ArticleFrontiers in immunology2026
CCL22-producing macrophages are associated with Th1-related sweat duct inflammation in acquired idiopathic generalized anhidrosis.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Acquired idiopathic generalized anhidrosis (AIGA) is a rare disorder characterized by generalized loss of sweating without identifiable causes. Because few biomarkers reflect its underlying mechanisms, diagnosis at the initial visit is often difficult. Although steroid pulse therapy is widely used, approximately half of patients respond insufficiently. We therefore aimed to elucidate the immune mechanisms underlying AIGA and identify potential biomarkers for diagnosis and treatment response. Methods: Fourteen patients with AIGA affecting more than 25% of body surface area were enrolled after exclusion of secondary causes of anhidrosis. Serum levels of 40 cytokines and chemokines were quantified using a multiplex assay and correlated with clinical parameters. Skin biopsy specimens were analyzed by histology and immunohistochemistry to characterize inflammatory cell infiltration and identify cellular sources of selected mediators. Results: Inflammatory cell infiltration was consistently observed around sweat ducts, predominantly composed of CD4 Conclusions: These findings suggest that AIGA involves a macrophage-CCL22-Th1-IFN-γ inflammatory axis associated with collapse of sweat duct immune privilege. Serum MIF may serve as a potential biomarker for predicting steroid responsiveness.
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