Host keratinocyte inflammatory response (None)

Keratinocytes, the predominant cells in the epidermis, drive the host inflammatory response in skin by acting as sentinels that detect pathogens, damage-associated molecular patterns, and alarmins through pattern recognition receptors like TLRs and NLRs. Upon activation, they initiate pro-inflammatory signaling via NF-κB, MAPK, and inflammasome pathways, secreting cytokines (IL-1, IL-6, TNF-α, IL-18), chemokines (CCL20, CCL27), and antimicrobial peptides to recruit neutrophils, T cells, and dendritic cells while promoting antigen presentation via MHC molecules. This response amplifies immunity during infections or wounds but also contributes to pathologies like psoriasis, atopic dermatitis, and autoinflammatory syndromes when dysregulated, as seen with NLRP1 mutations or IL-17/IL-22 overstimulation. Keratinocytes balance inflammation through anti-inflammatory factors like TSLP, TGF-β, and IL-10, supporting tolerance and memory T cell maintenance without systemic spread. Therapeutically, targeting components (e.g., IL-36R or TNF pathways) shows promise, but broad modulation risks barrier breakdown or opportunistic infections.

Other names

Keratinocyte-mediated inflammationEpidermal keratinocyte immune responseKeratinocyte pro-inflammatory signaling

TLR/NLR activation leading to NF-κB/MAPK pathway stimulation and cytokine/chemokine release; Inflammasome (NLRP3/NLRP1) activation for IL-1β/IL-18 processing; Cytokine receptor signaling (e.g., IL-1R, TNFR) inducing adhesion molecules (ICAM-1) and AMPs; IRF-mediated type I IFN production for antiviral states