research Lack of response of alopecia areata to pimecrolimus cream
Pimecrolimus cream is not effective for treating alopecia areata.
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research Anticytokine therapy, particularly anti-IFN-γ, in Th1-mediated autoimmune diseases
Blocking interferon-gamma might help treat various autoimmune diseases.
research Upadacitinib for the Treatment of Systemic Immune Co-Morbidity in One Case: Alopecia Areata, Vitiligo, Ankylosing Spondylitis, and Allergic Rhinitis-Asthma – Multifaceted Control
Upadacitinib improved multiple immune-related conditions in one patient.
research 033 IL-15 is an unexpected guardian of hair follicle immune privilege and promotes human hair growth ex vivo
IL-15 helps protect hair follicles from immune attacks and encourages hair growth.
research Immune cell regulation of the hair cycle
Immune cells affect hair growth and could lead to new hair loss treatments.
research Construction of regulatory network for alopecia areata progression and identification of immune monitoring genes based on multiple machine-learning algorithms
Researchers found four genes that could help diagnose severe alopecia areata early.
research Comparative investigation of immune-related biomarkers related to alopecia areata subtypes
Alopecia areata is linked to immune system differences, with specific biomarkers like CXCL9 and CXCL10 being key for diagnosis and potential treatment targets.
research Androgen receptor–mediated inhibition of cutaneous wound healing
Lowering testosterone speeds up wound healing in male mice.
research Immune Microenvironment of Hair Follicles in Tumor Immunotherapy
Tumor immunotherapy can cause hair loss by disrupting hair follicle immunity.
research Scarring hair follicle destruction is driven by the collapse of EGFR-protected JAK-STAT1-sensitive stem cell immune privilege
A protein called EGFR protects hair follicle stem cells, and when it's disrupted, hair follicles can be damaged, but blocking certain pathways can restore hair growth.
research TNC+ fibroblasts involve in skin inflammation via neuro-immune and interacting with T cells
TNC+ fibroblasts play a key role in skin inflammation by interacting with T cells.
research DKK1 Mediated Inhibition of Wnt Signaling in Postnatal Mice Leads to Loss of TEC Progenitors and Thymic Degeneration
Blocking Wnt signaling in young mice causes thymus shrinkage and cell loss, but recovery is possible when the block is removed.
research Moving Beyond Boundaries: Utilization of Longitudinal Exposure–Response Model for Bounded Outcome Score to Inform Decision Making in the Accelerated Drug Development Paradigm
A 50 mg daily dose of ritlecitinib is effective for alopecia areata, with temporary treatment breaks up to 6 weeks not affecting results.
research Inflammatory loops in the epithelial–immune microenvironment of the skin and skin appendages in chronic inflammatory diseases
Chronic inflammatory skin diseases are caused by disrupted interactions between skin cells and immune cells.
research Evidence for murine cutaneous immune surveillance localized to hair follicle epithelium
Hair follicles in mice help detect and respond to germs.
research Skin bacteriota ameliorates androgenetic alopecia via harmonizing skin immuno inflammatory balance
Restoring skin bacteria may help reduce hair loss.
research Ca 2+ -mediated protein citrullination regulates proliferation in the regenerating and malignant CNS
Ca²⁺-mediated protein citrullination controls cell growth in the CNS and may help treat brain tumors.
research Multiple Autoimmune Syndrome With Alopecia Universalis and Immune Thrombocytopenic Purpura
A man with four autoimmune diseases suggests a new category for multiple autoimmune syndrome.
research 1368 Does mitochondrial dysfunction drive immune privilege collapse in lichen planopilaris pathogenesis?
Mitochondrial dysfunction may contribute to chronic inflammation and immune system issues in Lichen planopilaris.
research Characterization of response of murine hair follicle-derived keratinocyte against androgen and testosterone 5α-redactase activity
Mouse hair cells respond to male hormones by growing less, and this can be stopped by certain blockers.
research EdnrB Governs Regenerative Response of Melanocyte Stem Cells by Crosstalk with Wnt Signaling
EdnrB signaling helps melanocyte stem cells regenerate and could be targeted to treat pigmentation issues.
research Integrated single-cell chromatin and transcriptomic analyses of peripheral immune cells in patients with alopecia areata
Early intervention with JAK inhibitors may prevent alopecia areata progression.
research Hair Follicle Immune Privilege Revisited: The Key to Alopecia Areata Management
Restoring hair bulb immune privilege is crucial for managing alopecia areata.
research Immune privilege and alopecia areata
Restoring immune privilege in hair follicles could help treat certain types of hair loss.
research Significant improvement with ivarmacitinib after suboptimal response to tofacitinib in severe alopecia areata: a case report and literature review
Ivarmacitinib significantly improved hair regrowth in severe alopecia areata after tofacitinib was less effective.
research The hair follicle as a neuro-immuno-endocrine organ: Implications in hair disorders and regenerative therapies
Understanding hair follicle signaling can improve hair disorder treatments.
research Influence of Immune Cells and Circulating Inflammatory Cytokines on Pathological Scars: A Mendelian Randomization Study
Immune cells and cytokines significantly affect pathological scar development.
research The IVIG treatment response in autoimmune polyendocrine syndromes type 2 with anti-GAD65 antibody-associated stiff person syndrome: a case report and literature review
IVIG therapy significantly improved symptoms in a patient with APS-2 and SPS.
research Immune niches for hair follicle development and homeostasis
Immune cells are crucial for hair growth and preventing hair loss.
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.