Evidence map›Paper›PMID 36426970›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2022

CD40 Drives Central Nervous System Autoimmune Disease by Inducing Complementary Effector Programs via B Cells and Dendritic Cells.

Ying Lu, Max Xu, Cayce E Dorrier, Ray Zhang, Christian T Mayer, David Wagner, Dorian B McGavern, Richard J Hodes

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 31% of its field
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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Association ofFrontiers in microbiology · 2026
    Article
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  3. Observational
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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 at 2 institutions in 1 country.

Ying LuExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Max XuExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Cayce E DorrierViral Immunology and Intravital Imaging Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD; and.
Ray ZhangExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Christian T MayerExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD.ORCID 0000-0002-0256-9650
David WagnerDepartment of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO.ORCID 0000-0002-3853-8039
Dorian B McGavernViral Immunology and Intravital Imaging Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD; and.
Richard J HodesExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD.ORCID 0000-0002-8142-5742
National Institutes of Health · USUniversity of Colorado Anschutz Medical Campus · US

Funding

RECEPTOR MEDIATED T AND B CELL ACTIVATIONZ01BC009281 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HODES, RICHARD J. · 1996 to 2008
$1.2M
Intramural NIH HHS Z01 BC009281
6 · The paper itself

Abstract

Costimulatory CD40 plays an essential role in autoimmune diseases, including experimental autoimmune encephalomyelitis (EAE), a murine model of human multiple sclerosis (MS). However, how CD40 drives autoimmune disease pathogenesis is not well defined. Here, we used a conditional knockout approach to determine how CD40 orchestrates a CNS autoimmune disease induced by recombinant human myelin oligodendrocyte glycoprotein (rhMOG). We found that deletion of CD40 in either dendritic cells (DCs) or B cells profoundly reduced EAE disease pathogenesis. Mechanistically, CD40 expression on DCs was required for priming pathogenic Th cells in peripheral draining lymph nodes and promoting their appearance in the CNS. By contrast, B cell CD40 was essential for class-switched MOG-specific Ab production, which played a crucial role in disease pathogenesis. In fact, passive transfer of MOG-immune serum or IgG into mice lacking CD40 on B cells but not DCs reconstituted autoimmune disease, which was associated with inundation of the spinal cord parenchyma by Ig and complement. These data demonstrate that CD40 supports distinct effector programs in B cells and DCs that converge to drive a CNS autoimmune disease and identify targets for intervention.

Indexed as

Autoimmune Diseases of the Nervous SystemCentral Nervous System DiseasesEncephalomyelitis, Autoimmune, ExperimentalAnimalsCD40 AntigensDendritic CellsHumansLymphocyte CountMiceCD40 Antigens

Identifiers

PMID36426970
PMCPMC10065987
OpenAlexW4306167958

What OpenQuestion holds

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Registered trials

None linked

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.