摘要:

SUMMARYFemale SJL/J mice are more susceptible to development of experimental autoimmune myositis than most other mouse strains. Since complement has been implicated in the pathogenesis of inflammatory muscle disease in humans, quantitative and qualitative studies of complement C3 were undertaken in SJL/J and BALB/c mice to determine whether complement may influence disease susceptibility in SJL/J mice. In accordance with previous studies, mature male and female BALB/c mice were shown to have similar serum C3 concentrations. However, differences were found between mature male and female SJL/J mice. Male SJL/J mice have significantly higher serum C3 concentrations than SJL/J females and both sexes of BALB/c mice suggesting that serum C3 concentration may be variably influenced by sex in some mouse strains. Qualitatively, SJL/J mice were shown to have a different allotypic form of C3 (C3F) compared to the common electrophoretically slow form (C3S) found in BALB/c mice and most other mouse strains. Furthermore, studies on the decay rate of C3 revealed that C3b/iC3b fragments are converted to C3c/d at a faster rate in sera from female SJL/J mice compared to female BALB/c mice. Because removal and solubility of immune complexes is influenced by complement C3, it is possible that the more rapid decay of the phagocytic ligands C3b/iC3b may account for the increased susceptibility to development of autoimmune disease in female SJL/J mice.

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1993.tb00090.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARYDeficiency of complement component C4 is considered playing a role in the genetic predisposition for systemic lupus erythematosus (SLE). The purpose of this study was to characterize the genomic alterations of the C4 and CYP21 genes in 40 caucasoid patients with SLE by C4 allotyping and by RFLP analysis. Nineteen patients (47.5%) carried C4A null alleles and eight patients (20.0%) C4B null alleles. SLE patients had more frequent C4A null alleles (47.5%) than healthy individuals (20%) (X2= 10.75;P<0.005). The commonest molecular alteration in the patients with C4A null alleles was a large gene deletion affecting both C4A and CYP21A genes. However, among the patients with C4A null alleles, 16.7% persons had no detectable C4A deletion. The non‐expression of C4A gene might be due to defects at various levels of gene expression (i.e. transcription and translation).Among the patients with C4B null alleles, 62.5% persons had no detectable gene lesion, whereas 37.5% showed a C4B deletion including both C4B/CYP21A or C4B/CYP21B genes.Duplication of the C4B gene was not rare in SLE patients, as we found 15.0% of the patients with a heterozygous C4B/CY21A gene duplication. The patients typed as having C4B gene homoduplication (B1,1) demonstrated two long C4B loci, whereas heteroduplication (B1,2) displayed two short loci, therefore the type of C4B gene duplication may be related to the gene length.In conclusion, C4 deficiencies observed in 26 of the 40 SLE patients studied were very heterogeneous. In every case, the gene alteration affected both C4 and CYP21 gene

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1993.tb00091.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARYRecognition sites of two monoclonal antibodies (mAbs), 1B7 and 1E4, specific for murine MHC class II were determined, using eleven L cell transfectants which express recombinant class II (I‐A) molecules. 1B7 positive cells possessed a haplotypekin the α‐helix of the β‐chain, whereas 1E4 positive cells had haplotypebat the α‐helix of the β‐chain. The α‐helix of the β‐chains is regarded as an important site for antigen binding. Thus, the 1B7 and 1E4 mAbs may be useful for analysis of functional sites on class II molecules involved in

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1993.tb00092.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARYThe HLA Class I sequences included in this compilation are taken from publications listed in the papers: Nomenclature for factors of the HLA system, 1991 (Bodmer et al., 1992), Nomenclature for factors of the HLA system, 1990 (Bodmeret al., 1991) and factors of the HLA system, 1989 (Bodmeret al., 1990). Due to the increased number of sequences we have only included sequences for exons 2, 3, and 4 in this compilation. Where discrepancies have arisen between reported sequences, the original authors have been contacted where possible, and necessary amendments to published sequences have been incorporated into this alignment. Future sequencing may identify errors in this list and we would welcome any evidence that helps to maintain the accuracy of this compilation. In the sequence alignments, identity between nucleotides is indicated by a hyphen (‐). An unavailable sequence is indicated by a period (.). Gaps in the sequence are inserted to maintain the alignment between different alleles showing variation in amino acid numbe

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1993.tb00093.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARYThe HLA Class II sequences included in this compilation are taken from publications listed in the papers: Nomenclature for factors of the HLA system, 1991 (Bodmeret al., 1992), Nomenclature for factors of the HLA system, 1990 (Bodmeret al., 1991) and Nomenclature for factors of the HLA system, 1989 (Bodmeret al., 1990). Where discrepancies have arisen between reported sequences, the original authors have been contacted where possible, and necessary amendments to published sequences have been incorporated into this alignment. Future sequencing may identify errors in this list and we would welcome any evidence that helps to maintain the accuracy of this compilation. In the sequence alignments, identity between residues is indicated by a hyphen (‐). An unavailable sequence is indicated by an asterisk (*). Gaps in the sequence are inserted to maintain the alignment between different alleles showing variation in amino acid numbe

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1993.tb00094.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:1744-3121    

DOI:10.1111/j.1744-313X.1993.tb00095.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY