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This study found that the succinate receptor, GPR91, plays a crucial role in the progression of androgenetic alopecia by affecting the immune system and hair follicle biology, and targeting it may offer new therapeutic strategies.

In this study, researchers found that children with alopecia areata exhibited immune system imbalances, including increased autoimmune and allergic markers and decreased phagocytic activity, along with a higher prevalence of autoimmune thyroiditis and allergic rhinitis compared to children without alopecia.

This study found that in mice, hyper-activated JAK-STAT1 signaling due to EGFR inhibitor treatment leads to scarring alopecia, but JAK1/2 inhibition can restore hair follicle immune privilege and promote new hair growth.

Removing GRK2 in skin cells causes hair loss similar to immune-related alopecia.

This study reported that COVID-19 patients treated with nirmatrelvir/ritonavir had lower anti-spike IgG levels and different cytokine patterns compared to those not receiving antiviral treatment, suggesting early antiviral use may alter immune response by reducing viral load and antigen presentation.

This study demonstrated that disrupting EGFR signaling in mice leads to immune sensitivity compromising the hair follicle's protective environment, but JAK1/2 inhibition can restore this immune privilege and stimulate hair growth, suggesting a potential therapy for scarring hair loss diseases like cicatricial alopecia.

This study constructed a comprehensive atlas of prenatal human skin, revealing that innate immune cells, such as macrophages, play a crucial role in skin morphogenesis by interacting with non-immune cells, influencing hair follicle formation and angiogenesis beyond their traditional immune functions.

In this animal study, the researchers found that biodegradable extracellular matrix scaffolds accelerated wound healing and enhanced hair follicle neogenesis in mice, suggesting a role for immune systems in tissue regeneration.

This study found increased infiltration of specific immune cells, such as γδ T cells and CD8+ T cells, in the bald scalp of male androgenetic alopecia patients, and identified four key immune-related genes potentially involved in hair loss development through interferon-γ signaling pathways.

This study found that TNC + fibroblasts are crucial in neuro-immune interactions in various skin diseases, particularly inflammation and tumors, by engaging extensively with immune cells and overexpressing inflammatory genes, suggesting their significant role in skin abnormalities.

This source reports that JAK inhibitors, commonly used in rheumatology, are being explored as new treatment options for autoimmune-driven hair loss, while new understanding of mechanisms is aiding research into androgenic alopecia.

In this study, researchers observed that Melan A, a melanocytic marker, was significantly expressed in hair follicles of alopecia areata patients and correlated with immune infiltrates, suggesting melanocytes might contribute to the autoimmune response in this condition.

This research observed that EGFR activity appears to maintain hair follicle quiescence and immune privilege, and its inhibition may lead to stem cell apoptosis and scarring alopecia during inflammation.

This study found that in an ex vivo model simulating alopecia areata, the DHODH inhibitor farudodstat reduced T-cell proliferation and MHC protein expression in hair follicles, suggesting it may protect against immune privilege collapse without cytotoxic effects.

This study reported that in mouse models, deletion of EGFR resulted in stem cell hyper-proliferation followed by apoptosis, leading to scarring alopecia, and implicated EGFR's role in maintaining hair follicle quiescence and immune privilege during inflammation.

This study found that deleting Ube2n in adult mouse skin leads to inflammation and other skin changes, and identifies IRAK1/4 as potential treatment targets for inflammatory skin disorders.

This study reports that CD200R expression is significantly reduced in an experimental mouse model of scarring alopecia, suggesting a potential role for this pathway in immune regulation and hair follicle protection.

This research developed new in vitro models for high-throughput screening of drugs that could protect or restore immune privilege in hair follicles, finding that Tofacitinib was effective in preventing inflammation-related marker upregulation, while Tacrolimus and αMSH worked specifically in outer root sheath keratinocytes.

In ex vivo organ culture of human scalp hair follicles, this study found that IL-9 signaling inhibits hair growth, reduces progenitor cell generation, and disrupts immune privilege.

This study observed that dandruff is linked to a weakened immunoprivilege in hair follicles, with reduced Langerhans cells and increased epidermal CD4+ and CD8+ T cell infiltration.

This study implicates EGFR as a critical regulator of immune privilege and stem cell quiescence in hair follicles, suggesting a link between EGFR inhibition and inflammation-driven hair loss during cancer therapy.

This study reported that IL-15 promotes human hair growth and protects hair follicle immune privilege, potentially stabilizing alopecia areata treatment outcomes when selectively stimulating IL-15Rα signaling.

In this case study, a 26-year-old female with PLEC mutations and features of muscular dystrophy and myasthenia gravis showed significant improvement in symptoms following steroid treatment.

This study found that a TYK2 inhibitor, BMS-986202, may restore immune privilege in hair follicles and promote hair regrowth in a humanized alopecia areata mouse model by inhibiting IL-12-mediated signaling.

This study found that epidermal growth factor receptor inhibitors used in cancer treatment induce a distinct inflammatory response in hair follicles, marked by immune privilege collapse and upregulation of inflammatory pathways.

This report describes a case of a patient with metastatic renal cell carcinoma who developed a psoriasiform skin lesion while undergoing immune checkpoint inhibitor therapy.

This review highlights the urgent need for increased research and policy support for autoimmune and immune-mediated skin diseases, which are on the rise and disproportionately affect women's health in the United States, suggesting a focus on gender and socioenvironmental factors.

This study found that the loss of papillary fibroblasts in the skin due to UV radiation is mainly caused by an uncontrolled inflammatory response, with T cells helping fibroblast survival.

This study suggests that a third Covid-19 vaccine dose is necessary to maintain protection, especially among immune-compromised individuals and those with comorbidities, emphasizing the urgent need for vaccine access in less developed regions.

This study found that interleukin-12 signals play a role in hair follicle immune privilege collapse in ex vivo alopecia areata models, and a TYK2 inhibitor may help prevent or reverse this process.