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IL-1 receptor absence in mice leads to skin cysts and changes in immune response after UVB exposure.

ASLAN004 was safe and well-tolerated, supporting further development for treating certain diseases.

This study suggests that erlotinib exacerbates inflammation in a mouse model of skin disease and that IL-1 inhibition could mitigate skin-related side effects of EGFR inhibitors.

This study found that IL-1 alpha inhibits the growth of cultured human hair follicles and hair fibers, suggesting a potential role in inflammatory hair loss conditions like alopecia areata.

This article explores potential mechanisms of acneiform skin eruptions linked to EGFR inhibition in cancer patients, focusing on EGFR's role in controlling IL-1-dependent inflammation at hair follicles, but reports no clinical results.

This study found that 1,25-dihydroxyvitamin D3 promotes hair growth and regeneration in mice by prolonging the anagen phase and counteracting DHT's inhibitory effects, suggesting its potential therapeutic role for androgenetic alopecia.

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 study found that VR1 activation in human hair follicles inhibited hair growth by suppressing proliferation and promoting apoptosis, suggesting VR1 plays an important role in hair growth regulation.

This study suggests that interleukin-1 α influences dermal papilla cell activity by modifying androgen receptor expression and increasing the secretion of several growth factors and cytokines.

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 elevated levels of IL-18 and free IL-18 in hidradenitis suppurativa patients compared to healthy controls, suggesting these cytokines may serve as novel biomarkers for disease activity, with correlations indicating their involvement in disease severity.

This study found that intracellular Toll-like receptors were significantly up-regulated in peripheral blood mononuclear cells of alopecia areata patients, suggesting a potential role in inflammatory signaling and pathogenesis.

This study found that dimethyl fumarate improved delayed wound healing in Il36rn-/- mice by reducing neutrophil extracellular trap formation and oxidative stress.

In this study, researchers found that certain cytokines can significantly down-regulate PDGF expression in dermal papilla cells and follicular keratinocytes, indicating a potential link between PDGF signaling and catagen induction.

In this laboratory study, Cucumis melo var. makuwa leaf extract significantly reduced DHT-induced apoptosis in human dermal papilla cells by modulating androgen receptor activity and gene expression, suggesting potential as a therapy for androgenetic alopecia.

This study found that intradermal injection of a cell-penetrating, AR-targeting asiRNA promoted hair growth and reduced androgen receptor expression in mouse models of androgenetic alopecia, suggesting its therapeutic potential.

Anti-IL-1 treatments might help with certain types of hair loss in people with high inflammation.

Blocking IL-1 could help treat some hair loss conditions; alopecia affects liver detox systems; spironolactone is better than finasteride for female hair growth; focusing on the catagen hair phase could lead to new alopecia treatments.

This article reviews the genetic and androgenic factors influencing the development of androgenetic alopecia and reports no new findings; the authors highlight a need for further research into the underlying mechanisms.

This study found that interleukin-1-alpha and oncostatin-M levels were positively associated with PCOS development, while interleukin-7, IL15RA, and CXCL11 were negatively associated, suggesting a connection between inflammatory factors and PCOS.

This study found that FGF21 suppresses inflammation induced by C. acnes in both human skin cells and mouse models, suggesting potential use in acne treatment.

This review discusses the potential of therapeutic antibodies as an alternative treatment for androgenetic alopecia, highlighting the initial development stages and the need for further validation and optimization of targets like the prolactin receptor and Interleukin-6 receptor.

This study found that type 2 immunity may play a role in the development of alopecia areata in patients with extrinsic atopic dermatitis, indicating different immunological states compared to non-atopic patients.

This study found that the peptide derivative beta-Ala-Pro-Dab-NHbenzyl may reduce wrinkles and sebum production in human skin by inhibiting dipeptidyl peptidase 4, suggesting potential for acne and skin inflammation treatment.

This research explores developing liposomal formulations to enhance the delivery of difficult-to-absorb agents directly to hair follicles and sebaceous glands, with minoxidil and plasmid DNA as study molecules.

This review discusses the epidemiology, clinical characteristics, pathogenesis, and genetic factors of alopecia areata, while stressing the need for targeted and effective treatments, but reports no new clinical results.

This study suggests that particulate matter can induce inflammation in human outer root sheath cells, potentially affecting hair growth, through oxidative stress-dependent MAPK and JAK-STAT signaling pathways.

This study found that mesenchymal stem cell treatment alleviated atopic dermatitis-like symptoms in a mouse model by modulating immune and inflammatory responses, with gene expression changes suggesting pathways for potential personalized treatment approaches.

This study found that 17β-estradiol inhibited RANTES production in human keratinocytes by suppressing nuclear factor κB activity, suggesting a potential mechanism for 17β-estradiol's modulation of psoriasis-related inflammation.