Pneumocystis pneumonia in an HIV-negative patient with no overt risk factors on presentation.

individuals are genetically predisposed to over-express HLA-G in response to specific signals. Once secreted, HLA-G could promote a cascade of events that result in worsening inflammation. Several polymorphisms in the promoter region of HLA-G coincide with transcription factor binding sites could account for inter-individual differences in expression of HLA-G [10]. We previously identified a polymorphism in the 3’ untranslated region of HLA-G which disrupts a microRNA target site and demonstrated allele-specific expression of HLA-G in the presence of microRNAs that bind to that target [5]. Therefore, either lack of suppression or over-expression of HLA-G could explain the association we report here with asthma. We note that the small numbers of subjects in this study precludes more detailed analysis of relationships between genetic variation and HLA-G expression. Futuremore, larger studies are required to clarify the potential modulating role of HLA-G on the clinical manifestations of asthma and the role of genetic variation on expression levels.