research Involvement of ILC1-like innate lymphocytes in human autoimmunity, lessons from alopecia areata
ILC1-like cells can independently cause alopecia areata.
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30 / 49 resultsresearch Author response: Involvement of ILC1-like innate lymphocytes in human autoimmunity, lessons from alopecia areata
ILC1-like cells may contribute to hair loss in alopecia areata.
research Editor's evaluation: Involvement of ILC1-like innate lymphocytes in human autoimmunity, lessons from alopecia areata
ILC1-like cells can independently cause alopecia areata by affecting hair follicles.
research Decision letter: Involvement of ILC1-like innate lymphocytes in human autoimmunity, lessons from alopecia areata
ILC1-like cells may contribute to hair loss in alopecia areata and could be new treatment targets.
research Involvement of ILC1-like innate lymphocytes in human autoimmunity, lessons from alopecia areata
ILC1-like cells can cause alopecia areata by attacking hair follicles.
research LB708 ILC1-like innate lymphocytes in human autoimmunity: Lessons from Alopecia Areata
ILC1-like cells can cause alopecia areata by disrupting hair follicle immunity, suggesting a new treatment approach.
research 331 Mitochondrial stress contributes to atopic dermatitis
Mitochondrial stress can lead to atopic dermatitis.
research 328 The transcription factor CEBPB is a novel hub gene and multi-functional disease driver in Psoriatic skin inflammation
ILC1-like cells can cause alopecia areata by themselves.
research 332 OTULIN maintains skin homeostasis by controlling keratinocyte death and stem cell identity
ILC1-like cells can cause alopecia areata by affecting hair follicles.
research 431 Innate lymphoid cells type 1 may be new, non-antigen-specific player in the pathogenesis of alopecia areata
Innate lymphoid cells type 1 may contribute to alopecia areata.
research 516 Possible role of ILC1 in the pathogenesis of alopecia areata (AA)
ILC1 cells contribute to hair loss in alopecia areata.
research 937 Disruption of the innate lymphoid cell network alters the hair cycle during induced anagen
Removing certain immune cells in mice causes their hair to enter the growth phase earlier than usual.
research Immune Cells in Cutaneous Wound Healing: A Review of Functional Data from Animal Models
Different immune cells like platelets, mast cells, neutrophils, macrophages, T cells, B cells, and innate lymphoid cells all play roles in skin wound healing, but more research is needed due to inconsistent results and the complex nature of the immune response.
research Immunological control of skin development: from homeostasis to developmental pathologies
Immune cells are crucial for normal skin development and their dysfunction can cause skin disorders.
research Decreased GATA3 levels cause changed mouse cutaneous innate lymphoid cell fate, facilitating hair follicle recycling
Lower GATA3 levels in mice help hair regrow by changing certain immune cells.
research A comparative analysis of immune privilege in pregnancy and cancer in the context of checkpoint blockade immunotherapy
The document concludes that pregnancy and cancer share immune evasion tactics, but more research is needed before using checkpoint blockade immunotherapy in pregnant cancer patients to avoid harm to the placenta.
research Sebaceous immunobiology - skin homeostasis, pathophysiology, coordination of innate immunity and inflammatory response and disease associations
Sebaceous glands play a key role in skin health, immunity, and various skin diseases.
research Understanding Type 3 Innate Lymphoid Cells and Crosstalk with the Microbiota: A Skin Connection
Type 3 Innate Lymphoid Cells help maintain skin health and balance, and are involved in skin diseases and healing.
research IL-15 Prolongs Anagen, Stimulates Proliferation, and Suppresses Apoptosis in the Hair Matrix of Human Scalp Hair Follicles
IL-15 helps hair grow longer and stronger by extending the growth phase and reducing cell death.
research 080 Mouse models of alopecia areata: C3H/HeJ mice versus the humanized AA mouse model
The humanized AA mouse model is better for testing new alopecia areata treatments.
research From mechanisms to therapies: current advances breakthroughs in alopecia areata immunopathology
JAK inhibitors are effective for treating moderate-to-severe alopecia areata.
research Maintenance of Barrier Tissue Integrity by Unconventional Lymphocytes
Unconventional lymphocytes are important for quick immune responses and healing of skin and mucosal barriers.
research Pathogenesis of Alopecia Areata and Vitiligo: Commonalities and Differences
Alopecia areata and vitiligo share immune system dysfunction but differ in specific immune responses and affected areas.
research Translational research in the generation of therapeutic medicine for wound healing: a review
New therapies show promise for wound healing, but more research is needed for safe, affordable options.
research How the Innate Lymphoid Cells Improved Our Understanding of the Mechanisms of Allergic Diseases and Influenced the Standpoint?
Innate lymphoid cells help us understand and manage allergic diseases better.
research Sphingolipid metabolism orchestrates the establishment of the adult hair follicle stem cell niche to control skin homeostasis
A specific enzyme is essential for proper hair follicle stem cell development and healthy skin.
research Epidermal Notch1 recruits RORγ+ group 3 innate lymphoid cells to orchestrate normal skin repair
Notch1 helps skin heal by attracting specific immune cells.
research The developing immune network in human prenatal skin
Human prenatal skin develops an immune network early on that helps with skin formation and healing without scarring.
research Updates In The Pathogenesis Of Alopecia Areata
Alopecia areata is an autoimmune condition causing hair loss, linked to genetic factors and immune system issues, with no cure yet.
research What’s Sex Got to Do With COVID-19? Gender-Based Differences in the Host Immune Response to Coronaviruses
Men generally have more severe COVID-19 cases and higher death rates than women due to biological differences.