ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1990.tb01749.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Abstract:A panel of monoclonal antibodies to the 69 kDa glycosyl phosphatidylinositol anchored lymphocyte differentiation antigen ecto‐5′‐nucleotidase (ecto‐5′‐NT, CD73) was produced using highly purified human placental 5′‐NT as immunogen. Antibodies 1E9.28.1 and 7G2.2.11 inhibit soluble placental 5′‐NT activity and recognize lymphocyte CD73 in indirect immunofluorescence and immunoprecipitation assays. In addition, 1E9.28.1 induces vigorous T cell proliferation in the presence of submitogenic doses of phorbol myristate and F(ab′): goat anti‐mouse Ig. Both antibodies can be used to purify the three major forms of placental 5′‐NT by affinity chromatography. By two‐color immunofluorescence, CD73 was found to be expressed on 19±5% of CD3+, 11±4% of CD4+, 51±14% of CD8+, 25±8% of CD28+, 15±5% of CD29+, 27±7% of CD45RA+, and 70±6% of CD19+lymphocytes. Within T cells, CD73 expression is restricted to the CD28+subset. Thus, CD73 is found on subsets of both T and B lymphocytes, with the highest expression on B cells and CD8+T cells. In sections of hyperplastic tonsil, CD73 expression is restricted to the small lymphocytes of the follicular mantle zone, a small subset of extrafollicular lymphocytes situated within the epithelium of the tonsillar crypt, and to follicular dendritic cells within the lower part of the “light‐zone.” CD73 is also detected on subsets of endothelial cells of capillaries and venules and the basal layer of non‐keratinizing squamous epithelium and transitional cell type mucosa of many tissues. Given the tissue distribution of CD73, along with its glycosyl phosphatidylinositol membrane anchoring and the observation that some CD73 antibodies are mitogenic, we propose that this interesting antigen may play a role in cell activat

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1990.tb01750.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Abstract:The polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) method, which we previously reported as an efficient and convenient typing technique for accurate definition of the HLA‐DQA1 and ‐DPB1 alleles, is now extended and applied to HLA‐DRB and ‐DQB typing. The second exon of the HLA‐DRB (B1 and B3 or B4) and DQB (B1 and B2) genes was selectively amplified from genomic DNAs of 70 HLA‐homozygous B cell lines by PCR. Amplified DNAs were digested with the restriction endonucleases, which can recognize allelic variations specific for HLA‐DR, ‐DQ, and ‐Dw allospecificities and then subjected to electrophoresis in polyacrylamide gel. Of DRB genes, FokI, HinfI, HhaI, HphI, KpnI and SacII were selected and the 20 different polymorphic patterns of the restriction fragments thus obtained were found to correlate with each HLA‐DR and ‐Dw type defined by serological and cellular typing. Of the DQB genes, FokI, HaellI, HhaI, RsaI and Sau3AI produced nine different polymorphic patterns of the restriction fragments, correlating with the HLA‐DQ and ‐Dw types. This PCR‐RFLP method provides a simple and rapid technique for accurate definition of the HLA‐DR, ‐DQ and ‐Dw types at the nucleotide level, eliminating the need for radioisotope as well as a

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1990.tb01751.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Abstract:HLA Class II polymorphisms were analysed in 27 families with at least one Type I diabetic proband using Southern blotting technique according to 10th Histocompatibility Workshop Standards. The probes used were DRB, DQA1, DQB1 and DOB. We have studied 108 haplotypes and performed segregation analysis with HLA serology and restriction fragment length polymorphism (RFLP) data and compared “affected” with “non‐affected” haplotypes (not inherited by IDDM patients). RFLPs correlated well with DR and DQ serology and detected additional polymorphisms. In particular, DQB polymorphism analysis showed segregation of the DQw3 splits with 88.5% of the DR4 affected haplotypes bearing the DQw3.2 split (now DQw8) and 11.5% the DQw3.1 split (now DQw7) while in the non‐affected DR4 haplotypes 33.3% were DQw3.2 and 66.6% were DQw3.1. Haplotype analysis showed that DR4‐DQw3.2 was in strong linkage with the U fragment (2.1 kb Taq I) of DQA2 (DXa) and with the L fragment (5.4 kb BamH I) of DOB. This study confirms previous observations of DQB polymorphisms in heterozygous IDDM patients, supports the protective effect of DQw3.1 (DQw7) against the development of the disease and demonstrates the importance of DQw3.2 (DQw8) for susceptibility to Ty

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1990.tb01752.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Abstract:It has been shown that Greek RA patients do not show an increased frequency of HLA‐DR4 compared with Greek controls. As only the Dw4 and Dwl4 subtypes of DR4 are implicated in RA, we have characterised DR4‐positive Greek RA patients and controls using serology, MLC typing and RFLP analysis to see whether the distribution of. DR4 subtypes or other HLA antigens associated with DR4 could account for these findings. In the 10 patients and 12 controls studied, Dw10 was common, being present in almost half the controls. Dw4 was not detected in the controls, but was present in three of the RA patients, indicating that there may be some relationship between Dw4 and RA in this population; Dw13 and Dw14 were also found, Dw15 was not detected. Eight of the subjects did not type as any of the HLA‐D antigens mentioned. Three controls had unusual DR4‐DQ associations, two having DR4‐DQw2 and one possessing DR4‐DQw4. Analysis of the TaqI DRB RFLP of the subjects showed that one control did not have the 6.1 kb band characteristic of DR4s. All these results indicate that DR4 is a heterogeneous antigen in this population and that several as yet undescribed variants of DR4 may

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1990.tb01753.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1990.tb01754.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY