Renal allograft rejection: The development and function of tubulitis

Robertson, Helen Lee; Kirby, John A.

doi:10.1053/trre.2001.24499

Cited by 24 publications

(35 citation statements)

References 119 publications

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“…The complex process of extravasation and influx of leukocyte subsets into the site of tissue injury appears to be mediated to a significant extent by the expression of specific chemokines and chemokine receptors (2). Specifically, the expression of the CC-chemokine MCP-1 together with the corresponding chemokine receptor CCR2 could be detected on the mononuclear cells infiltrating the kidney graft (3)(4)(5)(6)(7)(8). Furthermore, elevated levels of MCP-1 were also detected in the serum and urine of patients at the time of acute and chronic rejection (9,10).…”

mentioning

confidence: 94%

A Monocyte Chemoattractant Protein-1 (MCP-1) Polymorphism And Outcome After Renal Transplantation

Krüger¹,

Schröppel

Ashkan

et al. 2002

Journal of the American Society of Nephrology

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Abstract. Among the factors modulating transplant rejection and cardiovascular disease, chemokines and their respective receptors deserve special attention. In this respect, increased expression of MCP-1 and the corresponding receptor CCR2 have been demonstrated in renal transplant rejection and coronary artery disease. The impact of the MCP-1-2518G and CCR2-64I genotypes on renal allograft function was investigated in 232 patients who underwent transplantation over an 11-yr period. Genomic DNA was genotyped using PCR with sequence-specific primers followed by restriction fragment length polymorphism analysis. Eighteen (7.8%) patients were homozygous for the MCP-1-2518G mutation. The G/G allele of MCP-1 -2518 behaved as a determinant for long-term allograft survival and resulted in reduction of the mean graft survival, as compared with the heterozygous (A/G) or wild-type (A/A) allele (67 Ϯ 14 versus 95 Ϯ 4 mo; Log rank P ϭ 0.0052). The 64I mutation of CCR2 had no effect on kidney graft failure (93 Ϯ 6 and 91 Ϯ 5 mo, respectively; P ϭ 0.81). None of the investigated polymorphisms showed a significant shift in gene frequency in acute rejection and rejection-free groups. In conjunction with these findings, peripheral blood mononuclear cells from kidney transplant recipients carrying the G-allele were characterized by a 2.5-fold higher MCP-1 secretion (P Ͻ 0.05).

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mentioning

confidence: 94%

A Monocyte Chemoattractant Protein-1 (MCP-1) Polymorphism And Outcome After Renal Transplantation

Krüger¹,

Schröppel

Ashkan

et al. 2002

Journal of the American Society of Nephrology

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“…For example, the immediate posttransplant period is defined by the sequestration of neutrophils, which respond to early production of chemokines such as IL-8 (CXCL8) within the graft (13). At later time points the infiltrate is mononuclear, with chemokine receptors such as CXCR3 and CCR5 on T cells and monocytes responding to the local production of chemokines such as IP-10 (CXCL10), RANTES (CCL5), MIP-1a (CCL3), MIP-1b (CCL4) and MCP-1 (CCL2) (14,15 (20). The majority of T cell clones generated from renal allografts undergoing acute rejection produce a Th1 (Tc1)-polarized pattern of cytokines regardless of their CD4/CD8 phenotype (21).…”

mentioning

confidence: 99%

Post-Transplant Renal Tubulitis: The Recruitment, Differentiation and Persistence of Intra-Epithelial T Cells

Robertson

Kirby

2003

American Journal of Transplantation

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“…In addition, MCP-1, as anticipated, was involved in the interstitial nephritis (43). MCP-1 and other C-C chemokines were involved in the pathogenesis of allograft rejection (44). Interestingly, Met-RANTES reduced vascular and tubular damage during acute allograft rejection (45).…”

Section: Interstitial Renal Damage and Chemokinesmentioning

confidence: 58%