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In this mouse study, the researchers found that the monoclonal antibody ME1 causes hair follicle inflammation by up-regulating TNFα, which can be reduced by TNFα and interleukin-1 inhibitors.

This study found that intracellular Toll-like receptors were significantly up-regulated in peripheral blood mononuclear cells of alopecia areata patients, suggesting a potential role in inflammatory signaling and pathogenesis.

This study found that IL-1 alpha inhibits the growth of cultured human hair follicles and hair fibers, suggesting a potential role in inflammatory hair loss conditions like alopecia areata.

This study suggests that frontal fibrosing alopecia is a highly inflammatory disease involving TH1 and JAK-STAT pathways, without reduced hair keratins, highlighting JAK-STAT signaling as a potential therapeutic target.

Copper may protect against alopecia areata, while certain inflammatory markers increase risk.