Figure 1 Clinical findings and CNS immunoreactivity of CSF IgA of a patient with limbic encephalitis (A) Cranial MRI of a 69-year-old man with limbic encephalitis.

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Presentation transcript:

Figure 1 Clinical findings and CNS immunoreactivity of CSF IgA of a patient with limbic encephalitis (A) Cranial MRI of a 69-year-old man with limbic encephalitis demonstrates left mesiotemporal signal hyperintensities on coronal fluid-attenuated inversion recovery sequences (arrow, see also enlarged region) at first presentation in August 2013, which progressed into hippocampal atrophy (arrow, see also enlarged region) until September 2014. Clinical findings and CNS immunoreactivity of CSF IgA of a patient with limbic encephalitis (A) Cranial MRI of a 69-year-old man with limbic encephalitis demonstrates left mesiotemporal signal hyperintensities on coronal fluid-attenuated inversion recovery sequences (arrow, see also enlarged region) at first presentation in August 2013, which progressed into hippocampal atrophy (arrow, see also enlarged region) until September 2014. (B) Repeated cognitive screening by DemTect and Mini-Mental State Examination (MMSE) show mild cognitive impairment. (C) Time course of clinical symptoms, immunotherapies, and calculated percentage of intrathecally synthesized immunoglobulin A (IgA) or immunoglobulin G (IgG) of the total IgA or IgG in CSF. (D) Fixed and permeabilized mouse hippocampus sections were stained with patient CSF at a dilution of 1:100 (left panels) and a FITC-coupled antihuman IgA secondary antibody, demonstrating strong immunoreactivity within the neuropilar regions of the cornu ammonis and dentate gyrus including a prominent signal mapping to the mossy fiber tract. Immunoreactivity of the patient's CSF IgA colocalized with that of ZnT3, a marker of glutamatergic mossy fiber terminals expressed in synaptic vesicles. Control CSF adjusted to the same IgA concentration as the patient's CSF revealed no signal (right panels). Dapi staining was used to visualize nuclei. (E) Mouse cerebellum sections were stained with patient and control CSF as described above, demonstrating binding of patient CSF IgA to the molecular layer and the granule cell layer glomeruli, but not to Purkinje cells. AZT = azathioprine; CA = cornu ammonis; Dapi = 4′,6-Diamidin-2-phenylindol; DG = dentate gyrus; gcl = granule cell layer; IVIg = IV immunoglobulin; Mf = mossy fiber tract; ml = molecular layer; pcl = Purkinje cell layer; Slm = stratum lacunosum moleculare; So = stratum oriens; Sp = stratum pyramidale; Sr = stratum radiatum. Johannes Piepgras et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e169 © 2015 American Academy of Neurology