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This study used Cisd2 knockout mice models and found that these mice display premature aging characteristics and an increase in dysfunctional neutrophils, suggesting Cisd2's role in calcium homeostasis and neutrophil function via interactions with Calnexin and SERCA.

In this research, authors found that skin-resident ILCs regulate sebaceous gland function and microbial balance, emphasizing an immune-epithelia system that supports host-microbe symbiosis.

This study found that blocking interleukin-3 improved lupus nephritis symptoms in MRL/Ipr mice, suggesting IL-3 may play a role in the disease's progression.

In human hair follicle keratinocytes, this study found that treatment with the pharmacological inhibitor QLT0267 led to a strong inhibition of proliferation and migration and induced nearly 100% apoptosis.

In this study, targeted inactivation of the integrin-linked kinase gene in melanoblasts led to defects in cell migration, proliferation, and ability to populate the skin, implicating an integrin-linked kinase-Rac1 connection in melanocyte function.

This study found that ILC1-like cells can induce alopecia areata symptoms in both ex vivo human hair follicles and in vivo mouse models, challenging the view that alopecia areata is solely CD8+ T cell-driven.

This study found that innate lymphoid cells-type 1 (ILC1lc) can induce alopecia areata (AA) by disrupting hair follicle immune privilege and causing hair follicle dystrophy and regression in both ex vivo and in vivo settings.

In this study, researchers found that inhibiting IKKα in patient-derived CCS tumour models reduces tumour viability, supporting the potential for topical IKKα inhibitors as a treatment for CCS.

In this study, researchers identified CENPV as a new CYLD interacting partner that localizes to primary cilia and regulates acetylated tubulin levels, offering insights into the pathogenesis of skin appendage tumors.

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.

In this study, researchers reported that IL-17C plays a key pro-inflammatory role in human skin diseases and may be a promising therapeutic target for inflammatory skin conditions.

This study found that innate lymphoid cells-type 1 (ILC1) can induce alopecia areata by disrupting hair follicle immune privilege without the involvement of classical CD8+ T cells.

GLI2 activates GLI1, promoting skin tumor growth and hair development.

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.

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

In a murine model of alopecia areata, this study observed that the IL-2 fusion protein HCW9302 helped prevent disease development by expanding regulatory T cells and reducing disease-causing effector T cell infiltrates, suggesting potential for using IL-2 fusion proteins in alopecia areata treatment.

The researchers reported increased ubiquitination of proteins such as the insulin receptor in CYLD cutaneous syndrome skin tumors, suggesting that CYLD dysfunction may affect protein secretion and signaling processes.

This study found that in early retinal neurogenesis in mice, the transcription factor Lhx2 regulates Sonic Hedgehog signaling by controlling expression of pathway genes like the co-receptors Gas1 and Cdon.

In this study, subcutaneous recombinant human IL-12 showed a 43% partial response rate in early-stage mycosis fungoides patients refractory to previous treatments, with generally mild to moderate adverse events reported.

In this study, gene inactivation in mouse hair follicle stem cells lacking ILK impaired wound healing by reducing their progeny’s contribution to the regenerating epidermis, but did not affect hair follicle regeneration.

In this study, a mouse model of scarring alopecia demonstrated significantly reduced CD200R expression in affected skin, which may contribute to immune attacks on hair follicles.

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 case study of a neonate with ichthyosis and ILVASC demonstrates how an interdisciplinary approach facilitated a timely genetic diagnosis and management of complications.

This study demonstrated that litifilimab significantly reduced disease activity in cutaneous lupus erythematosus by Week 16, with improvements most notable in sunlight-exposed skin areas.

This article discusses the SLICC's revision and validation of the ACR SLE classification criteria to enhance clinical relevance and integrate recent immunological insights, but does not report new clinical results.

This study found that IL18 signaling plays a crucial role in the homing and retention of mature regulatory T cells in the mouse thymus, primarily by upregulating the chemokine receptor CCR6.

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

This case report highlights how chronic bacterial folliculitis may contribute to persistent inflammation in lichen simplex chronicus and emphasizes the value of DIF and IHC in diagnosing obscure cases.

This study found that IL-7 is crucial for the survival of memory regulatory T cells in the skin of mice, whereas IL-2 is essential for their initial generation but not for their maintenance.

This study identified major criteria including ectodermal malformations for diagnosing ichthyosis with confetti, and revealed significant genetic variation in the disease locus within the general population.