Both circulating and fibrotic tissue-infiltrating SSc immune cells display a type I interferon (IFN) signature and a bias towards Th2 polarization, resulting in high levels of interleukin (IL)-4, IL-13, and IL-31 which, together with IL-1β, IL-6, and transforming growth factor (TGF)-β, induce fibroblasts to proliferate and synthesize an excessive amount of extracellular matrix (ECM), further contributing to tissue fibrosis [1,3,4,5,7,8,10]. Here, IL4 is linked to systemic sclerosis.