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In this study, the researchers found that treatment with the JAK inhibitor tofacitinib in alopecia areata patients may reduce clonal CD8+ T cell expansions but does not eliminate them entirely, which could contribute to disease relapse.

In this study, researchers found that hair follicle stem cells activate an immune-modulatory program during wound healing, promoting Treg cell expansion and aiding skin repair, while deleting certain immune components impaired healing and increased inflammation in a mouse model.

In this study, alopecia areata patients treated with diphencyprone showed a significant increase in CD8 lymphocytes around hair bulbs, which may be associated with hair regrowth.

This study describes a new mouse model for vitiligo that mimics key clinical features such as skin depigmentation and CD8 + T cell infiltration, providing a useful tool for in-depth research and drug discovery.

This study suggests that hypersensitivity and increased serum IgE levels might contribute to the pathogenesis of diffuse alopecia areata through intense local inflammatory infiltration.

This study suggests that SOCS3 treatment may effectively inhibit alopecia areata by suppressing CD8+ T cell activity and IFN-γ production.

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 diphencyprone showed a significant clinical response for treating alopecia areata, while tacrolimus was not effective.

This study found that antroquinonol inhibited CD8+ T cell proliferation and reduced proinflammatory cytokine secretion in vitro, while also ameliorating H2O2-induced depigmentation and resisting reductions in hair follicle length, skin thickness, and tyrosinase expression in mice.

This case report highlights a rare instance of CD8-positive hypopigmented mycosis fungoides causing alopecia areata-like changes, emphasizing the necessity of scalp biopsy in such presentations.

This study observed that NSG-hu-BLT mice developed graft-versus-host disease characterized by CD8+ T lymphocyte-related cell death in the skin and liver, which may affect their utility in other research areas.

This review discusses the bidirectional interactions between human mast cells and CD8 T cells in the skin, particularly in the context of disorders like psoriasis, atopic dermatitis, and vitiligo, and reports no new findings.

This study found that B6.CD80CD86−/− mice developed autoimmune-like alopecia with nearly 100% incidence by 40 weeks, making them a promising model for studying human alopecia areata.

This study identified "HTLV-1-associated lichenoid dermatitis" as a skin condition in HTLV-1-infected individuals, characterized by reactive eruptions associated with increased immunity toward infected CD4+ T cells.

In this study using the C3H/HeJ mouse model of alopecia areata, researchers found that hyperexpanded CD8⁺ T cell clones were sufficient to initiate disease, establishing a causal link between T cell clonality and pathogenicity.

In this study, researchers observed significantly higher CD8+ T cell levels in Iraqi patients with Alopecia areata compared to healthy controls, alongside concluding that the condition is more prevalent in men.

This study found that both topical minoxidil and latanoprost effectively improved hair regrowth in patients with alopecia areata, but minoxidil showed higher efficacy.

This study found that in alopecia areata, treatment with the oral JAK-inhibitor tofacitinib decreased clonally expanded CD8⁺ T cells in the scalp, but many expanded clones did not completely disappear, potentially leading to relapse after stopping treatment.

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.

Certain CD8+ T cells attack hair follicles in alopecia areata, suggesting they could be targeted for treatment.

In this study, researchers observed elevated levels of epidermal γδ T cells, keratinocytes, and an upregulation of the BST2 gene among immune cells in C3H/HeJ mice with alopecia areata, suggesting a potential role in disease pathogenesis.

This study found that in alopecia areata, epidermal γδ T cells and macrophages contribute to the disease alongside CD8 T cells, with the expression of BST2 marking interferon-driven immune activation in both mouse and human skin, which decreases following treatment with the JAK inhibitor tofacitinib.

This study found that NK and CD8+ T cell infiltration may drive inflammation in androgenetic alopecia, suggesting that targeting IL-15 signaling could offer a new therapeutic approach for hair regeneration.

This study found that in mice with alopecia areata, CD8+ T cells showed clonal expansion and specific regulatory networks, which might help identify new therapeutic targets for patients not responding to JAK inhibitors.

Expanding regulatory T cells may help treat alopecia areata by reducing harmful immune cells.

This study found that Baricitinib significantly reduced hair loss and immune response in a mouse model of alopecia areata.

In this study of C3H/HeJ mice, researchers observed that alopecia areata is associated with the expansion of exhausted-memory CD8 T cells in multiple organs, with autoreactive activation not fully explained by known mechanisms, shedding light on the immunological dynamics underlying the condition.

This study observed two distinct groups of alopecia areata lesions based on PD-1 expression in T cells from biopsied skin samples, suggesting potential differences in subtypes or stages of the disease that warrant further investigation.

This study suggests that monitoring CD8+ TEMRA cells in patients with rapidly progressive alopecia areata treated with intravenous corticosteroids could help predict therapeutic outcomes.

This study found that in biopsied skin samples of alopecia areata, a lower anagen/telogen ratio was associated with increased T cell infiltration, and enhancing the PD-1/PD-L1 axis may inhibit CD8+T cell infiltration and improve the condition.