Glomerular infiltration by CXCR3+ ICOS+ activated T cells in chronic allograft nephropathy with transplant glomerulopathy

Enver Akalin; S. Dikman; B. Murphy; J. S. Bromberg; W. W. Hancock

doi:10.1034/j.1600-6143.2003.00151.x

Glomerular infiltration by CXCR3+ ICOS+ activated T cells in chronic allograft nephropathy with transplant glomerulopathy

Enver Akalin, S. Dikman, B. Murphy, J. S. Bromberg, W. W. Hancock

Research output: Contribution to journal › Article › peer-review

70 Scopus citations

Abstract

The pathogeneses of chronic allograft nephropathy (CAN), a leading cause of allograft failure, and one of its complications, transplant glomerulopathy (TGP), are unknown. Immunohistologic analysis of human renal transplant biopsies showed expression of inducible costimulator (ICOS), the chemokine receptor CXCR3, and its ligands, Mig and IP-10, by intraglomerular and periglomerular leukocytes in biopsies with CAN and TGP but not CAN alone. ICOS and CXCR3 are both characteristics of activated, effector T cells, suggesting different pathogenetic mechanisms underlying TGP vs. CAN. We conclude that targeting of specific chemokine and chemokine receptor pathways and/or ICOS may have clinical application in the prevention and treatment of TGP.

Original language	English (US)
Pages (from-to)	1116-1120
Number of pages	5
Journal	American Journal of Transplantation
Volume	3
Issue number	9
DOIs	https://doi.org/10.1034/j.1600-6143.2003.00151.x
State	Published - Sep 2003
Externally published	Yes

Keywords

CXCR3
Chemokines
Chronic allograft nephropathy
ICOS
Transplant glomerulopathy

ASJC Scopus subject areas

Immunology and Allergy
Transplantation
Pharmacology (medical)

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10.1034/j.1600-6143.2003.00151.x

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title = "Glomerular infiltration by CXCR3+ ICOS+ activated T cells in chronic allograft nephropathy with transplant glomerulopathy",

abstract = "The pathogeneses of chronic allograft nephropathy (CAN), a leading cause of allograft failure, and one of its complications, transplant glomerulopathy (TGP), are unknown. Immunohistologic analysis of human renal transplant biopsies showed expression of inducible costimulator (ICOS), the chemokine receptor CXCR3, and its ligands, Mig and IP-10, by intraglomerular and periglomerular leukocytes in biopsies with CAN and TGP but not CAN alone. ICOS and CXCR3 are both characteristics of activated, effector T cells, suggesting different pathogenetic mechanisms underlying TGP vs. CAN. We conclude that targeting of specific chemokine and chemokine receptor pathways and/or ICOS may have clinical application in the prevention and treatment of TGP.",

keywords = "CXCR3, Chemokines, Chronic allograft nephropathy, ICOS, Transplant glomerulopathy",

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AU - Akalin, Enver

AU - Dikman, S.

AU - Murphy, B.

AU - Bromberg, J. S.

AU - Hancock, W. W.

PY - 2003/9

Y1 - 2003/9

N2 - The pathogeneses of chronic allograft nephropathy (CAN), a leading cause of allograft failure, and one of its complications, transplant glomerulopathy (TGP), are unknown. Immunohistologic analysis of human renal transplant biopsies showed expression of inducible costimulator (ICOS), the chemokine receptor CXCR3, and its ligands, Mig and IP-10, by intraglomerular and periglomerular leukocytes in biopsies with CAN and TGP but not CAN alone. ICOS and CXCR3 are both characteristics of activated, effector T cells, suggesting different pathogenetic mechanisms underlying TGP vs. CAN. We conclude that targeting of specific chemokine and chemokine receptor pathways and/or ICOS may have clinical application in the prevention and treatment of TGP.

AB - The pathogeneses of chronic allograft nephropathy (CAN), a leading cause of allograft failure, and one of its complications, transplant glomerulopathy (TGP), are unknown. Immunohistologic analysis of human renal transplant biopsies showed expression of inducible costimulator (ICOS), the chemokine receptor CXCR3, and its ligands, Mig and IP-10, by intraglomerular and periglomerular leukocytes in biopsies with CAN and TGP but not CAN alone. ICOS and CXCR3 are both characteristics of activated, effector T cells, suggesting different pathogenetic mechanisms underlying TGP vs. CAN. We conclude that targeting of specific chemokine and chemokine receptor pathways and/or ICOS may have clinical application in the prevention and treatment of TGP.

KW - CXCR3

KW - Chemokines

KW - Chronic allograft nephropathy

KW - ICOS

KW - Transplant glomerulopathy

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Glomerular infiltration by CXCR3+ ICOS+ activated T cells in chronic allograft nephropathy with transplant glomerulopathy

Abstract

Keywords

ASJC Scopus subject areas

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