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A specific type of immune cell plays a key role in causing alopecia areata and could be a target for treatment.

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 review discusses the dual role of tissue-resident memory T cells in providing immune protection against infections and cancer and contributing to autoimmune skin disease pathology, without presenting new experimental results.

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

The research found that hair follicle–derived cytokines, particularly IL-15 and IL-7, regulate skin-resident memory T cells and their role in both immune homeostasis and lymphoma in the skin.

This review discusses how tissue resident memory T cells contribute to autoimmune skin diseases like vitiligo and psoriasis, highlighting their role in continuous immune activation, and reports no new clinical results.

Resident memory T cells and necroptosis may drive fibrosis in eosinophilic fasciitis and morphea.

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 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.

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 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.

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.

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.

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

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 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 paper proposes that the induction of HF-specific neo-antigens by peripheral CD8+ T cells may maintain self-tolerance but could also lead to immunopathology in conditions like alopecia areata.

This review highlights the possible role of T regulatory cells in the immune-related mechanisms of alopecia areata but reports no new clinical findings.

This review explores the role of Tregs in autoimmune skin diseases, transplantation, and skin cancer, and discusses Tregs-based therapies' potential for treating autoimmunity without reporting new experimental results.

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 observed that dandruff-affected scalp skin has increased T-cell infiltration in the epidermis and a reduction in the hair follicle's physiological immune privilege, particularly in the suprabulbar outer root sheath area, indicating a distinct immune microenvironment compared to healthy scalp.

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.

This study found that Th17 lymphocytes may play a more crucial role than cytotoxic T cells in the development of alopecia areata due to their infiltration around the hair bulb/bulge, which exacerbates hair loss as histopathological grade worsens.

This study found that terminally differentiated effector memory Vδ1T-cells and their cytotoxic activation markers were elevated in alopecia areata patients, suggesting these cells may contribute to its early pathogenesis.

Developing human skin has immune cells with memory-like features.

This research suggests that hair follicle-derived cytokines IL-7 and IL-15 are crucial for maintaining resident memory T cells in the skin, which may be relevant for diseases like cutaneous T cell lymphoma.

This study identified a reduced frequency of IL-10-producing regulatory B cells in alopecia areata patients, suggesting a protective role by these cells in disease development by regulating key immune mediators, such as IFN-γ and NKG2D+CD8+ T cells.

This review discusses the role of immune cells in the pathogenesis of alopecia areata and highlights emerging immunomodulatory strategies and novel therapeutic targets aimed at offering more effective and durable treatments for this autoimmune hair loss disorder.