Nrp1, or neuropilin 1, is expressed by neurons, blood vessels, immune cells, and many other cell types in the mammalian body. It binds a range of extracellular ligands to modulate organ development and function, playing roles in signaling pathways relevant to neuronal and vascular development in the brain and retina [2]. Mouse knockout models have been crucial tools for studying Nrp1 function [2].

Nrp1 has been found to be a receptor for mammalian orthoreovirus, contributing to viral dissemination and neurovirulence in mice. Capsid mutants unable to bind Nrp1 helped uncover this role [1]. In allergic airway inflammation, Nrp1 is a surface marker of ILC2s, with its down-regulation correlating with enhanced ILC2 responses during IL-33 challenge [3]. In liver fibrosis, Nrp1 expression is elevated in fibrotic livers, promoting HSC activation, and USP9X-mediated Nrp1 deubiquitination enhances this process [4]. In prostate cancer, Nrp1 promotes cancer progression by modulating the EGFR-dependent AKT pathway, and its inhibitor can suppress this process [5]. In colitis, Nrp1 is a positive regulator of IL-17-producing ILC3s, and its genetic deficiency or pharmacological inhibition can improve colitis outcomes [6].

In conclusion, Nrp1 is essential in various biological processes and disease conditions. Gene knockout models in mice have been instrumental in revealing its roles in viral pathogenesis, allergic inflammation, liver fibrosis, cancer progression, and colitis. Understanding Nrp1's functions through these models provides potential therapeutic targets for treating related diseases.