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Neuropilin 1 (NRP1); semaphorin 4A (SEMA4A)

Mouse studies suggest blocking SEMA4A-NRP1 signaling could increase an antitumor immune response without causing pathogenic autoimmunity. In mice with Treg-specific Nrp1 knockout, injection of cancer cell lines led to less tumor growth and greater antitumor immune responses than what was seen in mice with intact Nrp1. Mice with deletion of Nrp1 in Treg cells did not develop autoimmunity, and Nrp1-deleted Treg cells could maintain immune system homeostasis. In an ELISA, SEMA4A was shown to interact directly with NRP1. In mouse models of cancer, injection of SEMA4A- or NRP1-targeted antibodies decreased tumor growth compared with injection of control antibodies. Next steps include determining if the SEMA4A-NRP1 signaling axis in Treg cells is upregulated in human solid tumors (see Subverting Treg-mediated protection for tumors, page 8).

SciBX 6(32); doi:10.1038/scibx.2013.854
Published online Aug. 22, 2013

Patent application filed; available for licensing from St. Jude Children's Research Hospital
Contact: Scott Elmer, St. Jude Children's Research Hospital, Memphis, Tenn.

Delgoffe, G.M. et al. Nature; published online Aug. 4, 2013;
Contact: Dario A.A. Vignali,
St. Jude Children's Research Hospital, Memphis, Tenn.