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ATAs also known as anti-Scl-70 antibodies ; in a scleroderma patient is very strongly associated with the risk of development of pulmonary fibrosis relative risk 17 ; [83, 84]. In addition, ATA positivity was strongly associated with carriage of HLA-DRB1 * 11 alleles previously included as part of HLADR5 ; , i.e. 39 of 54 72% ; patients who tested positive for ATA carried these alleles versus , 18% carriership in controls p50.00006 ; [84]. Within HLA-DRB1 * 11, the allelic subtype * 1104 seems to be associated with ATA positivity and the presence of lung fibrosis [85]. GILCHRIST et al. [84] also showed that HLA DPB1 * 1301 was tightly associated with ATA presence. As the early phases of pathogenesis of systemic sclerosis are thought to involve a T-cell-mediated response to an antigenic trigger, possibly epitopes of DNA topoisomerase I, resulting in the production of antibodies directed against this enzyme ATA ; , the described HLA associations focus on the major histocompatibility complex MHC ; region on chromosome 6 for the identification of predisposing genetic factors for this disease. The contribution of genetic factors is further supported by the observation of familial clustering of the disease, the high frequency of autoimmune disorders and autoantibodies in family members of patients with systemic sclerosis, and differences in prevalence and clinical manifestations among different ethnic groups [82, 86, 87]. Besides MHC-based genes i.e. HLA genes and pro-inflammatory genes, such as TNF ; , non-MHC based genes encoding pro- anti-inflammatory cytokines and chemokines, and genes involved in fibroblast and endothelial cell functioning are also important candidates for a role in the genetics underlying systemic sclerosis. The genes and gene polymorphisms that have been evaluated to date in diffuse systemic sclerosis, i.e. systemic sclerosis associated with pulmonary fibrosis, are discussed below and summarised in table 2. Major histocompatibility complex Strong associations have been found between HLA-DRB1 * 11, and also HLA-DPB1 * 1301, and diffuse systemic sclerosis, and there is some evidence to suggest that it is an amino-acid motif, shared by the different class II susceptibility alleles, that may be pivotal in predisposing to autoantibody formation [84, 85]. However, the MHC region contains multiple extended haplotypes, and, therefore, HLA associations might also point to another nearby gene on chromosome 6p21 that is causally involved in systemic sclerosis. The known linkage disequilibrium between the TNF locus and HLA class II genes has led to studies to define complex haplotypes in that region. SATO et al. [88] have fine mapped across the TNF locus in scleroderma subsets and found an association between the potentially functional TNF -857C.T polymorphism and lung fibrosis. Intergenic haplotype construction revealed, however, that this was fully explained by linkage disequilibrium with HLA-DRB * 11. Remarkably, they found that another TNF allele, TNF -863A, was very strongly associated with positivity for anticentromere antibodies and therefore ``protective'' against pulmonary fibrosis [88]. This polymorphism has proven functionality, i.e. the TNF -863A allele is associated with high TNF-a production in vitro [94]. 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Gestation. These results are shown in Fig. 3. The mRNA content for all three SPs was low or undetectable at 99100 days gestation and increased progressively after 120 days gestation to term 145150 days gestation ; , with an apparent postnatal increase for SP-A. SP-C mRNA content appeared to increase somewhat faster than that for SP-A or SP-B. Human -actin mRNA did not vary with development, and normalization of the data with -actin yielded similar results data not shown.

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