Yurika Yogo et al. reported localization of CCL22 and CCR4 at CD68+ AMs, and an inverse correlation was observed between CCL22 levels in BALF and DLco/alveolar ventilation per minute (VA) values in IPF patients [72], suggesting that CCL22 might induce lung dysfunction in IPF patients by recruiting and activating CCR4+ AMs [72]. Here, CD68 is linked to idiopathic pulmonary fibrosis.