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  • 1
    Electronic Resource
    Electronic Resource
    Islet banking for transplantation in diabetes mellitus
    Amsterdam : Elsevier
    Cryobiology 25 (1988), S. 541-542 
    Details
    ISSN: 0011-2240
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0011-2240(88)90393-8
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Cryopreservation reduces pancreatic islet allo- and xenograft immunogenicity
    Amsterdam : Elsevier
    Cryobiology 25 (1988), S. 542 
    Details
    ISSN: 0011-2240
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0011-2240(88)90395-1
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Application of probabilistic fracture mechanics to optimize the maintenance of PWR steam generator tubes
    Amsterdam : Elsevier
    Nuclear Engineering and Design 142 (1993), S. 89-100 
    Details
    ISSN: 0029-5493
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Energy, Environment Protection, Nuclear Power Engineering
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0029-5493(93)90032-5
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Inhibition of monocyte and polymorphonuclear granulocyte immune phagocytosis by monoclonal antibodies specific for FcγRI, II and III (1997)
    Springer
    Annals of hematology 74 (1997), S. 15-22 
    Details
    ISSN: 1432-0584
    Keywords: Key words mAb ; CD64 ; CD32 ; CD16 ; FcγRIIa HR ; FcγRIIa LR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We tested two Fcγ receptor I (FcγRI); six FcγRII; and six FcγRIII-specific monoclonal antibodies (mAb) for their capacitiy to inhibit monocyte and polymorphonuclear granulocyte (PMN) immune phagocytosis which is mediated by FcγR. We used human red blood cells (rbc) coated with hIgG1 or mIgG1 as FcγRI- and FcγRII-specific target cells, respectively. The FcγRI-specific mAbs 22.2 and 32.2 did not inhibit FcγRI- or FcγRII-specific monocyte immune phagocytosis. The FcγRII-specific mAbs IV.3, CIKM5, FLI8.2, FLI 8.26, 2E1, and 41H16 inhibited FcγRII-specific monocyte immune phagocytosis in all FcγRIIa high-responder (HR) individuals but did not inhibit FcγRI-specific phagocytosis. Using PMN, FLI8.2 and 2E1 only partially inhibited phagocytosis in HR individuals, but the FcγRIII-specific mAbs 3G8, DJ130c, MFM-154, B88-9 and MG38 completely inhibited FcγRII-specific phagocytosis if the corresponding antigen was available on the cell surface. In these cases phagocytosis inhibition may be explained by cross-linking of FcγRII and FcγRIII via one antibody molecule, with the Fab portion binding to FcγRIII and the Fc portion binding to FcγRII.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050249
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    The NA"null" phenotype of a young man is caused by an FcγRIIIB gene deficiency while the products of the neighboring FcγRIIA and FcγRIIIA genes are present (1998)
    Springer
    Annals of hematology 76 (1998), S. 215-220 
    Details
    ISSN: 1432-0584
    Keywords: Key words FcγRIIIb deficiency ; NA1/NA2 polymorphism ; NA"null" ; SH antigen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  A 27-year-old man with an allergy to house dust mites was found to lack the FcγRIIIb on his neutrophils. Cell surface marker and PCR techniques were used to investigate possible reasons for this deficiency. Agglutination and immunofluorescence assays using the man's neutrophils together with NA1- and NA2-specific antibodies were negative, and there was no reaction with the FcγRIII-specific mAb 3G8. Indirect immunofluorescence demonstrated the presence of the CD24 molecule, which, like the FcγRIIIb, is anchored to the cell membrane by glycosylphosphatidylinositol. Thus a lack of the FcγRIIIb cell membrane anchor was excluded. PCR analysis confirmed the absence of the NA1 and NA2 alleles. The individual was therefore typed as NA"null". The products of those genes located together with the FcγRIIIB gene within a complex on chromosome 1 (q23–24) were examined. FcγRII was demonstrated on monocytes and B cells with the use of FcγRII-specific monoclonal antibodies. About 5% of the individual's peripheral blood monocytes were positive with the 3G8 antibody, indicating the presence of FcγRIIIa. From these data we concluded that the FcγRIIIb deficiency on the neutrophil cell surface of this individual is due to a lack of the FcγRIIIB gene while excluding a lack of the FcγRIIA and the FcγRIIIA genes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050392
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of ganglioside (Cronassial) treatment on MHC Ia antigen expression and allograft survival of pancreatic islets in diabetic rats (1990)
    Springer
    Diabetologia 33 (1990), S. 112-114 
    Details
    ISSN: 1432-0428
    Keywords: Gangliosides ; islet transplantation ; immunosuppression ; immunomodulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Streptozotocin-diabetic BdII rats were treated daily with 20 mg/kg body weight gangliosides for ten days beginning two days before transplantation. This treatment did not prolong allograft survival of untreated Lewis islets. Culture treatment of isolated Lewis islets with gangliosides (100 μg/ml in RPMI 1640) for one day resulted in a significant reduction of MHC Ia antigen positive cells but not of class I antigens within the islets. Tranplantation of the ganglioside pretreated islets into non-immunosuppressed BdII recipients prolonged allograft survival to 12 days only in one of five animals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401049
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    Paper (German National Licenses)
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  • 7
    Electronic Resource
    Electronic Resource
    Rat pancreatic islet pretreatment with anti-MHC class II monoclonal antibodies and culture: in vitro MLIC test response does not predict islet allograft survival (1993)
    Springer
    Acta diabetologica 30 (1993), S. 49-56 
    Details
    ISSN: 1432-5233
    Keywords: Antibody pretreatment ; Culture pretreatment ; Experimental diabetes ; Islet allotransplantation ; Mixed lymphocyte islet culture (MLIC)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Antigen presenting cells (APC) expressing MHC class II antigens have been attributed with stimulatory capacity for initiating islet allograft rejection (direct pathway). Therefore, we evaluated the effect of pretreating isolated islets with different monoclonal antibodies against MHC class II antigens and complement, with and without culture at 22°C or 37°C, on MHC class II antigen expression, on the allogeneic proliferative response in the mixed lymphocyte islet culture (MLIC) and on islet allograft survival in adult rats. Experiments were performed in two different strain combinations incompatible for MHC class II antigens and either incompatible or compatible for MHC class I antigens, in order to elucidate further the impact of class I antigens on islet allograft rejection. In terms of class II antigen suppression, pretreatment with anti-MHC class II antibodies together with complement and a 5-day (37°C) culture period proved most effective. After this procedure 92.7% of the islets. of LEW rats and 91.1% of the islets of LEW.1WR2 rats were negative for MHC class II antigens, as demonstrated by indirect immunofluorescence. Transfer of successfully pretreated islets to a MLIC in vitro test system provoked a significantly reduced allogeneic T-cell proliferative response in the case of additional MHC class I disparity (ratio 1.3 vs 4.7) and a response as low as that of a syngeneic setting when stimulator islets and allogeneic responder lymphocytes shared MHC class I antigens (ratio 1.0 vs 1.6). However, these encouraging in vitro results could not be confirmed in vivo after intraportal allotransplantation into streptozotocin-induced diabetic rats, neither in a strain combination incompatible for MHC class I antigens nor in a compatible combination. In conclusion, these findings provide evidence that an in vitro MLIC test response has a limited value for predicting in vivo islet allograft survival. In addition, the results are consistent with the notion that even near-total suppression of MHC class II antigens seems insufficient to prolong islet allograft survival; an indirect pathway coexisting in vivo may be involved in the antigen molecule processing and presentation by recipient APCs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00572875
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    Paper (German National Licenses)
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