Andreas Schulte-Mecklenbeck , Andre Dik , Christine Strippel , Laura Bierhansl , Niklas Meyer , Lisanne Korn , Matthias Pawlowski , Saskia Räuber , Judith Alferink , Sven G Meuth , Nico Melzer , Gerd Meyer zu Hörste , Harald Prüß , Heinz Wiendl , Catharina C. Gross , Stjepana Kovac
{"title":"脑脊液和血液特征支持边缘脑炎亚型的分类。","authors":"Andreas Schulte-Mecklenbeck , Andre Dik , Christine Strippel , Laura Bierhansl , Niklas Meyer , Lisanne Korn , Matthias Pawlowski , Saskia Räuber , Judith Alferink , Sven G Meuth , Nico Melzer , Gerd Meyer zu Hörste , Harald Prüß , Heinz Wiendl , Catharina C. Gross , Stjepana Kovac","doi":"10.1016/j.bbi.2024.10.018","DOIUrl":null,"url":null,"abstract":"<div><div>Autoimmune limbic encephalitis (ALE) represents a heterogeneous disease associated with antibodies targeting extracellular (ALE<sub>extra</sub>) epitopes, intracellular (ALE<sub>intra</sub>) epitopes, anti-glutamic acid decarboxylase65 ALE (ALE<sub>GAD65</sub>), and ALE without detectable antibodies (ALE<sub>abneg</sub>). Combining analysis of cellular parameters, investigated by flow cytometry, and soluble parameters in the blood and cerebrospinal fluid (CSF) from a large cohort of 148 ALE patients (33 ALE<sub>extra</sub>, 12 ALE<sub>intra</sub>, 28 ALE-GAD65, 37 ALE<sub>abneg</sub>) in comparison to paradigmatic examples for neuro-inflammatory (51 relapsing remitting MS patients (RRMS)), and neuro-degenerative (34 Alzheimer’s disease patients (AD)) diseases revealed discrete immune signatures in ALE subgroups. Identification of ALE-subtype specific markers facilitated classification of rare ALE-associated tumors, which may prompt further diagnostic efforts in clinical practice. While ALE<sub>intra</sub> exhibited features of neuro-inflammation, ALE<sub>extra</sub> displayed features of neuro-inflammation as well as neuro-degeneration. Moreover, ALE<sub>GAD65</sub> and ALE<sub>abneg</sub> lacked hallmarks of inflammation. This may explain the low efficacy of anti-inflammatory treatment regimens in ALE<sub>GAD65</sub> and presumably also ALE<sub>abneg</sub>.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"123 ","pages":"Pages 697-706"},"PeriodicalIF":8.8000,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"CSF and blood signatures support classification of limbic encephalitis subtypes\",\"authors\":\"Andreas Schulte-Mecklenbeck , Andre Dik , Christine Strippel , Laura Bierhansl , Niklas Meyer , Lisanne Korn , Matthias Pawlowski , Saskia Räuber , Judith Alferink , Sven G Meuth , Nico Melzer , Gerd Meyer zu Hörste , Harald Prüß , Heinz Wiendl , Catharina C. Gross , Stjepana Kovac\",\"doi\":\"10.1016/j.bbi.2024.10.018\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Autoimmune limbic encephalitis (ALE) represents a heterogeneous disease associated with antibodies targeting extracellular (ALE<sub>extra</sub>) epitopes, intracellular (ALE<sub>intra</sub>) epitopes, anti-glutamic acid decarboxylase65 ALE (ALE<sub>GAD65</sub>), and ALE without detectable antibodies (ALE<sub>abneg</sub>). Combining analysis of cellular parameters, investigated by flow cytometry, and soluble parameters in the blood and cerebrospinal fluid (CSF) from a large cohort of 148 ALE patients (33 ALE<sub>extra</sub>, 12 ALE<sub>intra</sub>, 28 ALE-GAD65, 37 ALE<sub>abneg</sub>) in comparison to paradigmatic examples for neuro-inflammatory (51 relapsing remitting MS patients (RRMS)), and neuro-degenerative (34 Alzheimer’s disease patients (AD)) diseases revealed discrete immune signatures in ALE subgroups. Identification of ALE-subtype specific markers facilitated classification of rare ALE-associated tumors, which may prompt further diagnostic efforts in clinical practice. While ALE<sub>intra</sub> exhibited features of neuro-inflammation, ALE<sub>extra</sub> displayed features of neuro-inflammation as well as neuro-degeneration. Moreover, ALE<sub>GAD65</sub> and ALE<sub>abneg</sub> lacked hallmarks of inflammation. This may explain the low efficacy of anti-inflammatory treatment regimens in ALE<sub>GAD65</sub> and presumably also ALE<sub>abneg</sub>.</div></div>\",\"PeriodicalId\":9199,\"journal\":{\"name\":\"Brain, Behavior, and Immunity\",\"volume\":\"123 \",\"pages\":\"Pages 697-706\"},\"PeriodicalIF\":8.8000,\"publicationDate\":\"2024-10-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Brain, Behavior, and Immunity\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0889159124006585\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain, Behavior, and Immunity","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0889159124006585","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
CSF and blood signatures support classification of limbic encephalitis subtypes
Autoimmune limbic encephalitis (ALE) represents a heterogeneous disease associated with antibodies targeting extracellular (ALEextra) epitopes, intracellular (ALEintra) epitopes, anti-glutamic acid decarboxylase65 ALE (ALEGAD65), and ALE without detectable antibodies (ALEabneg). Combining analysis of cellular parameters, investigated by flow cytometry, and soluble parameters in the blood and cerebrospinal fluid (CSF) from a large cohort of 148 ALE patients (33 ALEextra, 12 ALEintra, 28 ALE-GAD65, 37 ALEabneg) in comparison to paradigmatic examples for neuro-inflammatory (51 relapsing remitting MS patients (RRMS)), and neuro-degenerative (34 Alzheimer’s disease patients (AD)) diseases revealed discrete immune signatures in ALE subgroups. Identification of ALE-subtype specific markers facilitated classification of rare ALE-associated tumors, which may prompt further diagnostic efforts in clinical practice. While ALEintra exhibited features of neuro-inflammation, ALEextra displayed features of neuro-inflammation as well as neuro-degeneration. Moreover, ALEGAD65 and ALEabneg lacked hallmarks of inflammation. This may explain the low efficacy of anti-inflammatory treatment regimens in ALEGAD65 and presumably also ALEabneg.
期刊介绍:
Established in 1987, Brain, Behavior, and Immunity proudly serves as the official journal of the Psychoneuroimmunology Research Society (PNIRS). This pioneering journal is dedicated to publishing peer-reviewed basic, experimental, and clinical studies that explore the intricate interactions among behavioral, neural, endocrine, and immune systems in both humans and animals.
As an international and interdisciplinary platform, Brain, Behavior, and Immunity focuses on original research spanning neuroscience, immunology, integrative physiology, behavioral biology, psychiatry, psychology, and clinical medicine. The journal is inclusive of research conducted at various levels, including molecular, cellular, social, and whole organism perspectives. With a commitment to efficiency, the journal facilitates online submission and review, ensuring timely publication of experimental results. Manuscripts typically undergo peer review and are returned to authors within 30 days of submission. It's worth noting that Brain, Behavior, and Immunity, published eight times a year, does not impose submission fees or page charges, fostering an open and accessible platform for scientific discourse.