Morphometric Analysis of Cellular Infiltration Assessed by Monoclonal Antibody Labeling in Sequential Human Renal Allograft Biopsies

McWhinnie, Douglas; Thompson, John F.; Taylor, Helen; Chapman, J. R.; Bolton, Eleanor M.; Carter, N. P.; Wood, R. F.; Morris, Peter J.

doi:10.1097/00007890-198610000-00004

Cited by 128 publications

(75 citation statements)

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“…At 24 h after reperfusion, random corticomedullary junction fields were observed at a magnification of × 400. Using a method modified from McWhinnie et al (McWhinnie et al 1986), histopathologic assessment of the tubular necrosis was determined semiquantitatively by a person who was unaware of the treatment conditions (n = 4, each group). From each kidney, 100 intersections were examined, and a score from 0 to 3 was given for the tubular profiles involving an intersection: 0 = normal kidney; 1 = tubular cell swelling, brush border loss or nuclear condensation, with up to one-third of the tubular profiles showing nuclear loss; 2 = same as for score 1, but greater than one-third and less than two-thirds of the tubular profiles show nuclear loss; and 3 = greater than two-thirds of tubular profiles showing nuclear loss.…”

Section: Histopathologic Evaluationmentioning

confidence: 99%

Atrial Natriuretic Peptide Attenuates Ischemia/Reperfusion-Induced Renal Injury by Reducing Neutrophil Activation in Rats

Chujo

Ueki

Asaga

et al. 2008

Tohoku J. Exp. Med.

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Activated neutrophils have been implicated in the development of ischemia/reperfusion (I/R)-induced renal failure. Cytokine-induced neutrophil chemoattractant-1 (CINC-1), a major factor in acute inflammation, is responsible for the activation of neutrophils and for neutrophil chemotaxis to sites of injury. Atrial natriuretic peptide (ANP), a hormone synthesized by the cardiac atria, was shown to possess anti-inflammatory potential due to its potency to inhibit the production of inflammatory mediators. We examined whether the human form of ANP attenuates I/R-induced renal injury by reducing neutrophil activation in a rat model. Male Wistar rats weighing 200-240 g were observed for 24 h after reperfusion following 45-min renal ischemia. Rats were intravenously administered alphahuman ANP (α -hANP, 0.2 μ g/kg/min) beginning immediately after ischemia and continuing for 2 h after reperfusion. CINC-1 and myeloperoxidase (MPO) concentrations were measured to assess activation of the infiltrating neutrophil. Blood urea nitrogen and serum creatinine and urinary N-acetyl β -d-glucosaminidase (NAG) were measured as indicators of glomerular function and as a specific indicator of proximal tubular function, respectively. α -hANP significantly inhibited I/R-induced increases in renal CINC-1 and MPO concentrations. α -hANP also reduced I/R-induced increases in the concentrations of blood urea nitrogen and serum creatinine, and improved histopathologic changes, including acute tubular necrosis. These findings indicate that α -hANP attenuates I/R-induced acute renal injury, at least in part by reducing neutrophil activation, and may be useful in surgeries, associated with renal ischemia, as well as in renal transplantation.human atrial natriuretic peptide; neutrophils; kidney; ischemia/reperfusion; cytokine-induced neutrophil chemoattractant-1. Tohoku

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Section: Histopathologic Evaluationmentioning

confidence: 99%

Atrial Natriuretic Peptide Attenuates Ischemia/Reperfusion-Induced Renal Injury by Reducing Neutrophil Activation in Rats

Chujo

Ueki

Asaga

et al. 2008

Tohoku J. Exp. Med.

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“…The cell infiltrate was measured by immunochemistry using a three-step indirect immunoperoxidase technique with primary Ab and the corresponding biotin-conjugated anti-mouse Ig-Ab, HRP-conjugated streptavidin, and vasoactive intestinal peptide substrate. The area of each immunoperoxidaselabeled tissue section infiltrated by cells was determined by quantitative morphometric analysis as previously described (19). Briefly, the number of positively stained cells on each slide was counted by morphometric analysis using the point-counting technique, with a 121 intersection squared grid.…”

Section: Histology and Immunohistologymentioning

confidence: 99%

Dominant Tolerance to Kidney Allografts Induced by Anti-Donor MHC Class II Antibodies: Cooperation between T and Non-T CD103+ Cells

Degauque

Lair

Dupont

et al. 2006

The Journal of Immunology

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Allograft acceptance can be induced in the rat by pretransplant infusion of donor blood or spleen cells. Although promoting long-term acceptance, this treatment is also associated with chronic rejection. In this study, we show that a single administration of anti-donor MHC class II alloimmune serum on the day of transplantation results in indefinite survival of a MHC-mismatched kidney graft. Long-term recipients accept a donor-type skin graft and display no histological evidence of chronic rejection. The kidney grafts of tolerant animals display an accumulation of TCR Cβ, FoxP3, and IDO transcripts. Moreover, as compared with syngeneic recipients, tolerant recipients harbor a large infiltrate of MHC class II+ cells and CD103+ cells. In vitro, splenocytes from tolerant recipients exhibit decreased donor-specific proliferation, which is restored by depletion of non-T cells and partially restored by the blockade of IDO. Finally, splenocytes from tolerant recipients, but not purified T cell splenocytes, transfer donor-specific infectious tolerance without chronic rejection, after infusion into naive recipients, over two generations. However, splenocytes depleted of T cells or splenocytes depleted of CD103+ cells fail to transfer tolerance. Collectively, these data show that a single administration of anti-donor MHC class II alloimmune serum induces a tolerant state characterized by an infiltration of the kidney graft by regulatory T cells and CD103+ cells. These data also show that the transfer of tolerance requires the presence of both T cells and CD103+ dendritic cells. The precise mechanism of cooperation of these two cell subsets remains to be defined.

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“…The area of each immunoperoxydase-labeled tissue section that was infiltrated by cells was determined by quantitative morphometric analysis (24,25). Briefly, positively stained cells in the interstitium of each section were counted by morphometric analysis using a point counting method with a 121-intersection squared grid in the eyepiece of the microscope.…”

Section: Immunohistology and Quantitative Analysis Of Cellular Infiltmentioning

confidence: 99%

Highly Altered Vβ Repertoire of T Cells Infiltrating Long-Term Rejected Kidney Allografts

Gagne

Brouard

Giral

et al. 2000

The Journal of Immunology

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Chronic rejection represents a major cause of long-term kidney graft loss. T cells that are predominant in long-term rejected kidney allografts (35 ± 10% of area infiltrate) may thus be instrumental in this phenomenom, which is likely to be dependant on the indirect pathway of allorecognition only. We have analyzed the variations in T cell repertoire usage of the Vβ chain at the complementary determining region 3 (CDR3) level in 18 human kidney grafts lost due to chronic rejection. We observed a strongly biased intragraft TCR Vβ usage for the majority of Vβ families and also a very high percentage (55%) of Vβ families exhibiting common and oligoclonal Vβ-Cβ rearrangements in the grafts of patients with chronic rejection associated with superimposed histologically acute lesions. Furthermore, Vβ8 and Vβ23 families exhibited common and oligoclonal Vβ-Jβ rearrangements in 4 of 18 patients (22%). Several CDR3 amino acid sequences were found for the common and oligoclonal Vβ8-Jβ1.4 rearrangement. Quantitative PCR showed that biased Vβ transcripts were also overexpressed in chronically rejected kidneys with superimposed acute lesions. In contrast, T lymphocytes infiltrating rejected allografts with chronic rejection only showed an unaltered Gaussian-type CDR3 length distribution. This pattern suggests that late graft failure associated with histological lesions restricted to Banff-defined chronic rejection does not involve T cell-mediated injury. Thus, our observation suggests that a limited number of determinants stimulates the recipient immune system in long-term allograft failure. The possibility of a local response against viral or parenchymatous cell-derived determinants is discussed.

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Morphometric Analysis of Cellular Infiltration Assessed by Monoclonal Antibody Labeling in Sequential Human Renal Allograft Biopsies

Cited by 128 publications

References 0 publications

Atrial Natriuretic Peptide Attenuates Ischemia/Reperfusion-Induced Renal Injury by Reducing Neutrophil Activation in Rats

Atrial Natriuretic Peptide Attenuates Ischemia/Reperfusion-Induced Renal Injury by Reducing Neutrophil Activation in Rats

Dominant Tolerance to Kidney Allografts Induced by Anti-Donor MHC Class II Antibodies: Cooperation between T and Non-T CD103+ Cells

Highly Altered Vβ Repertoire of T Cells Infiltrating Long-Term Rejected Kidney Allografts

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