Idiopathic pulmonary fibrosis (IPF) is a chronic respiratory disease characterized by progressive scarring of the lung parenchyma. While two drugs have been approved by the US Food and Drug Administration (FDA) for IPF, median survival remains limited at 3 years, and the discovery of novel therapeutic targets is urgently needed. Recent studies indicate that immune cells play a critical role in regulating fibrosis. In this Mini Review, we discuss the recent literature focused on cells of the myeloid lineage that serve as key agents of pathologic interorgan communication in fibrosis. These cells are recruited from the bone marrow and have been found to be key drivers of the fibrotic process in the lung.