Cytokine mRNA Expression During Experimental Corneal Allograft Rejection

Torres, Paulo F.; Vos, Alex F. de; Gaag, R van der; Martins, Berta; Kijlstra, Aize

doi:10.1006/exer.1996.0135

Cited by 58 publications

(42 citation statements)

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“…A number of studies indicate that rejection of corneal allografts is mediated predominantly by a Th1-response identified on the distinct cytokine profile detected within rejected corneal grafts as well as in aqueous humor of experimental animals undergoing transplant failure. [4][5][6][7] Interleukin-10 (IL-10), originally described as cytokine synthesis inhibitory factor 8 is a potent immunomodulatory cytokine that interacts with antigen presenting cells. In addition, IL-10 inhibits production of monokines such as IL-1, IL-6, IL-8 and tumour necrosis factor (TNF)-a.…”

Section: Introductionmentioning

confidence: 99%

Effects of local and systemic viral interleukin-10 gene transfer on corneal allograft survival

et al. 2006

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Section: Introductionmentioning

confidence: 99%

Effects of local and systemic viral interleukin-10 gene transfer on corneal allograft survival

et al. 2006

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“…Corneal allograft rejection is histologically characterized by massive infiltration of CD4 + T cells and macrophages. Significant numbers of neutrophils and NK cells (NK cells) were also found in the cellular infiltrates (10)(11)(12)(13)(14). Furthermore, CD11c + CD11b + myeloid dendritic cells (DCs) are present throughout the anterior stroma.…”

mentioning

confidence: 99%

Topical Application of Soluble CD83 Induces IDO-Mediated Immune Modulation, Increases Foxp3+ T Cells, and Prolongs Allogeneic Corneal Graft Survival

Bock

Rößner

Onderka

et al. 2013

The Journal of Immunology

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Modulation of immune responses is one of the main research aims in transplant immunology. In this study, we investigate the local immunomodulatory properties of soluble CD83 (sCD83) at the graft-host interface using the high-risk corneal transplantation model. In this model, which mimics the inflammatory status and the preexisting vascularization of high-risk patients undergoing corneal transplantation, allogeneic donor corneas are transplanted onto sCD83-treated recipient animals. This model allows the direct and precise application of the immune modulator at the transplantation side. Interestingly, sCD83 was able to prolong graft survival after systemic application as well as after topical application, which is therapeutically more relevant. The therapeutic effect was accompanied by an increase in the frequency of regulatory T cells and was mediated by the immune-regulatory enzyme IDO and TGF-β. In vitro, sCD83 induced long-term IDO expression in both conventional and plasmacytoid dendritic cells via autocrine or paracrine production of TGF-β, a cytokine previously shown to be an essential mediator of IDO-dependent, long-term tolerance. These findings open new treatment avenues for local immune modulation after organ and tissue transplantation.

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“…17 Evidence from studies in mouse and rat models have shown the predominance of Th1 cytokine expression in cells infiltrating the graft during corneal allograft rejection. [18][19][20] The Th1 cytokine, interferon-g, as well as other cytokines, such as IL-1b, IL-2, IL-12, have also been shown to compromise ocular immune privilege, and their upregulation may contribute to graft rejection. 18,21 Recently, anti-interferon-g antibodies were reported to be effective in halting corneal transplant rejection after penetrating keratoplasty.…”

Section: Discussionmentioning

confidence: 99%

“…[18][19][20] The Th1 cytokine, interferon-g, as well as other cytokines, such as IL-1b, IL-2, IL-12, have also been shown to compromise ocular immune privilege, and their upregulation may contribute to graft rejection. 18,21 Recently, anti-interferon-g antibodies were reported to be effective in halting corneal transplant rejection after penetrating keratoplasty. 22 Rac2 has previously been demonstrated both in vitro and in vivo to be required for interferon-g production, 23 and in turn may indirectly contribute to graft rejection.…”

Section: Discussionmentioning

confidence: 99%

Increased Rac2 mRNA expression in peripheral blood during human corneal graft rejection

Huang

Tullo

Hillarby

2008

Eye

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Purpose Allograft rejection is the main cause of graft failure in human corneal transplantation, for which underlying pathomechanism is not yet clear. We compared gene expression in the peripheral blood of patients who after undergoing corneal transplantation experienced graft rejection with those patients who accepted grafts. Methods Sixty-six patients who underwent corneal transplantation were studied including 18 patients who suffered subsequent graft rejection. cDNA array technology was used to survey and quantify transcript expression . A semiquantitative reverse transcriptase-PCR (RT-PCR) was used to confirm the gene expression pattern measured by a cDNA array of selected genes. Results Among 265 genes present on the array, eight genes were found to be differentially expressed. Four genes (Rac 2, RhoA, paxillin, and CD18) were further analysed by semiquantitative RT-PCR, and significant differences in mRNA expression levels in the rejection group were confirmed. Conclusions Our study demonstrated that the expression of Rac2 mRNA was upregulated in the peripheral blood of patients experiencing corneal transplantation rejection compared to those patients who had no rejection episodes. In addition, three genes, RhoA, paxillin, and CD18, showed decreased expression in rejecting patients. cDNA array technology provides a potentially useful approach to identify novel genes that might participate in pathogenic pathways during corneal graft rejection.

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Cytokine mRNA Expression During Experimental Corneal Allograft Rejection

Cited by 58 publications

References 0 publications

Effects of local and systemic viral interleukin-10 gene transfer on corneal allograft survival

Effects of local and systemic viral interleukin-10 gene transfer on corneal allograft survival

Topical Application of Soluble CD83 Induces IDO-Mediated Immune Modulation, Increases Foxp3+ T Cells, and Prolongs Allogeneic Corneal Graft Survival

Increased Rac2 mRNA expression in peripheral blood during human corneal graft rejection

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