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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 case report describes a rare instance of thymoma associated with alopecia areata in a 60-year-old woman who had no signs of myasthenia gravis, highlighting the need for thoracic surgeons to consider alopecia in such cases due to its impact on quality of life.

Postmenopausal women may experience frontal hairline and eyebrow loss due to cicatricial fibrosis.

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.

In this case study, a 65-year-old male with hepatocellular carcinoma treated with the PD-1 inhibitor Sintilimab developed alopecia universalis alongside significant tumor regression and complete remission, highlighting a rare immune-related adverse event with effective anti-tumor outcomes.

This case report describes a 29-year-old woman with longstanding alopecia areata who experienced improvement in her scalp hair loss after 7 years of topical treatment with squaric acid dibutylester.

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 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 mechlorethamine restored hair growth in mice with alopecia-areata-like disease by eliminating infiltrated lymphocytes and inhibiting certain pro-inflammatory cytokines in treated skin areas.

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.

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

This review discusses the role of immune responses, especially Th1 cytokines, in alopecia areata pathogenesis and reports no new research findings.

In this case report, a woman developed severe alopecia areata approximately one year after starting belimumab for systemic lupus erythematosus, with hair loss improving upon discontinuation of the drug, suggesting a possible connection between belimumab and immune-mediated hair loss.

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 JAK inhibitors promote hair regrowth in both mice and human alopecia areata cases by blocking key immune pathways involved in disease development.

This study reports that a 14-year-old female rhesus monkey with alopecia universalis was found to have a T-cell-mediated autoimmune disease similar to human alopecia areata universalis.

This study found hair regrowth in the majority of AA-affected mice and rats treated with diphencyprone, suggesting its potential utility for understanding human alopecia areata and the drug's therapeutic action.

This case report describes the first dermoscopic evaluation of alopecia areata-like disease in a dog, where the condition mirrored human cases in terms of clinical presentation and treatment response.

This study showed that in C3H/HeJ mice, focal follicular inflammation starts before overt hair loss, with inflammation severity possibly reaching a threshold causing hair follicle dystrophy prior to visible hair loss.

This article reviews the pathogenesis, complications, and management of lichen planus, especially its persistent oral form, and highlights the need for further prospective studies.

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.

This study provides evidence that innate lymphoid cells-type 1 can induce alopecia areata in human hair follicles, challenging the view that it is solely a CD8+ T cell-driven autoimmune disease.

This study examines the similarities and differences in the pathogenesis of autoimmune conditions alopecia areata and vitiligo, highlighting shared features like immune cell involvement and cytokine pathways, while noting differing immune responses in skin and hair.

This case report highlights an unusual presentation of mycosis fungoides with photo-exacerbated lesions and a rare CD4+/CD8+ immunohistochemical phenotype, complicating diagnosis and treatment.

This review discusses the autoimmune nature of alopecia areata, potential therapeutic targets, and highlights the need for further studies on immunomodulatory treatments and genetic factors, but it reports no new clinical results.

This article proposes that alopecia areata may be caused by immune attacks on hair follicles after an immune privilege collapse, suggesting new therapeutic approaches targeting this immune response pattern.

This article hypothesizes that thymoma with aplastic anemia may result from abnormal autoimmune CD8⁺ T lymphocytes produced by the thymoma, potentially leading to other cytotoxic T-cell-mediated autoimmune diseases.