There is a prevalence of IFN signature in the CD14 monocytes of primary Sjögren’s syndrome patients, she said. These patients also show higher disease activity scores and expression of antibodies like SSA, SSB and IgG, Ms. Maria said. IFN may also induce IDO expression, and increased IDO may result in reduced tryptophan and increased kynurenine. IDO may also suppress effector T-cell function and promote Treg differentiation.
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To find out if IFN-induced IDO results in increased neurotoxicity that causes severe fatigue and depression, “we decided to look locally into the glands of these patients,” said Ms. Maria. “We found nice IDO expression in the glands, as well as MxA, and we had previously identified MxA as a good biomarker for interferon type-1 activity.”
These patients also showed higher levels of KAT neuroprotective enzymes and lower levels of KMO neurotoxic enzymes that are key players in the kynurenine-tryptophan pathway. They also showed upregulated Treg cells. Blocking that pathway may help prevent kynurenine from crossing into the brain and triggering fatigue and depression symptoms in these patients. Recent research suggests that exercise may increase KAT enzymes in muscle tissue, building resilience to stress-induced depression, she said.
Susan Bernstein is a freelance medical journalist based in Atlanta.