Evidence map›Paper›PMID 39325550›Full record

ArticleJCI insight2024

Dopamine receptor autoantibody signaling in infectious sequelae differentiates movement versus neuropsychiatric disorders.

Chandra M Menendez, Jonathan Zuccolo, Susan E Swedo, Sean Reim, Brian Richmand, Hilla Ben-Pazi, Abraham Kovoor, Madeleine W Cunningham

Abstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Article
  2. Cardiovascular pharmacology of dopaminergic agents in humans: a review.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2026
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Chandra M MenendezDepartment of Microbiology and Immunology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Jonathan ZuccoloDepartment of Microbiology and Immunology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Susan E SwedoIntramural Research Program of the National Institute of Mental Health, NIH, Bethesda, Maryland, USA.
Sean ReimDepartment of Microbiology and Immunology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Brian RichmandDepartment of Microbiology and Immunology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Hilla Ben-PaziDepartment of Pediatric Neurology, Shaare Zedek Medical Center, Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel.
Abraham KovoorCollege of Pharmacy, University of Rhode Island, Kingston, Rhode Island, USA.
Madeleine W CunninghamDepartment of Microbiology and Immunology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.

Funding

AUTOIMMUNE DETERMINANTS OF HUMAN CARDIAC MYOSINR01HL056267 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI COOPER, LESLIE T, CUNNINGHAM, MADELEINE W. · 1997 to 2013
$4.7M
MYOSIN--A LINK BETWEEN STREPTOCOCCI AND HEARTR37HL035280 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CUNNINGHAM, MADELEINE W. · 1999 to 2008
$3.0M
Autoimmune Determinants of Human Cardiac MyosinR56HL056267 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI COOPER, LESLIE T, CUNNINGHAM, MADELEINE W. · 2008 to 2015
$933k
NHLBI MERIT AwardNHLBI NIH HHS R01 HL056267NHLBI NIH HHS R37 HL035280NHLBI NIH HHS R56 HL056267
6 · The paper itself

Abstract

Despite growing recognition, neuropsychiatric diseases associated with infections are a major unsolved problem worldwide. Group A streptococcal (GAS) infections can cause autoimmune sequelae characterized by movement disorders, such as Sydenham chorea, and neuropsychiatric disorders. The molecular mechanisms underlying these diseases are not fully understood. Our previous work demonstrates that autoantibodies (AAbs) can target dopaminergic neurons and increase dopamine D2 receptor (D2R) signaling. However, AAb influence on dopamine D1 receptor (D1R) activity is underexplored. We found evidence that suggests GAS-induced cross-reactive AAbs promote autoimmune encephalitis of the basal ganglia, a region of high dopamine receptor density. Here, we report a mechanism whereby neuropsychiatric syndromes are distinguished from movement disorders by differences in D1R and D2R AAb titers, signaling, receiver operating characteristic curves, and immunoreactivity with D1R and D2R autoreactive epitopes. D1R AAb signaling was observed through patient serum AAbs and novel patient-derived monoclonal antibodies (mAbs), which induced both D1R G protein- and β-arrestin-transduced signals. Furthermore, patient AAbs and mAbs enhanced D1R signaling mechanisms mediated by the neurotransmitter dopamine. Our findings suggest that AAb-mediated D1R signaling may contribute to the pathogenesis of neuropsychiatric sequelae and inform new options for diagnosis and treatment of GAS sequelae and related disorders.

Indexed as

AutoantibodiesReceptors, Dopamine D1Receptors, Dopamine D2Signal TransductionStreptococcal InfectionsAdultAutoimmune DiseasesChoreaDopaminergic NeuronsFemaleHumansMaleMental DisordersMovement DisordersStreptococcus pyogenesAutoantibodiesDRD1 protein, humanDRD2 protein, humanReceptors, Dopamine D1Receptors, Dopamine D2Autoimmune diseasesAutoimmunityImmunologyNeurological disordersPsychiatric diseases

Identifiers

PMID39325550
PMCPMC11601707

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.