Expression of TLR2 and TLR4 on CD14 Monocytes in Female SLE Patients E

Abstract

Background: Systemic Lupus Erythematous (SLE) is a prototype autoimmune disease of multifactorial origin mainly assigned to defects in the adaptive immune system. However, evidences supported the crucial role of the innate immune system in its pathogenesis. Toll-like receptors (TLRs) have been proposed as important pathways in disease development. This relatively new idea holds promise for new therapeutic strategies. The aim of this work is to measure surface expression of TLR2 and TLR4 on CD14+ monocytes in SLE patients and compare it with healthy controls, also to find out their relation with disease activity and damage. Subjects and methods: The current study was carried out on Forty Egyptian female SLE patients and 20 matched control subjects. Disease activity was assessed by the SLE disease activity index (SLEDAI) and damage assessed by the Systemic Lupus International Collaborating Clinics (SLICC) index. Expression of TLR2 and 4 on CD14+ monocytes was studied using flow cytometry. Results: The age of the patients ranged between 16-56 years with a mean ± SD of 31.6 ± 9.2 years. Significant increase of TLR2 surface expression and a significant decrease of TLR4 surface expression on CD14+ monocytes in SLE patients compared to the control group (p=0.006, 0.004, respectively) were observed. No statistically significant associations were detected with both activity and damage indices. Conclusion: This study suggests that TLR2 and 4 plays a role in the pathogenesis of SLE but have no impact on disease activity.

Decreased toll-like receptor 4 and CD11b/CD18 expression on peripheral monocytes of hypertensive patients correlates with a lesser extent of endothelial damage: a preliminary study

“…Further studies have shown that this negative control of TLR4 surface expression not only appears in microbial infections but may also be a universal mechanism triggered in response to increased inflammation of various etiologies. Reduced expression of TLR4 on peripheral monocytes was observed in autoimmunology diseases, acute pancreatitis, or chronic kidney diseases [56][57][58][59][60]. Krejsek et al [61] observed TLR4 downregulation on monocytes of patients undergoing coronary artery bypass grafting, an invasive procedure associated with activating an inflammatory response.…”

“…Further studies have shown that this negative control of TLR4 surface expression not only appears in microbial infections but may also be a universal mechanism triggered in response to increased inflammation of various etiologies. Reduced expression of TLR4 on peripheral monocytes was observed in autoimmunology diseases, acute pancreatitis, or chronic kidney diseases [56–60]. Krejsek et al .…”