Upregulated expression of leukocyte immunoglobulin-like receptor A3 in patients with severe aplastic anemia

Exp Ther Med. 2021 Apr;21(4):346. doi: 10.3892/etm.2021.9777. Epub 2021 Feb 11.

Abstract

Severe aplastic anemia (SAA) is a rare and potentially life-threatening disease characterized by pancytopenia and bone marrow (BM) hypoplasia. In a previous study by our group, increased expression of leukocyte immunoglobulin-like receptors A (LILRA), LILRA3 in myeloid dendritic cells (mDCs) and LILRA5 in CD34+ cells in SAA was detected using proteomics techniques, highlighting their potential role in disease pathogenesis. In the present study, the expression of LILRA1-6 mRNA was assessed in the BM mononuclear cells of patients with SAA using reverse transcription-quantitative (RT-q)PCR. The expression of homogenic LILRA3 and LILRA5 isoform on mDCs, as well as CD34+, CD3+CD8+, CD19+ and CD14+ cells, was detected using flow cytometry. mDCs were then induced, cultured and sorted. The expression of LILRA3 was confirmed using RT-qPCR and western blot analyses. The serum levels of soluble LILRA3 were measured using ELISA. Furthermore, the relationship between LILRA3 expression and disease severity was assessed. The results indicated increased LILRA3 mRNA expression in patients with SAA. The percentage of LILRA3+ in BM mDCs and CD34+ cells was increased. Compared with controls, the relative LILRA3 mRNA expression and the relative protein intensity were highly increased in SAA mDCs. The serum LILRA3 levels in patients with SAA were also increased. The proportion of LILRA3+CD11C+ human leukocyte antigen (HLA)-DR+/CD11C+HLA-DR+ cells was positively correlated with the ratio of LILRA3+CD34+/CD34+ cells and the expression of LILRA3 mRNA. Taken together, the expression of LILRA3 on mDCs of patients with SAA was increased, which may affect the function of mDCs. LILRA3 may have a significant role in the immune pathogenesis of SAA.

Keywords: leukocyte immunoglobulin-like receptor A3; myeloid dendritic cells; proteomics; severe aplastic anemia.

Grants and funding

Funding: This work was supported by the National Natural Science Foundation of China (grant nos. 81970116, 81970115, 81870101 and 81500101) and the Tianjin Municipal Natural Science Foundation (grant nos. 18JCYBJC91700 and 18ZXDBSY00140).