CCL20, for instance, was found to be upregulatedduring infection at the blood–brain barrier,38 whereas CCL2 was strongly upregulated in cases with GBS-associatedsepsis.39 Taken together, these data indicatethat GBS MVs serve as a critical initiator of cytokine responses thatare commonly linked to disease. Here, CCL2 is linked to Guillain-Barre syndrome.