The Bruton tyrosine kinase (BTK)/NF-κB pathway plays a critical role in the progression of neuromyelitis optica spectrum disorder (NMOSD), according to a new study published in the European Journal of Medical Research. “Our results shed light on its important role as a therapeutic target for NMOSD,” the authors of the study wrote.

The pathogenesis of NMOSD is still not well understood. However, it is known that BTK and NF-κB are associated with the disease through the changes that take place in different periods.

To elucidate changes that occur in the BTK/NF-κB pathway at different stages of NMOSD, a team of researchers from China analyzed the BTK/NF-κB pathway and related chemokines in the cerebrospinal fluid and peripheral blood samples of 32 patients with NMOSD who were in the acute and remission phases of the disease and 32 healthy volunteers. 

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The results showed that the levels of BTK, NF-κB, PI3K, IKK, CXCL2, and CXCL12 mRNA were all elevated in patients with acute NMOSD compared to levels in the healthy controls.

Moreover, the levels of BTK, NF-κB, IKK, CXCL2, and CXCL12 mRNA were also significantly higher in patients with acute disease compared to those whose disease was in remission. Levels of PI3K were higher in patients whose disease was in remission compared to healthy controls.

Finally, levels of CXCL2 and CXCL12 in the serum of patients with acute disease and disease in remission were significantly higher compared to healthy volunteers.

“BTK, PI3K, IKK, NF-κB, and related inflammatory chemokines CXCL2 and CXCL12 are abnormally activated in the pathogenesis of NMOSD, which can induce B-cell proliferation and differentiation,” the researchers wrote.

NMOSD is a rare type of autoimmune disease that can cause neuritis and blindness. It is characterized by an autoimmune attack against aquaporin-4 channels.


Qiao H, Mao Z, Wang W, et al. Changes in the BTK/NF-κB signaling pathway and related cytokines in different stages of neuromyelitis optica spectrum disorders. Eur J Med Res. 2022;27(1):96. doi:10.1186/s40001-022-00723-x