Аннотация:Abstracts of the 34th FEBS Congress
Abstract
BACKGROUND: The PDCD1 gene encodes the PD-1 protein, which is involved in the immunomodulation. The PD-1.3 polymorphism of the PDCD1 gene is previously shown to be associated with several autoimmune inflammatory disorders including systemic lupus erythematosus and multiple sclerosis. The aim of our study was to assess an effect of PD-1.3 in another inflammatory disorder with strong immune component in its pathogenesis, atopic bronchial asthma (BA).
METHODS: A group of 232 asthma patients (BA+ group) and 189 control subjects (BA- group) of Russian origin was collected . BA+ group was divided into subgroups of 117 moderate/severe asthma (SA) and 115 mild asthma (MA) patients according to Global Initiative for Asthma (GINA) criteria. PD-1.3 polymorphism was typed as previously described (Prokunina et al., 2002).
RESULTS: No significant difference in allele and genotype frequencies is found between BA+ and BA- groups as well as between two subgroups with mild (MA) and moderate/severe (SA) asthma. AG and AA genotypes were pooled together because genotype AA was found in only one asthma patient. AG+AA genotypes are correlated with lower concentrations of total serum IgE (313± 79.4 kU/L vs. 649± 65.3, p=0.010) and IL-4 (33.5± 10.7 vs. 111.5± 16.6 pkg/ml, p=0.015) as compared to wild type (GG) in asthma patients.
CONCLUSION: We found for the first time significant association of PD-1.3 polymorphism with main biochemical markers of atopic bronchial asthma - total serum IgE and IL-4, in a case-control study of 421 Russians. Our findings are consistent with hypothesis of general role of PDCD1 gene polymorphisms in susceptibility to diseases with immune inflammation.
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