J Clin Invest: Study uncovers the pathogenic effects γ intestinal vascular activation mediated by IFN-2000.

Inflammatory bowel disease (IBD) is a chronic inflammatory disease with an increasing incidence.
large number of blood vessels in the lesions tissue, however the pathogenic effects and potential regulatory mechanisms of blood vessels in IBD are not yet known, the results of which have been published online in J Clin Invest.
IFN-γ is the main cytokine in the onset of IBD, but in the context of the disease, it is almost simply its immunomodulation and corted cell-oriented functions that are considered.
recent studies by our team have shown that IFN-γ also has a powerful effect on blood vessels.
these considerations, we analyzed ifN-γ's vascular-directed pathogenicity and found that it drives the onset of IBD by breaking the vascular barrier.
specifically, we have shown that ifN-γ reactions in blood vessels can be inhibited by nepeopenheal knockout of IFN-γ subject 2, which can improve experimentally induced colitis in mice.
IFN-γ can cause disease by destroying the adhesive protein VE-cadherin, causing damage to the vascular barrier.
it is worth noting that intestinal vascular barrier dysfunction has also been confirmed in human IBD patients, supporting the clinical significance of our findings.
use of imatinib therapy can restore VE-cadherin/objectns junctions, inhibit vascular permeability, and significantly reduce colon inflammation of experimental colitis.
, the findings shed light on the pathogenic effects of IFN-γ-mediated intestinal vascular activation in IBD and opened up new avenues for vascular-oriented treatment of the disease.
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