Christmann et al. (2014) compared the gene expression levels of lung tissues between SSc-ILD patients and controls, and the results revealed that M2 macrophage markers, such as CD163 and CCL18, were upregulated in SSc patients, which were related to the progression of pulmonary fibrosis. Pechkovsky et al. (2010) illustrated the importance of M2 macrophage phenotype in the pathogenesis of lung fibrosis, and IL-4 and IL-10 could induce the shift of alveolar macrophages to M2. Here, CCL18 is linked to systemic sclerosis.