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This study found that human hematopoietic mesenchymal stem cells increased the viability and migration of human outer root sheath cells in an in vitro alopecia areata model, involving Wnt/β-catenin and JAK/STAT pathways.

This study in a murine model of alopecia areata found that IFNg is crucial while perforin is not necessary for CD8 T cell-mediated disease development.

In this study, IFN-γ-stimulated iPSC-derived mesenchymal stem cell extracellular vesicles improved atopic dermatitis in mice by reducing Th2 cytokine activity, suppressing inflammation, and restoring skin barrier function, as evidenced by decreased itching and inflammatory markers.

This study observed that Epigallocatechin-3-gallate (EGCG) can inhibit phosphorylation of STAT1 and reduce a specific subset of immune cells in vitro and ex vivo, suggesting a potential role in maintaining immune privilege in alopecia areata.

This study found that injecting interferon gamma into C3H/HeJ mice did not alter the frequency or onset of alopecia areata, suggesting the protein alone does not trigger the disease.

This study developed and analyzed a mathematical model for alopecia areata involving interactions among immune cells and cytokines, establishing conditions under which hairless patches can become stable and pervasive, particularly with certain biological rate levels and chemotactic sensitivities.

This study suggests that NKG2D+ Vδ1 T cells may contribute to hair follicle pathology in alopecia areata by recognizing stressed keratinocytes and inducing immune privilege collapse.

In this study, researchers found that CD4 T cells from the skin draining lymph nodes of mice with alopecia areata can transfer the disease to recipient mice, highlighting the key role of these cells and their interaction with CD8 T cells in the disease's development.

This study found that Enz_MoriL, a compound derived from Morus alba L., promotes hair follicle cell proliferation by affecting the Wnt/β-catenin pathway and can counteract an alopecia areata-like condition by suppressing the JAK-STAT signaling in human hair follicle dermal papilla cells.

In this experimental study, laser irradiation significantly altered the gene expression of cytokines in cultured human T-cell lymphocytes, suggesting that such laser light may photobiomodulate cytokine production in vitro.

This study found that topical ginsenoside Rg1 may protect skin from UVB-induced damage in mice by reducing pathological changes and modulating cytokine mRNA expression associated with inflammation and immune response.

Specific immune cells cause alopecia areata and blocking certain proteins can prevent it.

In this study, researchers observed that a topical gel containing 20% hypoxia mesenchymal stem cell secretome significantly reduced IL-15 and IFN-γ mRNA expression and baldness by 60% in male Wistar rats with fluconazole-related alopecia.

This study found that IFN-γ plays a critical role in T cell activation and the pathogenesis of alopecia areata in C3H/HeJ mice.

This study found that mycophenolate may stabilize β-catenin and counteract interferon-γ-induced catagen changes in human dermal papilla cells, which could promote hair growth.

In this study, researchers developed a mouse model of scarring alopecia and observed significant reductions in CD200R expression in affected skin, potentially linking this signaling pathway to immune attacks on hair follicles and suggesting new treatment targets for scarring hair loss.

This study suggests that the neuropeptide CGRP may protect against, but not restore, IFNγ-induced collapse of hair follicle immune privilege in alopecia areata.

This study identifies substance P, TNFα, and IFNγ as novel regulators of prolactin and its receptor expression in human skin, suggesting intracutaneous prolactin is not controlled by dopamine.

In this study, certain cytokines and growth factors were found to significantly regulate hair growth in vitro, with EGF, TNFα, and IL-1β particularly inhibiting it.

This study found that human placenta hydrolysate effectively inhibited atopic dermatitis development in stimulated human cells and a mouse model, suggesting its potential as a therapeutic agent for related skin diseases.

This study suggests that IL-17 may play a more significant role than IFN-γ in the pathogenesis of chronic alopecia areata, with increasing severity linked to Th17 lymphocytes and cytotoxic T lymphocyte infiltration.

In this study, patients with alopecia areata showed significantly elevated serum levels of IFN-γ and severely deficient vitamin D3 levels compared to healthy controls.

In this study, combining compound glycyrrhizin with topical minoxidil was more effective and as safe as minoxidil alone for treating alopecia areata.

A JAK1 variant causes hair loss, skin issues, and thyroid disease, but treatment with a specific inhibitor can help.

In this study, researchers demonstrated that CD4 T cells from skin-draining lymph nodes in mice with alopecia areata can transfer the disease to recipient mice, revealing a critical role for CD4 T cells in disease development and suggesting potential therapeutic targets.

This study found that subcutaneous injection of a CXCL12 neutralizing antibody significantly promoted hair growth in androgenic alopecia and inhibited hair loss in alopecia areata in mouse models, suggesting its potential as a promising treatment for hair loss.

This study found that in chronic alopecia areata, increased IL-17 expression and CD8+CD49a-Trm cell infiltration in hair follicles were associated with more severe histopathologic gradings, while Foxp3+mTreg infiltration decreased.

This study suggests that lithocholic acid may enhance hair regeneration in alopecia by activating vitamin D receptors in human dermal papilla cells.

This case report describes how anifrolumab, used beyond trial-eligible populations, led to significant clinical and serological recovery in a 45-year-old woman with organ-threatening systemic lupus erythematosus complicated by infection and resistant to conventional treatments like cyclophosphamide and rituximab.

This study systematically reviewed literature on paradoxical reactions during biologic treatments for psoriasis, identifying immune dysregulation mechanisms and diverse clinical manifestations, highlighting that mild cases often respond well to topical treatments, while severe cases may require switching to different IL-23 inhibitors.