A monoclonal antibody that detects HLA-D region antigen in routinely fixed, wax embedded sections of normal and neoplastic lymphoid tissues.

Epenetos, A A; Bobrow, Lynda G.; Adams, Timothy E.; Collins, C. D.; Isaacson, Peter G.; Bodmer, W F

doi:10.1136/jcp.38.1.12

Cited by 74 publications

(8 citation statements)

References 10 publications

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“…26,27 In addition to reagents defining MHC class I glycoproteins, panel antibodies included the monomorphic MHC class II HLA-DR marker TAL IB5. 28 Differentiation markers included TMH1 defining the melanocytic 75 kD tyrosinase-related protein TRP1 [29][30][31] and Dako T6 (CD1a). 32 Immunocytochemistry was performed on 5 m cryostat sections using a streptavidin-peroxidase technique.…”

Section: Methodsmentioning

confidence: 99%

An Immunocytochemical Study of MHC Class I Expression on Human Langerhans Cells and Melanocytes

et al. 1997

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Section: Methodsmentioning

confidence: 99%

An Immunocytochemical Study of MHC Class I Expression on Human Langerhans Cells and Melanocytes

et al. 1997

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“…The primary dilutions were 1:20, 1:5000, 1:5000 and 1:10000 respectively. In addition to the hormonal antibodies, we used two antibodies against the non-polymorphous region of the HLA-DR antigen, EPl13 (gift of Dr. H. G. Thiele, Hamburg, FRG [16[) and TAL-B 5 (gift of C. Dixon, London, UK [17]) known to react on paraffin embedded tissue at dilutions of I : 10 000 and 1 : 20 respectively.…”

Section: Methodsmentioning

confidence: 99%

Residual insulin positivity and pancreatic atrophy in relation to duration of chronic Type 1 (insulin-dependent) diabetes mellitus and microangiopathy

1987

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Summary.The relationship of residual insulin positivity in chronic Type I (insulin-dependent) diabetes and atrophy of the exocrine pancreas to duration of diabetes, age at onset and microangiopathy was studied in 26 patients (disease duration 2 to 54 years, mean 26 years). Islets containing insulin cells were found in 13/26 pancreata. In 5/13 pancreata insulin positive cells were detected in only one lobule, while in 8/13 insulin positivity was multifocal. All patients with diabetes duration less than 11 years had residual insulin cells; whereas, the rate of insulin positivity was near 40% with diabetes duration of more than 11 and 21 years, respectively. Survival of insulin cells was not clearly related to age at onset. HLA-DR expression on insulin cells was seen in one case. lnsulitis was lacking. Pancreatic volume determined in 18 patients ranged from 14-110ml (age adjusted mean 56.3 ml) and was significantly less than that of control subjects (age adjusted, mean 89.9 ml, p < 0.0001). Computerized morphometry of the exocrine pancreas revealed severe acinat atrophy due to a reduction in size of acinar cells. Acinar atrophy correlated neither with the degree of insulin positivity, disease duration nor severity of microangiopathy. The findings suggest that in about 40% of patients with Type 1 diabetes a small population of insulin cells may escape autoimmune destruction, irrespective of disease duration or age at onset. Though exocrine atrophy and insulin deficiency are associated, the variable extent of pancreatic atrophy could not to be related to such factors as amount of surviving insulin cells, duration of diabetes or microangiopathy.Key words: Chronic Type 1 (insulin-dependent) diabetes, residual insulin cells, exocrine atrophy, HLA-DR expression, diabetic microangiopathy.Loss of insulin cells characterises the islet lesions in patients with Type 1 (insulin-dependent) diabetes mellitus [1][2][3][4]. This loss, however, need not to be complete, since B cells, though severely reduced, have been demonstrated even in patients with a diabetes duration up to 37 years [1,3], The mechanisms which may protect some insulin cells from destruction by the autoimmune process underlying Type I diabetes are largely unkrlown.Another finding that characterises the pancreas in chronic Type 1 diabetes is a reduction in weight and volume [3,[5][6][7][8]. The pancreatic atrophy is attributed to the lacking trophic effect of insulin on the acinar cells [2,3,[9][10][11][12][13]. The extent of the exocrine atrophy, however, appears to vary considerably from patient to patient and has not yet been related to the remaining insulin positivity in the pancreas, to diabetes duration or to the degree of microangiopathy. * Presented in part at the 22 nd EASD meeting in Rome, 1986 ** Present address: Department of Pathology, Free University of Brussels, BelgiumThe aim of the present study was to investigate the degree and distribution of residual insulin positivity in the pancreas of patients with long-standing Type 1 diabetes by immunocyt...

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“…The murine monoclonal antibody TAL-1 B5 to a monomorphic determinant of the HLA-DR a-chain (weakly cross-reacting with the fl-chain) originally raised by Adams et al (1983) and shown to react with fixed and paraffinembedded tissues (Epenetos et al, 1985) Immunoperoxidase staining The indirect immunoperoxidase technique used in this study was performed as previously described (Bartek et al, 1985a) using peroxidase conjugated rabbit anti-mouse immunoglobulin antiserum (Dako, Copenhagen, Denmark) as the second antibody, diaminobenzidine (Sigma, Deisenhofen, FRG) as chromogen and haematoxylin to counterstain nuclei.…”

Section: Monoclonal Antibodiesmentioning

confidence: 99%

HLA-DR antigens on differentiating human mammary gland epithelium and breast tumours

Bártek

Petřek²,

Vojtěšek³

et al. 1987

Br J Cancer

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Summary The staining pattern of a monoclonal antibody directed to the monomorphic determinant of HLA-DR antigens was examined on sections of human mammary gland tissues at various stages of differentiation as well as on 50 benign and 72 malignant breast lesions. Normal resting breast epithelium lacked HLA-DR, whereas late-pregnant and lactating epithelia expressed high levels of HLA-DR antigens, followed by a decline in the post-weaning regression period. Most benign breast lesions revealed heterogeneous staining ranging from very few up to 20-25% positive epithelial cells. Greater variability was observed among carcinomas, where a small group (-7%) of cases showing 40-95% positive tumour cells was found, in addition to negative tumours and those with the minority of HLA-DR expressing carcinoma cells. The density of the leukocytic infiltrate was higher in carcinomas than in either normal breast tissue or benign lesions, the HLA-DR phenotype of the mononuclear infiltrating cells lacking any obvious correlation with the HLA-DR status of the epithelial component. Immunoblotting analyses of whole-tissue lysates separated by SDS-PAGE confirmed the immunohistochemical data and demonstrated the reactivity with only one protein band predicted for HLA-DR a-chain. The combination of immunohistochemistry and autoradiography on sections of human reduction mammoplasty organoids cultured in collagen gels and labelled with tritiated thymidine revealed a lack of HLA-DR expression on proliferating breast epithelial cells suggesting factors other than cell kinetics must be responsible for induction of HLA-DR antigens seen in pregnant and lactating breast epithelium and some tumours.

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A monoclonal antibody that detects HLA-D region antigen in routinely fixed, wax embedded sections of normal and neoplastic lymphoid tissues.

Cited by 74 publications

References 10 publications

An Immunocytochemical Study of MHC Class I Expression on Human Langerhans Cells and Melanocytes

An Immunocytochemical Study of MHC Class I Expression on Human Langerhans Cells and Melanocytes

Residual insulin positivity and pancreatic atrophy in relation to duration of chronic Type 1 (insulin-dependent) diabetes mellitus and microangiopathy

HLA-DR antigens on differentiating human mammary gland epithelium and breast tumours

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