ReviewFrontiers in medicine2026
Hair follicle immune privilege in autoimmune and immune-mediated alopecias: paths toward reestablishing immune tolerance.
Review in Frontiers in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Engineering immune-competent hair follicle microphysiological systems: from organoid assembly to dynamic immune modelling.Frontiers in bioengineering and biotechnology · 2026Review
- Unraveling the autoimmune architecture of pemphigus: from B-cell depletion to network-based immune engineering.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Autoimmune and immune-mediated alopecias demonstrate how a site-specific failure of immune privilege can produce reversible or irreversible hair loss. In alopecia areata (AA), cytotoxic injury is concentrated at the anagen bulb but preserves the stem cell pool, permitting regrowth following immune suppression. Lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) feature a spectrum of chronic interface dermatitis that destroys the stem cell niche, leading to permanent fibrosis. These entities overlap in bulge-targeted inflammation and histopathology but diverge in clinical distribution and demographic risk. Discoid lupus erythematosus (DLE) of the scalp reflects immune-complex-driven complement injury to the upper follicle, whereas central centrifugal cicatricial alopecia (CCCA) represents a fibroblast-dominant process associated with chronic stress and is sustained by stromal remodeling. Here, we frame these entities as four follicular immune network archetypes defined by the axial locus of immune privilege collapse, effector programs, loss of tolerogenic programs, stromal trajectories, and dermoscopic correlates. Using a Network Engineering for Site-Specific Tolerance (NEST) framework, we situate these archetypes within a three-tier taxonomy comprising intrinsic follicular privilege, local tolerogenic repertoires, and stromal checkpoint circuits. Specifically, AA localizes to the anagen bulb, DLE spans the upper follicle and interfollicular epidermis, LPP/FFA targets the bulge stem cell niche, and CCCA converges on the upper follicle-interfollicular epidermis unit. Within their respective niches, AA and DLE exhibit comparatively resolved clonotypic effector modules dominated by pathogenic T cells or B cells, whereas LPP/FFA and CCCA are framed as polyclonal networks in which the failure of tolerogenic programs or stress signaling pathways constitutes the dominant archetypal engine.
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