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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 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.

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

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 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.

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.

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 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 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.

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

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 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.

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

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 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 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.

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

This study found that phosphodiesterase inhibitors may suppress the proliferation of benign prostatic hyperplasia epithelial cells by modulating CCL5 levels in low androgen conditions.

In this study, treatment with a 5a-reductase inhibitor increased CD8+ T cell infiltration in benign prostatic hyperplasia tissues, suggesting an impact on inflammatory responses.

This research explored the roles of various T cell types in chronic alopecia areata, finding that increased severity of lesions and hair loss may be linked to decreased lesional Foxp3+ Tregs, with a notable role for IL-17 and Th17 lymphocytes in the pathological process.

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 mouse skin CD4(+) memory T cells are in equilibrium with the circulation under steady state but increase in specific clusters in response to infection or inflammation.

In this study, iNKT10 cells were found to play a significant role in preventing and treating alopecia areata in a humanized mouse model, suggesting these cells could have potential in managing related autoimmune disorders.

This study demonstrates that T-cell responses in extensive alopecia areata scalp may be aberrantly regulated, with reduced cytokine production but activated phenotype, providing insight into the disease's immune mechanisms.

In this narrative review, researchers outlined the role of T cells in the autoimmune pathogenesis of alopecia areata and highlighted ongoing research into therapeutic pathways, beyond current JAK inhibitors, aimed at developing new treatments for the disease.