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This study found that an E-cadherin mutant preserved normal cadherin levels and prevented inflammation and lethality in mouse skin lacking p120, highlighting p120's role in regulating cadherin-mediated cell adhesion and inflammation.

In a conditional knockout mouse model, this study found that loss of the transcription elongation factor SPT6 in basal keratinocytes led to psoriasis-like skin inflammation and delayed wound healing, suggesting SPT6 plays a crucial role in maintaining epidermal immune quiescence by suppressing proinflammatory NF-κB signaling.

This study found that H-Ras activation in aged mouse skin leads to increased dysplasia and progression to in situ squamous cell carcinoma, highlighting an age-linked connection between immune changes, senescence, and cancer risk.

This study found that loss of epidermal PPARγ in mice altered the expression of many genes related to skin inflammation, keratinization, and sebaceous gland function, indicating its key role in maintaining skin homeostasis.

This study found that selective deletion of Ctip2 in epidermal keratinocytes in adult mice leads to atopic dermatitis-like inflammation and suggests Ctip2 plays a crucial role in skin barrier maintenance and inflammatory regulation.

This study found that Schistosoma mansoni cercariae stimulate epidermal keratinocytes in mice, initiating pro-inflammatory responses and barrier repair mechanisms akin to those in wound healing.

This study found that overexpression of Gsdma3 in mice led to epidermal hyperplasia, skin inflammation, and hair growth defects, suggesting gain-of-function mutations in Gsdma3 cause these conditions.

The study observed that mRAGE expression is prevalent in keratinocytes of the healthy human epidermis and may regulate inflammation and apoptosis to maintain skin homeostasis rather than responding to aging processes.

This case report describes a woman who developed extensive nonscarring inflammatory hair loss after two years of gefitinib treatment, highlighting potential cutaneous side effects associated with epidermal growth factor receptor blockers.

This study found that sulfated CCK octapeptide reduces psoriasis-like skin inflammation in mice, suggesting a new pathophysiological role for CCK in regulating epidermal inflammation.

This study found that aging in the epidermis disrupts cytokine balance and stem cell function, which may contribute to broader tumor-suppressive mechanisms.

This study found that overexpression of PKCα in mouse epidermis increases expression of specific proinflammatory mediators and induces inflammation but does not significantly affect epidermal differentiation, proliferation, or tumor promotion with TPA.

This study found that TRPV3 ion channels on human epidermal keratinocytes suppress cell proliferation, induce cell death, and trigger a proinflammatory response, suggesting a role in cutaneous inflammatory processes.

In this study, CD109 overexpression in transgenic mice led to reduced inflammation and improved collagen organization during wound healing without affecting wound closure.

This review discusses how inflammation influences hair follicle stem cell activities like wound healing and follicle cycling and suggests a potential link between inflammation, stem cell activation, and programmed cell death.

This review highlights advances in understanding inflammatory memory in epidermal stem cells, focusing on their capacity to remember prior inflammatory responses and respond more quickly to future stimuli, potentially aiding strategies against skin-related diseases.

In this study, epidermal EGFR ablation in a mouse model led to significant local and systemic inflammatory responses, highlighting EGFR's role in maintaining skin immuno-homeostasis.

This study found that N,N-dimethylglycine sodium salt promoted proliferation and migration of cultured human epidermal keratinocytes and had anti-inflammatory and antioxidant effects in vitro.

This study found that neutrophil-rich hair follicle inflammation caused by a monoclonal antibody targeting murine EGFR in mice involved TNFα and interleukin-1, suggesting these cytokines play a role in EGFR antibody-induced rashes in cancer patients.

This study in mice found that a monoclonal antibody targeting EGFR resulted in skin inflammation mediated by TNFα, suggesting potential pathways for addressing EGFR antibody-induced skin rash in cancer patients.

This study found that treatment with EGFR inhibitors or mitogen-activated kinase inhibitors may compromise the immune privilege of human scalp hair follicles, suggesting new directions for managing drug-induced folliculitis.

In this mouse study, the researchers found that the monoclonal antibody ME1 causes hair follicle inflammation by up-regulating TNFα, which can be reduced by TNFα and interleukin-1 inhibitors.

This article discusses the cutaneous side effects of erlotinib, an EGFR inhibitor, in a patient with non-small cell lung cancer, reporting nonscarring alopecia and indicative scalp biopsy findings.

This study found that epidermal growth factor receptor inhibitors used in cancer treatment induce a distinct inflammatory response in hair follicles, marked by immune privilege collapse and upregulation of inflammatory pathways.

In this study, CTCF was found to play essential roles in epidermal differentiation and skin barrier formation, simultaneously acting as a suppressor of epithelial inflammatory responses in mouse skin.

This study investigated how keratinocytes in the skin respond to different iron levels and found they play a significant role in regulating iron homeostasis by storing iron, affecting epidermal differentiation, and influencing inflammation-related gene expression in mice.

This study found that epidermal VEGF is crucial for maintaining skin barrier function in mice and may help explain psoriasis development following skin trauma due to its effects on angiogenesis and hyperplasia.

This study found that deletion of c-Jun and JunB in mouse bulge hair follicle stem cells was sufficient to trigger psoriasis-like skin disease through thymic stromal lymphopoietin signaling.