This program provides a blueprint for subsequent tissue repair; however, as we will discuss in Section 3.5, the aberrant reactivation and persistent activation of this very developmental program is also a core pathological mechanism in fibrotic diseases such as Systemic Sclerosis (SSc).During hair follicle development, macrophages maintain the cell density of the placode region by clearing excess epidermal cells, while simultaneously releasing TGF-β, IL-1, and Wnt-related factors that co-regulate follicle morphogenesis and inward growth (48). This evidence concerns the gene IL1B and systemic sclerosis.