Investigating the effect of native-LDL and oxidized-LDL on peripheral T cell-mediated immune responses in patients with stable angina pectoris

Abstract

Oxidized and native low-density lipoproteins (ox-LDL, n-LDL) are instrumental factors in atherogenesis; however, their effect on immunoregulation in stable stages of coronary syndrome is still unclear. CD4+CD25+FoxP3+ regulatory T (Treg) cells and Th17 cells, a new subset of T-helper cells, play an important role in peripheral immunity. Their imbalance leads to the development of tissue inflammation and autoimmune diseases. Few studies have explored the effect of ox-LDL and n-LDL on altering the balance between T-reg and Th17 cells. In order to increase our understanding about the regulatory mechanism underlying Th17/T-reg cells, we examined the frequencies of T-reg cells with its relevant secreted cytokine interleukin-10. We measured also the levels of interleukin-6 known to act as an inducer signal for Th17 responses, and interleukin-17 levels the signature cytokine of Th17 cells from peripheral blood mononuclear cells (PBMCs) of patients with stable angina (SA) and normal coronary artery (NCA) groups. The addition of ox-LDL and n-LDL on both patients and control cells lead to an anergy or hyporesponsivness effect in T-regulatory and Th17 responses. We suggest that this effect of peripheral cellular tolerance would be altered under the influence of a definite cytokine milieu that can shift the immune system dramatically to an inflammatory or even to an anti-inflammatory response depending on the cytokines nature and lipoproteins concentration that can exist in the cell culture media.