TLR activation of airway epithelial cells enhances the production of NRTN, which binds to constitutively expressed GFRα2 on the surface of lung macrophages (1). Viral TLR activation on lung macrophages (2) triggers the release of IFNβ (3), which acts in an autocrine manner and binds to the IFNα/β receptor, IFNAR (4), to stimulate the production of RET at the mRNA and protein level (5). RET translocates to the cytoplasm and binds to GFRα2 (6), stimulating the production of MMP-2 (7) and dampening the pro-inflammatory cytokine response.