Neutrophils and redox stress in the pathogenesis of autoimmune disease

Glennon-Alty, Laurence ORCID: 0000-0002-6416-0711, Hackett, Angela P, Chapman, Elinor A ORCID: 0000-0002-4398-1705 and Wright, Helen L ORCID: 0000-0003-0442-3134
(2018) Neutrophils and redox stress in the pathogenesis of autoimmune disease. FREE RADICAL BIOLOGY AND MEDICINE, 125. pp. 25-35.

[thumbnail of Redox-review-Wright-accepted.docx] Text
Redox-review-Wright-accepted.docx - Author Accepted Manuscript

Download (626kB)


Polymorphonuclear leukocytes, or neutrophils, are specialist phagocytic cells of the innate immune system. Their primary role is host defence against micro-organisms, which they kill via phagocytosis, followed by release of reactive oxygen species (ROS) and proteolytic enzymes within the phagosome. ROS are generated via the action of the NADPH oxidase (also known as NOX2), in a process termed the 'Respiratory Burst'. This process consumes large amounts of oxygen, which is converted into the highly-reactive superoxide radical O<sub>2</sub><sup>-</sup> and H<sub>2</sub>O<sub>2</sub>. Subsequent activation of myeloperoxidase (MPO) generates secondary oxidants and chloroamines that are highly microbiocidal in nature, which together with proteases such as elastase and gelatinase provide a toxic intra-phagosomal environment able to kill a broad range of micro-organisms. However, under certain circumstances such as during an auto-immune response, neutrophils can be triggered to release ROS and proteases extracellularly causing damage to host tissues, modification of host proteins, lipids and DNA and dysregulation of oxidative homeostasis. This review describes the range of ROS species produced by human neutrophils with a focus on the implications of neutrophil redox products in autoimmune inflammation.

Item Type: Article
Uncontrolled Keywords: Neutrophil, ROS, Redox, Auto-immune, Rheumatoid arthritis, Systemic Lupus Erythematosus, Vasculitis, Behcets disease, Psoriasis, Multiple sclerosis
Depositing User: Symplectic Admin
Date Deposited: 06 Apr 2018 15:24
Last Modified: 19 Jan 2023 06:36
DOI: 10.1016/j.freeradbiomed.2018.03.049
Related URLs: