Distinct patterns of chemokine secretion and chemokine receptor expression shape the inflammatory response in rejecting human liver transplants  

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Sarah Goddard, Stefan Hubscher and David Adams

The Liver Research Laboratories, MRC Centre for Immune Regulation, University of Birmingham UK.


Graft rejection after liver transplantation is associated with infiltration of the liver by monocytes & lymphocytes and the nature of this inflammatory response will be determined in part by the local activity of chemotactic cytokines (chemokines) that attract particular subsets of effector T cells to the graft. The liver is a source of chemokines during rejection but little is known about the chemokine receptors used by leukocytes infiltrating the liver. We studied the expression of chemokines and chemokine receptors in human liver by immunohistochemistry and flow cytometry. Normal human liver contained a light infiltrate of lymphocytes most of which expressed CXCR3 and some of which stained weakly for CXCR4. Kupffer cells stained weakly for CCR3. In contrast lymphocytes infiltrating portal tracts during acute and chronic graft rejection were strongly positive for CXCR3, CXCR4 & CCR5. This was associated with increased staining for the respective ligands IP-10 (CXCR3), MIP-1a and MIP-1ß (CCR5), and SDF-1a and SDF-1ß (CXCR4) in the graft. Moreover these ligands show distinctive expression patterns with IP-10 expressed on sinusoids, MIP-1a and ß on vascular endothelium and SDF on parenchymal cells. Kupffer cells showed a change in phenotype becoming positive for CXCR1, CXCR2, CXCR4, CCR2 and especially CCR3 and CCR5. In vitro alloactivation of lymphocytes resulted in increased expression of all chemokine receptors studied, but with particularly high levels of CXCR4, CXCR3 and CCR5. Further evidence that these receptors are functionally important in recruiting lymphocytes to rejecting allografts is provided by our observation that CXCR3 and CXCR4 are increased on peripheral blood T cells following liver transplantation. Thus the patterns of local chemokine expression and the induction of specific chemokine receptors on alloactivated lymphocytes will determine the nature of the inflammatory infiltrate in graft rejection.

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