Neuropilin-1 is important for proper suppression of inflammation and autoreactivity (143.23)

• Published in: The Journal of immunology (1950) Vol. 184; no. 1_Supplement; pp. 143 - 143.23
• Main Authors: Bynoe, Margaret, Solomon, Benjamin, Chae, Wookjin, Mueller, Cynthia, Alabanza, Leah
• Format: Journal Article
• Language: English
• Published: 01-04-2010
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.184.Supp.143.23

The surface molecule Neuropilin-1 (Nrp1), was originally identified for its role in neuronal development. Recently, Nrp1 has been implicated in several aspects of immune function, including maintenance of the immune synapse and development of regulatory T cells (Treg). We provide the first evidence for a role of Nrp1 in the pathogenesis of an immune mediated disease, experimental autoimmune encephalomyelitis (EAE), which serves as an animal model for the central nervous system inflammatory disorder multiple sclerosis (MS). Using a mouse cell type specific deletion system, we observed that the lack of Nrp1 on CD4+ T cells results in increased EAE disease severity. These Nrp1 conditional knockout mice exhibit preferential Th17 lineage commitment. Further, CD4+ T cells expressing Nrp1 can suppress Th17 cell expansion and cytokine production both in vitro and in vivo. These findings suggest that Nrp1 is essential for proper maintenance of peripheral tolerance and its absence can result in unchecked autoreactive responses.