Roles of Reactive Oxygen Species in Rheumatoid Arthritis Pathogenesis
Journal of Rheumatic Diseases
;
: 340-347, 2016.
Artigo
em Inglês
| WPRIM
| ID: wpr-34293
ABSTRACT
Rheumatoid arthritis (RA) is an autoimmune disease that starts with decreased tolerance to modified self-antigens and eventually leads to synovitis and destruction of bone and cartilage. Age is a risk factor for developing RA. Major changes in the immune system come with age due to chronic oxidative stress on the deoxyribonucleic acid (DNA) damage pathway, somatic mutation, modifications of auto-antigens, T cell tolerance and activation of fibroblast-like synoviocytes (FLS). Reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate oxidase 2 (NADPH oxidase 2) suppress T cell receptor signaling. Sirtuin 1 (SIRT1) is a critical immune suppressor of T cell activation and a key regulator of oxidative stress. When oxidative stress reduces activity of SIRT1, the breakdown of tolerance to modified self-antigens is expected. Generation of ROS can be perpetuated by enhanced DNA damage and dysfunctional mitochondria in a feedback loop during the development of RA. Through major T cell loss and selective proliferation of peripheral T cells, pro-inflammatory T cell pools with abnormal features are established in the T cell compartment. Hypoxic and inflammatory condition in synovium perpetuates ROS generation, which leads to the activation of FLS. In both T cell and synovium compartment, oxidative stress reshapes the immune system into the development of pre-clinical RA.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Oxirredutases
/
Artrite Reumatoide
/
Autoantígenos
/
Doenças Autoimunes
/
Membrana Sinovial
/
Sinovite
/
Dano ao DNA
/
DNA
/
Receptores de Antígenos de Linfócitos T
/
Linfócitos T
Tipo de estudo:
Estudo de etiologia
/
Fatores de risco
Idioma:
Inglês
Revista:
Journal of Rheumatic Diseases
Ano de publicação:
2016
Tipo de documento:
Artigo
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