A similar pattern was observed when assessing tight junctional integrity: while occludin, claudin-5 and ZO-1 gene expression were disrupted at the peak of demyelination, consistent with increased intestinal permeability and compromised barrier function well-documented in both MS patients and EAE models (6, 47), a noteworthy level of recovery took place during remyelination. This evidence concerns the gene OCLN and myeloid sarcoma.