Itaconic acid, a mitochondrial immune metabolite, is known to suppress inflammatory and oxidative stress responses. In this study, the authors showed that a derivative of itaconic acid, 4-octyl itaconate, significantly reduced murine lupus through modulation of the JAK/STAT pathways. This opens the possibility of further exploring itaconate-derived agents for lupus therapeutics.

What is exciting about this article?

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder associated with severe morbidity and mortality. The first line of treatment to control systemic inflammation in SLE is immunosuppressive drugs and immunomodulators. Finding a novel drug that has minimal side effects is of critical importance in the treatment of this disease. This study showed that therapeutic use of an itaconic acid derivative improved disease outcomes in mice with established lupus, paving the way for a potential treatment strategy for SLE and other autoimmune diseases.

How does this fit into the larger NIAMS portfolio?

The focus of this study is to describe potential mechanisms of immune dysregulation and identify novel therapeutic targets to prevent premature vascular damage in systemic autoimmune diseases like SLE. The study findings provide evidence that itaconate-derived therapeutics may have an important role in autoimmune disorders.

Grant support


Research Areas:

Autoimmunity Cell Biology Immunology Molecular Biology and Biochemistry


Modulation of the Itaconate Pathway Attenuates Murine Lupus.

Blanco LP, Patino-Martinez E, Nakabo S, Zhang M, Pedersen HL, Wang X, Carmona-Rivera C, Claybaugh D, Yu ZX, Desta E, Kaplan MJ
Arthritis Rheumatol.
2022 Dec;
doi: 10.1002/art.42284
PMID: 35791960

Research reported in this publication was supported by the Intramural Research Program of the NIHʼs National Institute of Arthritis and Musculoskeletal and Skin Diseases.