B. K.
Publication year - 2006
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/j.1399-0012.2006.00540.x
Subject(s) - medicine , graft rejection , expression (computer science) , transplantation , immunology , computer science , programming language
The exact mechanism of acute and chronic allograft rejection still remains unclear. The chemokine SDF‐1 as mediator of allograft rejection has been under intensive investigation in liver, cardiac and bone marrow transplantation, whereas in renal transplantation, there are no reports about SDF‐1 to date. This study was performed to evaluate if SDF‐1 might also play an important role in human renal graft biopsies. One hundred and ninety formalin‐fixed, paraffin‐embedded renal allograft biopsies were included in the analysis from patients with normal renal graft morphology (according to Banff 97 classification grade 1, n = 84), with acute interstitial rejection (Banff grade 4 type I, n = 10), with acute vascular rejection (Banff grade 4 type II, n = 21), with chronic allograft nephropathy (CAN, Banff grade 5, n = 23), and without rejection but with various other lesions (Banff grade 6, n = 42). SDF‐1 was localized by immunohistochemistry. In biopsies with CAN, SDF‐1 expression was significantly elevated in interstitial infiltrates and infiltrating neointimal cells of arteries compared with biopsies with normal renal graft morphology. This is the first study describing a role of SDF‐1 in human renal allograft rejection. We were able to demonstrate in a large number of biopsies an upregulation of SDF‐1 in patients with CAN. Whether SDF‐1 has pro‐inflammatory or protective properties in this setting has to be evaluated in further trials.