The immune function of dermal fibroblasts in skin defence against pathogens

Abstract

Dermal fibroblasts are the main resident cells of the dermis. They have several significant functions related to wound healing, extracellular matrix production and hair cycling. Dermal fibroblasts can also act as sentinels in defence against infection. They express pattern recognition receptors such as toll‐like receptors to sense pathogen components, followed by the synthesis of pro‐inflammatory cytokines (including IL‐6, IFN‐β and TNF‐α), chemokines (such as IL‐8 and CXCL1) and antimicrobial peptides. Dermal fibroblasts also secrete other molecules‐like growth factors and matrix metalloproteinases to benefit tissue repair from infection. Crosstalk between dermal fibroblasts and immune cells may amplify the immune response against infection. Moreover, the transition of a certain adipogenic fibroblasts to adipocytes protects skin from bacterial infection. Together, we discuss the role of dermal fibroblasts in the war against pathogens in this review. Dermal fibroblasts have important immune functions in anti‐infection immunity, which should not be overlooked.

Modeling of solar UV-induced photodamage on the hair follicles in human skin organoids

“…Generally, the hair follicle is composed of keratinocytes and fibroblasts, both of which play crucial roles in skin inflammatory response. 34 , 35 Remarkably, we observed a drastic suppression of IkBα, which is normally expressed throughout the entire hair follicle, particularly in the ORS keratinocytes in the vehicle group ( Figure 6(c) and ( d )). Accordingly, sUV exposure induced a marked increase in p-NF-κB expression the ORS and matrix of hair follicles ( Figure 6(c) and ( d )).…”

Piezoelectric and Triboelectric Nanogenerators for Enhanced Wound Healing

“…During the inflammatory phase, the platelet-derived growth factor and transforming growth factor promote the multiplication of fibroblasts [42]. By generating pro-inflammatory cytokines and chemokines including IL-1, IL-6, IL-10, TNF-α, IL-1β, IFN-γ, CCL2, and CXCL5, these activated fibroblasts participate in a crosstalk that enhances the immune cell activation [43,44]. Monocytes, endothelial cells, and neutrophils attach to the fibrin scaffold generated during platelet activation [38,45].…”