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This study provides evidence that innate lymphoid cells-type 1 can induce alopecia areata in human hair follicles, challenging the view that it is solely a CD8+ T cell-driven autoimmune disease.

This study developed a DPC cell line by introducing mutant CDK4, Cyclin D1, and TERT, making it a promising tool to study downstream signaling pathways activated by testosterone in androgenetic alopecia.

This article reviews the roles of dendritic cells in alopecia areata and highlights emerging precision therapies that target these cells, reporting no new experimental findings.

In this study, cyclic ADP-ribose (cADPR) treatment in human hair follicle dermal papilla cells was associated with increased intracellular calcium retention and activated anagen-related signaling without causing significant cytotoxicity, indicating its potential impact on hair growth processes.

This study found that stabilizing β-catenin in a specific mouse model led to temporarily increased hair density but ultimately accelerated hair follicle aging and hair thinning.

This study developed PiSCES biosignatures that distinguished alopecia areata patients from controls, revealing enhanced basal TCR signaling and a potential disease-specific signaling network signature.

Testosterone metabolism in balding scalp cells may not be the main cause of hair loss.

This study found that dermal papilla and peribulbar dermal sheath cup cells in mice can both induce hair follicle formation, suggesting they may have similar functional roles in hair growth.

This study found that plasmacytoid dendritic cells are central to the pathogenesis of alopecia areata, suggesting they may help differentiate it from trichotillomania and androgenetic alopecia.

This study observed that cells from androgen-sensitive areas like the beard and scrotum showed higher androgen receptor levels compared to those from non-balding scalp areas, supporting the role of dermal papilla in follicle growth responses to androgens.

This study identifies a bipotent stem cell in adult hair follicles that self-renews and contributes to dermal sheath and papilla cell populations, potentially aiding hair regrowth after injury, disease, or aging.

This study suggests that macrophages, especially CD206+ subsets, play a key role in hair growth induced by squaric acid dibutyl ester, a therapy used for alopecia areata.

Allergic contact dermatitis may promote hair growth by activating hair follicle stem cells.

This study found that LEF1/TCF3 is necessary but not sufficient for TOPGAL activation in hair follicle development, indicating complex regulation in the skin.

This study indicates that innate lymphoid cells-type 1 may provoke alopecia areata by disrupting hair follicle immune privilege and inducing characteristic lesions, challenging the view that alopecia areata is purely an autoantigen-dependent, T cell-driven condition.

This study explored how T cells interact with hair follicles in primary cicatricial alopecias by using spatial transcriptomics across mice, dogs, and human samples, revealing specific communication pathways and potential drug targets like CFD and S100A8/9 for future therapeutic research.

This study suggests that label-retaining cells in the hair follicle contribute to follicular renewal, indicating a specific role in the hair cycle by proliferating during the late telogen phase.

This study suggests that macrophages, particularly CD206⁺ macrophages, play a crucial role in squaric acid dibutylester-induced hair growth in alopecia areata treatment.

This study suggests that in alopecia areata, innate lymphoid cells type 1 may contribute to the disease’s pathogenesis by inducing hair follicle changes similarly to CD8+ T cells.

This study reported that the anti-γc antibody hC2 restored hair follicle homeostasis and suppressed hair loss in an AA-like mouse model by inhibiting autoreactive T-cell activity, suggesting that hC2 may offer a safer and more effective treatment for alopecia areata compared to current Jak inhibitors.

This study provides evidence that ILC1-like cells can induce alopecia areata in previously healthy human hair follicles, challenging the view that it is solely an autoantigen-dependent autoimmune disease.

This study found that androgenetic alopecia may involve a defect in the conversion of hair follicle stem cells to progenitor cells, as demonstrated by a reduced presence of progenitor cells in bald scalp samples.

This study identified a large deletion in the desmoglein 4 gene as the genetic basis of the Iffa Credo "hairless" rat's skin phenotype, linking it to lanceolate hair mutations.

This study found that immune-mediated destruction of bulge stem cells is a key factor in the alopecia observed in AE mice, suggesting it as a model for studying primary cicatricial alopecias, particularly lichen planopilaris.

This research suggests that innate lymphoid cells type 1 (ILC1) may contribute to the development of alopecia areata, alongside CD8+ T cells, by disrupting hair follicle immune privilege and promoting features of the disease.

Cedrol promotes hair growth better than baricitinib by regulating immune cells.

This study found that loss of the ACER1 gene in mice led to increased ceramide levels and progressive hair loss, highlighting ACER1's role in maintaining hair follicle stem cell homeostasis.

This study found that the Plcd3(mNab) mutation in mice worsens the alopecia caused by Plcd1 loss, suggesting synergistic effects between Plcd1 and Plcd3 on hair follicle health.

This study found that ALRN-6924, a clinical-stage dual inhibitor, can selectively protect human scalp hair follicles from paclitaxel-induced toxicity and damage by inducing transient cell cycle arrest in healthy cells without affecting cancer cells, potentially reducing chemotherapy-induced alopecia.

Bulge progenitor cells show promise for regenerating hair follicles and increasing hair density.