Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown aetiology. The results of experimental studies point to the involvement of innate immunity receptors—toll-like receptors (TLR)—in the pathogenesis of the disease. The aim of the study was to assess the expression of TLR3, 7, and 9 in the population of peripheral blood mononuclear cells (PBMC) and in B lymphocytes (CD19+), T lymphocytes (CD4+ and CD8+) using flow cytometry. The study group included 35 patients with SLE and 15 healthy controls. The patient group presented a significantly higher percentage of TLR3- and TLR9-positive cells among all PBMCs and their subpopulations (CD3+, CD4+, CD8+, and CD19+ lymphocytes) as well as TLR7 in CD19+ B-lymphocytes, compared to the control group. There was no correlation between the expression of all studied TLRs and the disease activity according to the SLAM scale, and the degree of organ damage according to the SLICC/ACR Damage Index. However, a correlation was observed between the percentage of various TLR-positive cells and some clinical (joint lesions) and laboratory (lymphopenia, hypogammaglobulinemia, anaemia, and higher ESR) features and menopause in women. The results of the study suggest that TLR3, 7, and 9 play a role in the pathogenesis of SLE and have an impact on organ involvement in SLE.
Highlights
Systemic lupus erythematosus (SLE) is an autoimmune disease of connective tissue involving multiple organs
Higher percentages of TLR3- and TLR9positive peripheral blood mononuclear cells (PBMC) and CD3+ T lymphocytes, including those positive for CD4 and CD8 antigens, as well as CD19+ B lymphocytes were observed among patients with SLE, compared to healthy controls (Figures 2 and 3)
A higher percentage of CD19+ B lymphocytes expressing TLR7 was found in patients with SLE than in healthy subjects (P < 0.006) (Figure 4)
Summary
Systemic lupus erythematosus (SLE) is an autoimmune disease of connective tissue involving multiple organs. Recent studies have shown that abnormal stimulation of innate immunity may have a great influence on the immunopathogenesis of SLE. The receptors for Pathogen-Associated Molecular Patterns (PAMPs) have been the source of much recent attention. One of the representatives of this group is toll-like receptors (TLRs). They are associated with innate immunity insofar as they are agents in the pathogenesis of SLE and lupus-like syndromes [2]. TLR3, TLR7, and TLR9 seem to be involved in the development of autoimmune diseases [4]. These receptors are located in the membrane of endosomes. The ligation of a TLR activates a chain of proteins which transmit a signal to the nucleus, which in turn leads to increased
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