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E Adafer

Publications and source records attributed to E Adafer.

6 recordsLinked to original sources

[Longitudinal study of histocompatibility antigen expression in renal transplants followed for 10 years].

Using monoclonal antibodies against class I and class II (DR antigen) major histocompatibility complex antigens, 65 renal transplant biopsies from 21 recipients whose renal transplants survived ten years or more were studied. Seven biopsies were performed while acute rejection of the renal transplant was under way. The other biopsies were carried out on a routine basis, 6 months (10 biopsies), 2 years (15 biopsies), 4 years (12 biopsies), and 10 years (21 biopsies) after transplantation. Semiquantitative evaluation of fibrous tubulointerstitial lesions was carried out on the biopsies taken after ten years. During episodes of acute rejection, strong expression of class I and class II HLA molecules by transplant tubule epithelial cells was found. When there was no acute rejection, tubule expression of class I and class II HLA molecules was more common in earlier biopsies as compared with later biopsies. In the long-term, persistence of DR antigen in tubule epithelium was associated with increased severity of fibrous tubulointerstitial lesions. A last remarkable finding in some patients was loss of expression of class I antigens in tubule cells from transplants with the longest survivals.

Adolescent↗

Cell differentiation in Wilms' tumor (nephroblastoma): an immunohistochemical study.

Using an indirect immunoperoxidase technique, we tested frozen specimens from 12 Wilms' tumors with monoclonal antibodies (MoAbs) reacting against a large panel of molecules including laminin, fibronectin, cytokeratin, vimentin, villin, CD24, CALLA/CD10, CR1, CD26, class I and class II major histocompatibility complex (MHC) molecules, and endothelium factor VIII. These molecules were chosen because they are markers of specific segments of the mature kidney and because their loss or acquisition is indicative of different steps of human nephrogenesis. KI67 MoAb was used to evaluate the proliferating activity of the cells. The blastemal component (cell compact areas) of Wilms' tumors consisted of vimentin-positive cells with a fibronectin network. However, signs of epithelial maturation were present in compact areas where cytokeratin-positive cells producing laminin were observed. The cells exhibited a high degree of proliferating activity. The tubule formations consisted of cytokeratin-positive cells and had a defined laminin border. All the cells, whether in compact areas or in tubules, were strongly CD24-positive. Some tubular formations showed signs of proximal maturation with the presence of CALLA, CD26, and even villin. In four cases class I-MHC molecules were expressed by some tubular cells. Large cystic cavities present in five cases were edged by cytokeratin, CD24-positive cells, or by vimentin, CALLA, CR1-positive cells. Some glomeruloid bodies, present in two cases, were also composed of vimentin, CALLA, and CR1-positive cells which correspond to the mature podocyte phenotype. The interstitial tissue contained mainly laminin and fibronectin network with macrophages and few CD3 lymphocytes. The presence of large cells with muscular differentiation was noted; round vimentin and CD26-positive cells were also seen. The endothelial cells of the vessels exhibited vimentin, factor VIII, and class I and class II MHC molecules as do mature cells, but in some cases the endothelial cells lacked class II molecule expression and were CALLA-positive. These results which confirmed and extended those previously described show that cell differentiation in Wilms' tumor mimics that observed during metanephros development. Moreover, this study shows that tumoral cells in nephroblastoma share several antigens with cells from lymphoid lineage (CD24, CALLA, and CD26) as do developing and mature kidney cells. Such cell phenotype dissection provides a useful and reliable tool for testing the influence of various factors on the development of hetero-transplanted or cultured Wilms' tumors.

Antigens, CD↗

Relationship between the integrity of Bowman's capsule and the composition of cellular crescents in human crescentic glomerulonephritis.

Cell constituents of glomerular crescents still remain controversial. We examined cellular crescents in ten cases of crescentic glomerulonephritis (GN) using indirect immunoperoxidase technique and monoclonal antibodies against T cells (OKT3) and subsets: T helper/inducer cell (T4), T suppressor/cytotoxic cell (OKT8), T activated cell (IoT14 and IoT15); B cells (B1, B4, OKB2 and IoB3) and subsets (B2 and IoB1); monocytes/macrophages (LeuM3); DR Ag (I2) and renal native cells: podocytes (IoT5), Bowman's capsule (BC) parietal epithelial cell (OKB2, IoB3). Studied cases were 2 anti-glomerular basement membrane (GBM) GN, 4 immune complex GN, 3 vasculitis and 1 idiopathic GN. When the BC continuity was preserved almost all crescent cells were identified; they originated in majority from the BC parietal epithelium and ranged from 55 to 95 per cent. The other main constituents which represented 15 to 35 per cent of the crescent cells were monocytes (LeuM3+) and T-activated cells (IoT15+). In the interstitial infiltrate, which was mostly periglomerular, LeuM3+ cells and IoT15+ cells accounted for more than 70 per cent of the cell population. On the other hand, when BC were ruptured, mononuclear inflammatory cells, mainly LeuM3+ and IoT15+ cells accompanied by significant number of T4+ and T8+ cells, constituted the glomerular crescents. At this time, BC parietal epithelial cells were rarely identified (15 per cent). These findings strongly support the importance of BC integrity to discriminate the nature of crescent cells.

Antibodies, Monoclonal↗

Characterization of mononuclear cell subsets in renal cellular interstitial infiltrates.

Indirect immunoperoxidase analysis using monoclonal antibodies (Mo Ab) was performed in 33 renal biopsies with interstitial cellular infiltration obtained from non-transplanted patients. We reviewed four acute interstitial nephritis (IN), three chronic IN, four granulomatous IN, four acute tubular necrosis, four vasculitis, seven primary glomerulonephritis and seven active lupus nephritis (LN). We used Mo Ab recognizing T and B cell markers [OKT3, OKT8, T4, B1, IOT14 (IL2 receptor)], HLA-DR related antigen (I2) and monocytes/macrophages (LeuM3). In all cases the interstitial cellular infiltrates were predominantly T cells, whereas the B cell population accounted for less than 20% of the infiltrate. LeuM3+ cells were present in 28 of 32 cases, usually in a lesser proportion than T cells. IOT14+ cells were exceptional. T4+/T8+ cells were clearly greater than one in three acute IN, three granulomatous IN, two LN and two vasculitis. The T8+ cell population predominated in one case of chronic IN related to a non-steroidal anti-inflammatory drug. In all the remaining cases T4+ and T8+ cells were equally present. Aberrant strong HLA-DR expression within tubular cells was noted in nine cases (4 LN) irrespective of the presence of tubular lesions. On the basis of the phenotypic analysis, our data do not support a specific pattern of the infiltrate in regard to a given etiology and thus cannot be used as a diagnostic tool. However, such analysis may aid in understanding the mechanisms of tissue injury.

Adult↗