In Situ Expression of Tumor Necrosis Factor-Alpha, Interferon-Gamma, and Interleukin-2 Receptors in Renal Allograft Biopsies

Noronha, Irene L.; Eberlein-Gonska, Maria; Hartley, B; Stephens, Sue; Js, Cameron; Waldherr, Rüdiger

doi:10.1097/00007890-199212000-00015

Cited by 97 publications

(40 citation statements)

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“…A possible explanation may be that unknown antigens are released from the damaged tissue, and that these, in turn, are capable of stimulating the immune system. [8] As expected the inflammatory infiltrates were more severe in acute rejection and borderline cases when compared to the control group. The results showed that the number of CD8+ lymphocytes and macrophages were greater in the rejection group versus the borderline and control groups (p < 0.001).…”

Section: Discussionsupporting

confidence: 68%

“…The receptors for interleukin-2 are essential for lymphocyte interaction, cell growth, and new synthesis of other cytokines. [8] Knowledge of the phenotype of the mononuclear cell population infiltrating the transplanted kidney has proved to be of great value in establishing the precise diagnosis of post-transplant renal dysfunction as well as determining its severity and reversibility. The allograft survival is dependent on the detection and treatment of acute rejection episodes as early as possible.…”

Section: Introductionmentioning

confidence: 99%

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In Situ Expression of Mononuclear Cell Markers and Interleukin-2 Receptor in Renal Allograft Biopsies of Acute Rejection and Borderline Cases

et al. 2007

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The correct diagnosis of renal allograft rejection may be difficult using only clinical and/or histopathological criteria. Immunological assays should be considered in order to evaluate the phenotype of inflammatory infiltrate in renal allograft biopsies. Immunohistochemical studies were performed to detect mononuclear cells, CD4 and CD8 T lymphocytes, B lymphocytes, macrophages, null cells, and positive cells for interleukin-2 receptors. A total of 41 allograft biopsies classified into three groups were studied: acute cellular rejection (28 biopsies/22 patients), borderline (7 biopsies/5 patients) and control (6 biopsies/6 patients).In the rejection group (RG), increased cellularity was found mainly at the tubulo-interstitial level. Expression of CD8 positive cells was higher in RG when compared to borderline (BG) and control (CG) groups, respectively (0.

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Section: Discussionsupporting

confidence: 68%

Section: Introductionmentioning

confidence: 99%

In Situ Expression of Mononuclear Cell Markers and Interleukin-2 Receptor in Renal Allograft Biopsies of Acute Rejection and Borderline Cases

et al. 2007

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“…We restored some of the effects of IFN-␥ in GKO hosts by rIFN-␥ administration. This probably indicates that these changes (e.g., MHC and MIG induction, graft protection against necrosis) reflect the large quantities of IFN-␥ produced by host cells in rejecting grafts in close proximity with graft cells (33). Perhaps the local continuous administration of Ab or of rIFN-␥ by osmotic minipumps into the transplant artery will be able to manipulate the local conditions effectively, but technical difficulties have limited the application of this method in the small vessels of the mouse.…”

Section: Discussionmentioning

confidence: 99%

IFN-γ Alters the Pathology of Graft Rejection: Protection from Early Necrosis

Halloran

Miller

Urmson

et al. 2001

The Journal of Immunology

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We studied the effect of host IFN-γ on the pathology of acute rejection of vascularized mouse heart and kidney allografts. Organs from CBA donors (H-2k) were transplanted into BALB/c (H-2d) hosts with wild-type (WT) or disrupted (GKO, BALB/c mice with disrupted IFN-γ genes) IFN-γ genes. In WT hosts, rejecting hearts and kidneys showed mononuclear cell infiltration, intense induction of donor MHC products, but little parenchymal necrosis at day 7. Rejecting allografts in GKO recipients showed infiltrate but little or no induction of donor MHC and developed extensive necrosis despite patent large vessels. The necrosis was immunologically mediated, since it developed during rejection, was absent in isografts, and was prevented by immunosuppressing the recipient with cyclosporine or mycophenolate mofetil. Rejecting kidneys in GKO hosts showed increased mRNA for heme oxygenase 1, and decreased mRNA for NO synthase 2 and monokine inducible by IFN-γ (MIG). The mRNA levels for CTL genes (perforin, granzyme B, and Fas ligand) were similar in rejecting kidneys in WT and GKO hosts, and the host Ab responses were similar. The administration of recombinant IFN-γ to GKO hosts reduced but did not fully prevent the effects of IFN-γ deficiency: MHC was induced, but the prevention of necrosis and induction of MIG were incomplete compared with WT hosts. Thus, IFN-γ has unique effects in vascularized allografts, including induction of MHC and MIG, and protection against parenchymal necrosis, probably at the level of the microcirculation. This is probably a local action of IFN-γ produced in large quantities in the allograft.

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“…Evidence has been presented that TNF infusion can prolong survival of islet xenografts from rats to mice (24); however, a systemic immunosuppressive effect on the recipient animal, rather than a local masking of immunogenicity of the donor cells, could be responsible for the latter results. In contrast, the levels of TNF have been observed to rise both preceeding and during allogeneic graft rejection in humans (25)(26)(27), and antibodies to TNF have been observed to prolong allogeneic cardiac transplants in mice (28)(29)(30). Expression of TNF in ,B cells in transgenic mice results in insulitis but does not progress to diabetes (31,32 (35).…”

Section: Discussionmentioning

confidence: 99%

Prolonged survival of pancreatic islet allografts mediated by adenovirus immunoregulatory transgenes.

Efrat

Fejér

Brownlee

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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The adenovirus (Ad) early region 3 (E3) genes code for at least four proteins that inhibit the host immune responses mediated by cytotoxic T lymphocytes and tumor necrosis factor a. To evaluate the potential use of these immunoregulatory viral functions in facilitating allogeneic cell transplantation, the Ad E3 genes were expressed in pancreatic beta cells in transgenic mice under control of the rat insulin II promoter. Transgenic H-

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In Situ Expression of Tumor Necrosis Factor-Alpha, Interferon-Gamma, and Interleukin-2 Receptors in Renal Allograft Biopsies

Cited by 97 publications

References 0 publications

In Situ Expression of Mononuclear Cell Markers and Interleukin-2 Receptor in Renal Allograft Biopsies of Acute Rejection and Borderline Cases

In Situ Expression of Mononuclear Cell Markers and Interleukin-2 Receptor in Renal Allograft Biopsies of Acute Rejection and Borderline Cases

IFN-γ Alters the Pathology of Graft Rejection: Protection from Early Necrosis

Prolonged survival of pancreatic islet allografts mediated by adenovirus immunoregulatory transgenes.

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