Suppressed immune status facilitates immune escape mechanisms that allow chronic lymphocytic leukemia cells to proliferate and expand. The expression of HLA-G could effectively inhibit the immune response. In immune response inhibitory signals follow activation of immune system which might be occur during bacterial or viral infection in CLL patients. In the current study we characterized two components of immune system, inhibitory molecule HLA-G with its receptor - CD85j and Toll-like receptor 9. The material was obtained from 41 CLL patients and 41 HV with similar median age. In CLL patients expression of intracellular and surface HLA-G and soluble HLA-G levels were significantly higher than in HV. We found higher expression of CD85j compared to HV and the positive correlation between expression of HLA-G and CD85j. All the CLL cells expressed TLR-9, and the level of expression positively correlated with expression of HLA-G and CD85j. Patients with higher expression of intracellular expression of TLR-9 have significantly longer treatment-free survival than patients with low expression of TLR-9 (57 months vs. 8 months, respectively). Summarizing in CLL we characterized activatory and inhibitory components of immune system that might be connected functionally. Analysis of TLR-9 expression might have additional prognostic value for CLL patients.
Keywords: CLL; CpG ODN; CpG oligodeoxynucleotides; DC; ELISA; FBS; HV; IL; MFI; MHC; Mean Fluorescence Intensity; NK; PAMPs; PBMC; PBS; TFS; TLR-9; TLRs; TNF; Toll-like receptor 9; Toll-like receptors; Treg; chronic lymphocytic leukemia; dendritic cells; enzyme-linked immunosorbent assay; fetal bovine serum; healthy volunteers; interleukin; major histocompatibility complex; natural killer cells; pathogen-associated molecular patterns; peripheral blood mononuclear cells; phosphate buffered saline; regulatory T cells; sHLA-G; soluble HLA-G; treatment-free survival; tumor necrosis factor.
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