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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: VPAC1 receptor (Vipr1)-deficient mice exhibit ameliorated experimental autoimmune encephalomyelitis, with specific deficits in the effector stage

Fig. 7

Scheme suggesting potential roles of VPAC1 on EAE. Upon MOG administration, EAE has two phases: the induction or priming phase and the effector phase. In the induction phase, MOG drains to the local lymph nodes and T cells are activated and polarized towards Th1 and Th17 cells. In the effector phase, these cells migrate to the CNS, where they mount an inflammatory response amplified by immune cell recruitment. Our data suggests that VPAC1 signaling on non-immune cells or microglia may be required for the effector phase of EAE and may explain the lack of clinical disease in VPAC1 KO mice or upon pretreatment of WT mice with a VPAC1 antagonist (VPAC1 antago). VPAC1 anti-inflammatory actions would be prevalent only during ongoing disease, and thus a VPAC1 agonist (VPAC1 ago) administered during this time blocked the disease. A treatment with a VPAC1 antagonist during ongoing disease during the same time frame post-EAE induction did not prevent and may have exacerbated the disease. Mice deficient in one of the two VPAC1 ligands, VIP, are also resistant to EAE, whereas PACAP-deficient mice exhibit exacerbated EAE, implying a critical VIP/VPAC1 interaction that is required for the development of EAE

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