Treatment with interferon-beta (IFN-β) reduces the inflammatory response in immune cells from Sjögren’s syndrome patients, a study reports.
The findings suggest that treatment with IFN-β may be a potential way of controlling inflammation in Sjögren’s patients.
The study, “Interferon‑β inhibits infammatory responses mediators via suppression of iNOS signaling pathway in PBMCs from patients with primary Sjögren’s syndrome,” was published in the journal Inflammopharmacology.
Several cell subsets of the immune system have been associated with primary Sjögren’s syndrome (where the disease is not a consequence of other autoimmune disorders), including T- and B-cells, macrophages, dendritic cells, and tissue-resident cells.
All of these cells can contribute to chronic inflammation through the release of pro-inflammatory cytokines — messenger mediators of inflammation — but also through the production of nitric oxide (NO).
NO is a highly reactive molecule that can be produced by cells to perform signaling roles, particularly to control vessel dilation and immune responses. One of its major roles is to work as a toxic agent to help the immune system kill parasites and bacteria.
Sjögren’s patients, though, seem to have an imbalance in nitric oxide, which appears to be involved in the onset and continuation of chronic inflammation and its associated lesions.
In fact, an excess of nitric oxide is thought to be a possibly important event in the development of other autoimmune and inflammatory diseases, including rheumatoid arthritis.
In this study, researchers investigated if treatment with human interferon β-1a (IFN-β) might control NO production in immune cells of Sjögren’s patients and prevent inflammation.
IFN-β is a cytokine produced by many cell types in response to environmental threats, and also plays important roles in cancer and autoimmune disorders. Therapy with IFN-β is already approved in the U.S and Europe for relapsing forms of multiple sclerosis, an autoimmune disease, under the brand names Rebif, Avonex, and Plegridy, among others.
Researchers compared the impact of IFN-β treatment on blood immune cells – peripheral blood mononuclear cells (PBMCs) consisting on lymphocytes, monocytes, and dendritic cells – from 41 primary Sjögren’s patients and 21 healthy controls.
As expected, immune cells from Sjögren’s patients produced greater amounts of NO and pro-inflammatory cytokines than did immune cells from controls.
But IFN-β significantly reduced the secretion of NO and pro-inflammatory cytokines (TNF-α and IL-6) in patients’ cells, lowering their levels closer to those of healthy individuals.
The anti-inflammatory effect of IFN-β was accompanied by a decrease in the expression of an enzyme called inducible nitric oxide synthase, which is responsible for the production of NO inside cells.
This result suggests that IFN-β is able to reduce nitric oxide production, likely through inhibition of nitric oxide synthase expression.
Interestingly, the strongest effect of IFN-β was observed in patients with neurological lesions (neuropathies), compared to patients with other clinical manifestations (articular involvement, Raynaud’s phenomenon, vasculitis plus purpura, and hypergammaglobulinemia).
“Our findings highlight a consistent ex vivo inhibitory effect of IFN-β on pro-inflammatory cytokine production and NO pathway in pSS patients,” the researchers wrote.
“Our data suggest that IFN-β could represent a potential candidate for targeting inflammation during pSS,” they concluded.
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