Our results demonstrated that the sera obtained from the patients with three clinical phenotypes of CIDP all significantly decreased claudin-5 expression and the TEER value in the FH-BNBs, suggesting that humoral factors present in the sera of MADSAM and DADS patients, as well as t-CIDP patients, induce the BNB malfunction. This evidence concerns the gene PMP22 and chronic inflammatory demyelinating polyradiculoneuropathy.