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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.

This study observed that in human scalp hair follicles, BTNL2 expression is lower in stressed conditions, which correlates with increased cytotoxic activity by gamma/delta and CD8+ T cells, suggesting a possible role for BTNL2 in controlling immune responses relevant to alopecia areata.

This study suggests that autoimmune dysregulation involving HLA-DR+ T and NK cell subsets may contribute to severe patchy alopecia areata and alopecia universalis, with normalization seen after betamethasone treatment.

This study found that patients with alopecia areata had significantly lower T cell numbers and reduced lymphocyte responses compared to healthy controls, correlated with hair loss severity and presence of antithyroid antibodies.

This study suggests that mechanical tension significantly impacts lymphocyte function, and that a complete lymphocyte population is essential for effective wound healing and reducing inflammation.

This study investigates whether lymphocytes from mice with secondary alopecia areata can effectively induce the disease in a C3H/HeH mouse model, similar to lymphocytes from mice with spontaneous disease.

This study found that the presence of CD3(+) T-cells within empty follicular fibrous tracts is a reliable indicator for diagnosing diffuse alopecia areata instead of pattern hair loss.

In this study, a thoroughbred mare exhibited a unique case of alopecia areata with lymphocytic infiltration at both the bulbar and isthmic levels of hair follicles.

This study found that peribulbar lymphocytic infiltration can effectively differentiate between alopecia areata and androgenetic alopecia using T-cell infiltration patterns in skin tissue.

This review examines the interplay of genetics and neuroimmunology in alopecia areata, highlighting its potential to inform broader autoimmunity research, but reports no new findings.

This review discusses the role and mechanisms of unconventional lymphocytes in promoting tissue repair and maintaining mucosal barrier integrity in the skin, gut, and lungs, but reports no new findings.

Minoxidil may help hair regrowth in alopecia areata by affecting T-cells.

This study found that CD44 and CD49d together enhance signaling pathways in lymphocytes in mice with alopecia areata, influencing their activation and function.

In this study, researchers identified unique prenatal lymphocyte features in human fetal skin, including proliferative naive T cells and memory-like T cells, which may influence antigen and allergen responses in utero and infancy.

Scarring alopecia involves increased immune cells and specific gene changes near damaged hair follicles.

This study describes a form of lymphocytic mural folliculitis in tigers causing hair loss, concluding it may represent a nonspecific hypersensitivity reaction distinct from T-cell lymphoma.

Enhancing regulatory T cells may help treat autoimmune diseases like alopecia areata.

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.

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.

Alopecia areata patients have more activated T cells in their blood, which may help in developing treatments.

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

In this study, four dogs with a novel skin disease showed clinical lesions involving verrucous, crusted papules and plaques, and responded variably to immunosuppressive therapy, suggesting an immune-mediated cause.

This study suggests that contact sensitizers may treat alopecia areata by expanding suppressor cells and interfering with antigen presentation to lymphocytes.

This study suggests that CD8+ cytotoxic T lymphocytes play a crucial role in the development of alopecia areata, based on observations in rodent models that mimic human autoimmune disease.

This study found that macroscopic vesiculobullous lesions with epidermal devitalization in dogs are part of the clinical spectrum of canine cutaneous epitheliotropic T-cell lymphoma.

In this study using a mouse model and human data, researchers found that CD8+ T cells are central to driving alopecia areata, while regulatory T cells offer some protection, highlighting CD8+ T cells as key targets for future therapy development.

This study indicates that innate lymphoid cells-type 1 may provoke alopecia areata by disrupting hair follicle immune privilege and inducing characteristic lesions, challenging the view that alopecia areata is purely an autoantigen-dependent, T cell-driven condition.

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 (ILC1) can induce alopecia areata by disrupting hair follicle immune privilege without the involvement of classical CD8+ T cells.

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.