Systemic lupus erythematosus (SLE) is an autoimmune disease in which the body mistakenly attacks healthy tissue.
The condition makes the body’s immune system malfunction and begins assaulting various organs, particularly the skin and kidneys. The underlying reasons for lupus are obscure, yet contaminations are thought to play a role.
A previous study suggested that immune cells called CD8 T cells, which generally help destroy threats to the body such as viruses, appear to malfunction in SLE patients.
A new study by the Imperial College London has shed light on how these CD8 T cells malfunction.
Scientists observed immune cells from both healthy individuals and lupus patients. They found that these T cells have certain genes switched ‘on’ by specific immune proteins, called type I interferons- that are generally present during viral infections.
In any case, in lupus patients, the interferons actuate genes in the CD8 T cells that modify how the cells make their energy endure. As an aftereffect of these progressions, the cells die without any problem.
Professor Marina Botto, lead author and Head of the Department of Immunology and Inflammation at Imperial, explained: “The type I interferons are known to be produced by the body during virus infections. Although the initial trigger for lupus remains unknown, the condition could be sustained by viral infections that trigger an expansion of the CD8 T cells. Here we show that the type I interferons cause the cellular power stations, called mitochondria, to malfunction. This malfunction of the mitochondria reduces the lifespan of the CD8 T cells and may fuel the disease.”
- Journal Reference:
- Buang, N., Tang, L., Gray, V. et al. Type I interferons affect the metabolic fitness of CD8+ T cells from patients with systemic lupus erythematosus. Nat Commun 12, 1980 (2021). DOI: 10.1038/s41467-021-22312-y