Expression of "non-classical" MHC molecules in bronchial asthma and atopic dermatitis

Currently, bronchial asthma (BA) and atopic dermatitis (AD) are among the most common allergic diseases. According to available data, the worldwide incidence of bronchial asthma is about 260 million people. Prevalence of BA in adult population is 6.9%, and about 10% among children and adolescents. AD occurs in approximately 10-30% of children and 2-10% of adults in developed countries. Every year, a steady increase in AD and BA incidence is noted, but the pathogenesis of these diseases remains poorly known. Recently, the research is being devoted to the studies of interactions between the immune cells and molecules of the major histocompatibility complex (MHC, human leukocyte antigens, HLA), especially, to “non-classical” HLA. HLA-E are among the less studied antigens. Its gene is located in the short arm of chromosome 6 between the HLA-A and HLA-C genes. HLA-E transcription is found in almost all cell types. HLA-E expression is predominantly present on the surface of lymphoid cells (T and B lymphocytes, monocytes and macrophages), to greater extent, and, to lesser degree, on the surface of endothelial cells. Currently, the role of HLA-E in allergic disorders has not been described in the literature. Therefore, it seems relevant to study the role of HLA-E in allergic diseases, in particular, in bronchial asthma and AD. The biological material for this study were PBMCs taken from the patients with bronchial asthma (n = 19), AD (n = 7) and healthy donors (n = 16). We have found that the proportion of T helper cells carrying surface HLA-E was decreased in allergic disorders when compared to healthy donors. At the same time, the level of HLA-E expression in patients with atopic dermatitis was significantly lower than in patients with bronchial asthma. The level of HLA-E expression on CD14⁺ and CD8⁺T cells was significantly lower in patients of the AD group compared to the donor group, whereas no statistically significant differences were observed between the AD group and the donor group. Thus, the level of HLA-E expression on immunocompetent cells differed between the group of donors and the patients with Th2 diseases. A significantly decreased expression of this molecule on immunocompetent cells of the patients with bronchial asthma may suggest a possible role of this molecule in pathogenesis of this disease.