Background: Alopecia areata (AA) is an autoimmune disorder characterized by non-scarring hair loss. Janus kinase inhibitors (JAKi), such as baricitinib, show therapeutic benefit; however, the underlying mechanisms and reliable predictors of response remain insufficiently defined. Methods: In this real-world study, 74 Chinese patients with severe AA received baricitinib for up to 36 weeks. Clinical outcomes were assessed by Severity of Alopecia Tool (SALT) scores. Serum from 51 patients and 22 healthy controls underwent Olink proteomics; candidate biomarkers were validated by ELISA. Results: At week 24, 45.9% achieved SALT20 (responders), 21.6% met SALT 30 (partial responders), and 32.4% failed to reach SALT 30 (non-responders); by week 36, 56.8% achieved SALT20. Proteomics revealed elevation of Th1/Th2/Th17-axis cytokines, common γ-chain (γc) cytokines, growth factors, and GDNF-family ligands in AA, with responders showing broad cytokine suppression after treatment. Patients with longer disease duration, higher baseline SALT, and AT/AU or ophiasis type were significantly over represented among non-responders. These patients also exhibited a low proinflammatory profile and poorer prognosis, collectively defining a chronic, treatment-resistant state. Plasma CCL11 decreased stepwise from responders to non-responders and discriminated non-responders with high predictive accuracy, indicating it to be a precise biomarker of this chronic, treatment-resistant state. Conclusions: Baricitinib demonstrated robust efficacy and safety in severe AA. The data delineate a chronic, treatment-resistant phenotype characterized by low proinflammatory profile with impaired hair regrowth, in which JAKi responses are limited. These findings support earlier therapeutic intervention to avoid transition to refractoriness and identified CCL11 as a biomarker to guide timely, personalized treatment strategies.