Antilymphocytic antibodies in mixed connective tissue disease

✍ Scribed by Efraín Díaz-Jouane; Donato Alarcó-Segovia

• Publisher: John Wiley and Sons
• Year: 1983
• Tongue: English
• Weight: 118 KB
• Volume: 26
• Category: Article
• ISSN: 0004-3591
• DOI: 10.1002/art.1780261223

✦ Synopsis

alleles may actually operate against its formation. Alternatively, it is possible that immune response genes which promote antibodies to nRNP may not be represented on DRZlMBl/MTl and DR3/MT2 bearing haplotypes. Thus, the presence of both sets of alleles, as seen in our patients, might exclude this antibody response.

The actual genes primarily responsible for these HLA-autoantibody associations, whether DR, MB/MT, or closely linked loci, have not yet been defined, and it remains unclear why differences in HLA-SLE and HLA-autoantibody correlations have been reported in other series (1-5). Moreover, it is possible that several major histocompatibility complex loci and/or alleles are acting in concert. Regardless, the inconsistent segregation of HLA haplotypes with SLE, other autoimmune diseases, and serologic abnormalities in multiplex families implies that other non-HLA-linked genes are also necessary for the development of SLE (9,lO). Thus, HLA may act only as a modifier of other "immunoregulatory" genes, perhaps via the promotion of certain autoantibody responses which in turn produce the lesions clinically characteristic of SLE.