2026-05-28 イェール大学
＜関連情報＞
- https://news.yale.edu/2026/05/28/yale-study-links-some-long-covid-patients-autoimmune-responses
- https://www.cell.com/cell/abstract/S0092-8674(26)00509-X
長期COVIDにおける自己抗体と神経症状との因果関係 A causal link between autoantibodies and neurological symptoms in long COVID
Keyla Santos Guedes de Sá ∙ Julio Silva ∙ Rafael Bayarri-Olmos ∙ … ∙ David Putrino ∙ Tamas L. Horvath ∙ Akiko Iwasaki
Cell Published: May 28, 2026
DOI:https://doi.org/10.1016/j.cell.2026.04.042
Graphical abstract
Highlights
- Long COVID features autoantibodies targeting neural and vascular tissues
- Patients’ IgG shows increased ADCP activity against MED20
- Passive transfer of IgG induces pain and fatigue-like phenotypes in mice
- Mouse pain behavior after IgG transfer correlates with patient-reported chronic pain
Summary
Acute SARS-CoV-2 infection triggers the de novo production of diverse, functional autoantibodies (AABs) that remain elevated in long COVID (LC), but their pathogenic role remains unclear. Using tissue-based immunofluorescence, ELISA, human protein array, and mass spectrometry assays, we identified a broad range of AAB targets among individuals with LC. Individuals with neurocognitive symptoms showed increased AABs against central nervous system (CNS) and peripheral nervous system proteins. Purified immunoglobulin G (IgG) reacted with human locus coeruleus, thalamus, adrenal gland, and thyroid and cross-reacted with mouse sciatic nerve and meninges. CNS-reactive AABs correlated with several neurological symptoms. MED20-targeting IgG from patients with LC showed enhanced antibody-dependent phagocytosis. Passive transfer of IgG from individuals with LC into mice induced fatigue-like behavior, loss of balance/coordination, thermal hyperalgesia, small fiber nerve damage, and increased pain-related neuronal activity, recapitulating patients’ symptoms. These findings suggest that targeting AABs might offer therapeutic benefits for this LC subgroup.
