{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T11:19:01Z","timestamp":1788261541285,"version":"build-2803163510"},"reference-count":160,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Autoimmune encephalitis (AE) is an antibody-mediated brain disorder involving self-antibody-driven inflammation. Different subtypes present unique clinical and pathological features, influenced by variations in target antigens and underlying pathophysiological processes. Although the precise pathogenesis of each AE subtype remains incompletely understood, recent research has provided valuable insights into their immunopathological mechanisms. This article critically evaluates current discoveries regarding the immunobiology of diverse autoimmune encephalitis categories, elucidating their multifaceted etiological pathways. 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