Molecular mechanisms regulating immune responses in thromboangiitis obliterans: A comprehensive review

Abstract

Thromboangiitis obliterans (TAO) is a thrombotic-occlusive as well as an inflammatory peripheral vascular disease with unknown etiology. Recent evidence has supported the immunopathogenesis of the disease, however, the factors contributing to the altered immune function and vascular tissue inflammation are still unclear. This review was intended to collate the more current knowledge on the regulatory molecules involved in TAO from an immunoreactive perspective. The homeostasis of the immune system as well as a variety of progenitor cell populations appear to be affected during TAO and these alterations are associated with intrinsic signaling defects that are directing to an improved understanding of the crosstalk between angiogenesis and the immune system, as well as the potential of new co-targeting strategies applying both immunotherapy and angiogenic therapy.

Keywords: Angiogenesis; Immune system; Molecular biology; Signal pathways; Thromboangiitis obliterans.

Figure 1

Oxidative stress through the stimulation of the endothelial NF-ĸB--iNOS--NO pathway and upregulation of homocysteine; eNOS: endothelial nitric oxide synthase, iNOS: inducible nitric oxide synthase, NADPH: nicotinamide adenine dinucleotide phosphate, NF-κB: nuclear factor kappa B, NO: nitric oxide, ROS: reactive oxygen species

Figure 2

Schematic presentation of COX inflammatory pathway; COX: cyclooxygenase,CRF: corticotrophin-releasing factor, ICAM-1: intercellular adhesion molecule-1, PG: prostaglandin