PMID- 34560071
OWN - NLM
STAT- MEDLINE
DCOM- 20211129
LR  - 20211129
IS  - 1872-7905 (Electronic)
IS  - 0022-1759 (Linking)
VI  - 499
DP  - 2021 Dec
TI  - Evaluation of the concordance between GluN1-GluN2 heteromer live-cell-based assay 
      and GluN1 monomer biochip kit assay on anti-NMDAR autoantibody detection.
PG  - 113150
LID - S0022-1759(21)00195-2 [pii]
LID - 10.1016/j.jim.2021.113150 [doi]
AB  - Anti-N-methyl-d-aspartate receptor (NMDAR) antibodies are most frequently 
      detected in autoantibody-related autoimmune encephalitis. Anti-NMDAR encephalitis 
      mainly affects young women with ovarian teratoma, including acute to subacute 
      onset of psychosis, seizures, consciousness disturbance, dyskinetic involuntary 
      movements, autonomic dysfunction, and others. Diagnosis is based on the detection 
      of anti-NMDAR autoantibodies in cerebrospinal fluid (CSF). The autoantibody 
      recognizes the conformational epitope of the NMDA receptor. NMDA receptors 
      contain hetero-tetramers of GluN1 (NR1) and GluN2/3 (NR2/3), in which GluN1 is 
      essential to form functional receptors on the synaptic membrane in the brain. 
      Thus, the autoantibodies are detected using neurons or culture cells expressing 
      conformational receptors on their cell membrane, the natural form in the brain. 
      The antibodies detected using artificial GluN1 monosubunit expressing cells as 
      the antigens have been widely used for anti-NMDAR-antibody test. In the present 
      study two detection systems were compared, a live-cell-based assay using human 
      embryonic kidney (HEK) 293 cells expressing both of GluN1 and GluN2B, and a 
      commercially available GluN1-monotransfected HEK cell biochip system. As the 
      result, both the methods were equivalent, and the clinical features of both 
      groups were similar, suggesting both tests have equal clinical significance.
CI  - Copyright (c) 2021 Elsevier B.V. All rights reserved.
FAU - Tanaka, Keiko
AU  - Tanaka K
AD  - Department of Life Science, Medical Research Institute, Kanazawa Medical 
      University, Kanazawa, Japan; Department of Animal Model Development, Brain 
      Research Institute, Niigata University, Niigata, Japan; Department of Multiple 
      Sclerosis Therapeutics, Fukushima Medical University, School of Medicine, 
      Fukushima, Japan. Electronic address: k-tana28@bri.niigata-u.ac.jp.
FAU - Kitagawa, Yoko
AU  - Kitagawa Y
AD  - Department of Life Science, Medical Research Institute, Kanazawa Medical 
      University, Kanazawa, Japan.
FAU - Hori, Kiyoe
AU  - Hori K
AD  - Department of Life Science, Medical Research Institute, Kanazawa Medical 
      University, Kanazawa, Japan.
FAU - Kinoshita, Masako
AU  - Kinoshita M
AD  - Department of Neurology, National Hospital Organization, Utano National Hospital, 
      Kyoto, Japan.
FAU - Tanaka, Masami
AU  - Tanaka M
AD  - MS Center, Kyoto Min-Iren Chuo Hospital, Uzumasa, Kyoto, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210922
PL  - Netherlands
TA  - J Immunol Methods
JT  - Journal of immunological methods
JID - 1305440
RN  - 0 (Autoantibodies)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
SB  - IM
MH  - Adult
MH  - Autoantibodies/*analysis/cerebrospinal fluid/immunology
MH  - Female
MH  - HEK293 Cells
MH  - Humans
MH  - Male
MH  - Receptors, N-Methyl-D-Aspartate/immunology
OTO - NOTNLM
OT  - Autoantibody
OT  - BIOCHIP mosaics
OT  - Cell-based assay
OT  - GluN1 and GluN2B-heteromer detection
OT  - GluN1-monomer detection
OT  - NMDAR
EDAT- 2021/09/25 06:00
MHDA- 2021/11/30 06:00
CRDT- 2021/09/24 20:13
PHST- 2021/05/06 00:00 [received]
PHST- 2021/08/04 00:00 [revised]
PHST- 2021/09/15 00:00 [accepted]
PHST- 2021/09/25 06:00 [pubmed]
PHST- 2021/11/30 06:00 [medline]
PHST- 2021/09/24 20:13 [entrez]
AID - S0022-1759(21)00195-2 [pii]
AID - 10.1016/j.jim.2021.113150 [doi]
PST - ppublish
SO  - J Immunol Methods. 2021 Dec;499:113150. doi: 10.1016/j.jim.2021.113150. Epub 2021 
      Sep 22.