摘要:

SUMMARYThe cDNA sequence and serological data for HLA‐B73 are reported. Anti‐B73 sera are found relatively frequently, considering the rarity of the antigen. It was noted early that in some cases the antibodies in sera of multiparous women did not react with the eliciting cells (fathers) and thus all behaved as a naturally occurring antibody. We report on 18 B73 antisera found during the screening of 55000 Danish sera. Only one of the 17 stimulators typed also had the B73 tissue type. Ten of the stimulators had antigens from the B7 CREG (B7, B22, B27, B42, B67, B73), whereas none of the responders had such tissue types. In seven cases the serum was not able to react with the stimulator's lymphocytes in a cytotoxicity assay and in four cases the stimulator lymphocytes could not deplete the anti‐B73 activity from the serum in absorption experiments. The cDNA of B73 was expressed correctly in COS cells and was recognized on the cell surface by a monospecific serum. The α1α2domains of B73 are most similar to those of the HLA‐B22 family. Interestingly, the α3and transmembrane domains of HLA‐B73 are not standard human domains, but are most similar to the corresponding domains of some gorilla and chimpanzee

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1995.tb00237.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

SUMMARYAn Abelson virus‐transformed immature B cell line, AT8‐1‐12‐5‐2, produced truncated μ‐chains. Sequencing analysis of the VHDJHcomplex on the expressed H‐chain allele revealed the deletion of 75 nucleotides that involved leader‐variable region intron and the 5’ end of the variable region, which resulted in the loss of the 3′ splice site of leader‐variable region intron. Sequence studies of a leader‐ and CH1‐containing cDNA clone showed that leader region was directly spliced to the CH1exon, resulting in the production of the truncated μ‐chains without variable portion. Our results demonstrated for the first time that the only loss of the 3′ splice site of leader‐variable region intron could induce an aberrant splicing b

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1995.tb00238.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

SUMMARYNineteen horse MHC class I specificities have been serologically identified previously at a single locus (ELA‐A), and two other specificities appear to be coded at other loci. Biochemical studies indicate that there are at least two expressed loci. In order to establish the number of transcribed horse MHC class I genes, we made a cDNA library from a heterozygous animal (ELA‐A3/A7), and screened for positive clones using a bovine class I probe. More than 200 class I clones were isolated in this way, and so far seven unique full length sequences have been identified. All of the sequences are predicted to code for surface expressed, functional molecules. The number of different sequences identified demonstrate that at least four genes are transcribed, although variations in transmembrane length (which is generally conserved in class I loci) suggest that five genes could be represented. Evolutionary analysis of these sequences (and two additional sequences known to represent different horse class I loci) reveals no firm relationships, such that the division between the different loci cannot be discerned. These results suggest an unusual evolutionary history for the horse MHC, the precise nature of which may be revealed only following further cross‐species compar

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1995.tb00239.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1995.tb00240.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

SUMMARYHuman IgE synthesis requires the presence of both interleukin 4 (IL‐4) and T‐cells. However, it is not clear what role IL‐4 and T‐cells play in the induction of IgE synthesis at the level of gene regulation. B cells that were obtained from patients with a high level of serum IgE and from healthy donors were immortalized by Epstein‐Barr virus. We examined IgE production of these B cells stimulated with IL‐4. Supernatant IgE levels of patient's B cells cultured with or without IL‐4 were higher than those of healthy donor's B cells. Our results indicated that B cells stimulated with IL‐4 from patients produced IgE, germline C ε transcript, and S μ S ε recombination. The germline C e transcript was dose‐dependently induced in the presence of IL‐4 and related to the supernatant IgE level. In B cells stimulated with IL‐4 that were obtained from patients, (some of the) DNA near or within the I e region was (already partly) unmethylated, unlike those from healthy donors, and there was a loss of methyl groups of the DNA upon the addition of IL‐4 in B cells from both patients and normal donors. IgE synthesis of B cells stimulated with IL‐4 in patients with a high level of serum IgE is due to an accessibility in the immunoglobulin heavy‐chain isotype switch, and this may reflect the accessibility in synthesis of germline C ε transcript, which may be caused by the increase of opening chromatin structures because of their

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1995.tb00241.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

SUMMARYThe polymorphism of the LST‐1 gene (the human homologue of the mouse B144 gene) can be identified by Pvu II restriction enzyme digestion. We investigated the contribution of this RFLP to disease susceptibility in 117 patients with type I diabetes mellitus (IDDM), 110 with Graves’ disease (GD) and 93 healthy controls. The distribution of the different LST‐1 alleles (LST‐1*1:1323bp, LST‐1*2:610bp/713) was similar among IDDM and GD patients as well as in controls. The combination of DQA1*0501, DQB1*0201 and DQB1*0301, all predisposing to endocrine autoimmune disease, with LST‐1*1 or LST‐1*2 was not increased in patients. Analysis of two informative families with IDDM demonstrated cosegregation of DQA1 and DQB1 alleles with LST‐1 alleles. No association of LST‐1 polymorphisms with IDDM nor GD coul

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1995.tb00242.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1995.tb00243.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1995.tb00244.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY