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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 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 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 (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 found that innate lymphoid cells-type 1 can induce alopecia areata characteristics in human hair follicles both ex vivo and in vivo, challenging the view of it as solely an autoimmune disease driven by CD8+ T cells.

This study found that ILC1-like cells can induce alopecia areata in healthy human hair follicles, challenging the traditional belief that the disease is primarily driven by CD8+ T cells.

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 research suggests that innate lymphoid cells type 1 (ILC1) may contribute to the development of alopecia areata, alongside CD8+ T cells, by disrupting hair follicle immune privilege and promoting features of the disease.

This review discusses the roles and interactions of intestinal intraepithelial lymphocytes in maintaining mucosal barrier integrity and highlights how their dysregulated responses may contribute to intestinal pathologies.

This study found that ILC1-like cells can induce alopecia areata in healthy human hair follicles, suggesting that these cells might be a therapeutic target in AA management.

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.

ICL is a condition with low CD4+ T cells like AIDS but not caused by HIV, and normal CD4+ T cell counts may vary between men and women.

This study found that in immunodeficient mice lacking T cells, certain innate lymphoid cell subsets increased and influenced the hair growth cycle, with specific ILC subsets shown to promote anagen, the active phase of hair growth.

This study reviews current evidence on the role of ILC3s in the skin, highlighting their potential involvement in responding to microbiome changes such as those associated with acne and suggesting gaps in understanding their mechanisms.

This review examines the role of innate lymphoid cells in allergic diseases and the influence of an allergic microenvironment on their plasticity, without reporting new clinical outcomes.

In this study, researchers observed that dysregulated innate lymphoid cells type 1, alongside CD8+ T cells, may contribute to the pathogenesis of alopecia areata by affecting hair follicle health.

In human hair follicle keratinocytes, this study found that treatment with the pharmacological inhibitor QLT0267 led to a strong inhibition of proliferation and migration and induced nearly 100% apoptosis.

This study found that ILK deficiency disrupts hair follicle development by impairing cell polarity and laminin-511 assembly, but these defects can be partially reversed with exogenous laminin-511.

This study suggests that in alopecia areata, innate lymphoid cells type 1 may contribute to the disease’s pathogenesis by inducing hair follicle changes similarly to CD8+ T cells.

This study found that DC-HIL+ myeloid derived suppressor cells are increased in the blood and skin of patients with cutaneous lupus erythematosus and show immunosuppressive properties.

IL-1 receptor absence in mice leads to skin cysts and changes in immune response after UVB exposure.

This study identified a high-risk allele in the PLCD1 gene associated with hereditary trichilemmal cyst formation, proposing a monoallelic two-hit mechanism as the underlying genetic pathogenesis.

This case study of a neonate with ichthyosis and ILVASC demonstrates how an interdisciplinary approach facilitated a timely genetic diagnosis and management of complications.

In this research, authors found that skin-resident ILCs regulate sebaceous gland function and microbial balance, emphasizing an immune-epithelia system that supports host-microbe symbiosis.

This study found that ICAM-1 expression in murine skin is developmentally regulated and crucial for skin and hair follicle remodeling beyond its recognized role in immune responses.

In this study, PINCH-1 gene loss in mouse epidermis led to detachment from the basement membrane, thickened skin, and hair loss, with findings suggesting PINCH-1 plays a role in keratinocyte adhesion through both ILK and EPLIN pathways.

In this study, targeted inactivation of the integrin-linked kinase gene in melanoblasts led to defects in cell migration, proliferation, and ability to populate the skin, implicating an integrin-linked kinase-Rac1 connection in melanocyte function.

In this study, researchers reported that IL-17C plays a key pro-inflammatory role in human skin diseases and may be a promising therapeutic target for inflammatory skin conditions.

In this study, researchers found that the cell surface protein Lrig1 plays a crucial role in regulating the suppressive function of regulatory T cells, suggesting it as a potential target for treating autoimmune diseases, as evidenced by experiments in mouse models.