摘要:

Abstract:HLA‐B15 embraces a multiplicity of antigenic specificities which vary in their distribution amongst human populations. To correlate B15 molecular structure with the serological picture we have sequenced alleles encoding the various subspecificities of the B15 antigen: B62, B63, B75, B76 and B77, and a number of “variants” of these antigens including the 8w66 split of B63. HLA‐B63 (B*1517) and 8w66 (B*1516) heavy chains have sequence identity to B17 in the α1helix correlating with the antigenic crossreactivity of these molecules. HLA‐B77(B*1513) and B75 (B*1502) heavy chains differ solely in segments determining the Bw4 and Bw6 public epitopes, consistent with the serological description of the B77 and B75 antigens. One allele encoding the B76 antigen (B*1512) appears to be the product of gene conversion between the HLA‐A and ‐B loci and differs from B*1501 in codons 166 and 167. In contrast, a second allele encoding the B76 antigen (B*1514) differs from B*1501 by an unrelated substitution in codon 167 which confers similarily with B45, an antigen crossreactive with B76. A third allele encoding B76. B*1519, differs from B*1512 by a unique point substitution in exon 4. Three alleles encoding variant B15 and B62 antigens (B*1508, B*1511 and B*1515) differ from B*1501 by localized clusters of substitutions that probably result from interallelic conversion. The B15 sequences described in this paper, in combination with those previously determined, define a family of 22 alleles, including those encoding the B46 and B70 antigens. Within this family the patterns of allelic substitution are analogous to those of other HLA‐A and ‐B families, in that pairwise differences almost always involve functional positions of the antigen recognition site and recombination is the major agent

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1994.tb02327.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Abstract:Oral erosive lichen planus is a distinct subtype of the common dermatosis lichen planus. Although the etiology of lichen planus is still obscure, it is known that cell‐mediated immune mechanisms and genetic factors underlie its pathogenesis. Previous studies have found an association between lichen planus and HLA‐DR3 or DR9 in different population groups. The present work was designed to elucidate, at the serologic and molecular levels, whether and which HLA genes are associated with oral erosive lichen planus in Israeli Jewish patients. A significant association with HLA‐DR2 (RR = 4.7; pc<0.0013) and a decrease in DR4 (RR = 0.3; p<0.03) among the patients were noted. Oligotyping of DR2 alleles showed the presence of all three common variants (DRB1*1501, DRB1*1502 and DRB1*1601) in the patients, although none of the variants was overrepresented significantly. Three possible explanations for the role of HLA genes in the predisposition to oral erosive lichen planus are discussed. The most attractive theory for the pathogenesis of the disease seems to include the involvement of non‐classical HL

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1994.tb02328.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1994.tb02329.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Abstract:Analysis of the reaction patterns of 57 putative class II MHC alloantisera revealed 18 B‐cell serum clusters, named Ds01–Ds18. These clusters were grouped together in such a manner that 17 provisional serological class II haplotypes were defined. Segregation in half‐sib families of these class II haplotypes with serologically defined class I and ID‐IEF defined DRB3 types indicated that the 18 clusters identify class II polymorphisms in cattle and can be considered as local specif

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1994.tb02330.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Abstract:Previous HLA serological studies showed positive associations of the DR52 antigen, the DR52‐associated antigens (DR3, DR5 and DR6) and the DR8 antigen with sarcoidosis. To investigate the HLA alleles that may contribute to the genetic susceptibility to sarcoidosis at the DNA level, HLA‐DRB1, ‐DRB3, ‐DQA1 and DQB1 genotyping using the polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) method was performed in 63 Japanese patients with sarcoidosis. The frequencies of the DR52‐associated DRB1 alleles (DRB1*11, DRB1*12 and DRB1*14 except DRB1*1302), DRB1*08, DRB3*0101, DQA1*0501 and DQB1*0301 were significantly increased in patients compared with healthy controls. The significant increase of DRB3*0101, DQA1*0501 and DQB1*0301 could be explained by linkage disequilibrium with the DR52‐associated DRB1 alleles. It must be noted that the DR8 haplotype, which does not possess the DRB3 gene, also showed a significant increase in sarcoidosis. These results suggest that the HLA‐alleles responsible for the susceptibility to sarcoidosis are located at the HLA‐DRB1 locus rather than the HLA‐DRB3, ‐DQA1 and ‐DQB1 loci. In contrast, DRB1*1302 may confer

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1994.tb02331.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Abstract:The protocols represented in this report can resolve all 22 DQB1 alleles. The second exon of DQB1 was subjected to PCR using two group‐specific primers to obtain DQB1 group 1 (DQ5 and DQ6) and group 2 (DQ2, DQ3, DQ4) specific amplified products, respectively. Three endo‐nucleases, Apal, BssHII and Ncil, can provide typing of DQ5 and DQ6 based on easy‐to‐read uncleaved, cleaved and a combination of uncleaved/cleaved patterns. Similarly, two endonucleases, FokI and BgII can define the specificities DQ2, DQ3 and DQ4. Moreover, all 13 group 1 DQB1 alleles and all but one of their 78 possible heterozygotes can be unambiguously resolved using an extended panel of 10 endonucleases. The remaining pair of heterozygotes, DQB1*05031/0603 and 05032/0608, can however be resolved by double digestion with BsmFI and SfaNI. RsaI splits the previously unresolved alleles DQB1*0602 and 0603 in the amplified products of the modified primer SDQ‐01. Fnu4HI can resolve DQB1*0606 from 0605. DQB1*0603, 0607 and 0608 can be resolved by SfaNI and the new endonuclease BsmFI. The comprehensive typing of group 2 DQB1 alleles can be achieved using five endonucleases. All 9 group 2 DQB1 alleles and all but one pair (DQB1*0301/0302 from DQB1*03032/0304) of 36 possible heterozygotes can be resolved. Thus, PCR‐RFLP remains a simple, inexpensive and reliable method for DQB1 typing. The PCR‐RFLP can be used for comprehensive DQB1 typing either independently or to complement the PCR‐SSP and P

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1994.tb02332.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1994.tb02333.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1994.tb02334.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1994.tb02335.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

ISSN:0001-2815    

DOI:10.1111/j.1399-0039.1994.tb02336.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY