IL4 and pulmonary fibrosis: Meanwhile, in BLM-treated mice, deficiency of PIR-B increases lung histopathology (such as excessive destruction of lung architecture, increased fibrocystic foci, and increased monocytes infiltration), and induces collagen expression and the IL-4-associated profibrogenic markers RELMα, MMP-12, TIMP-1 and osteopontin in alveolar macrophages, indicating that PIR-B can inhibit pulmonary fibrosis [27].