Evidence map›Paper›PMID 36719648›Full record

ArticleThe Journal of experimental medicine2023

Myeloid-like B cells boost emergency myelopoiesis through IL-10 production during infection.

Masashi Kanayama, Yuta Izumi, Megumi Akiyama, Toyoki Hayashi, Koji Atarashi, Axel Roers, Taku Sato, Toshiaki Ohteki

Open access · hybridAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

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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 3 institutions in 2 countries.

Masashi KanayamaDepartment of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University , Tokyo, Japan.ORCID 0000-0001-8366-5275
Yuta IzumiDepartment of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University , Tokyo, Japan.ORCID 0000-0001-5816-3257
Megumi AkiyamaDepartment of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University , Tokyo, Japan.ORCID 0000-0002-8308-382X
Toyoki HayashiDepartment of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University , Tokyo, Japan.ORCID 0000-0001-8355-6407
Koji AtarashiDepartment of Microbiology and Immunology, Keio University School of Medicine , Tokyo, Japan.ORCID 0000-0001-5422-0736
Axel RoersInstitute for Immunology, Heidelberg University Hospital , Heidelberg, Germany.ORCID 0000-0003-1806-6158
Taku SatoDepartment of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University , Tokyo, Japan.ORCID 0000-0003-2801-1521
Toshiaki OhtekiDepartment of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University , Tokyo, Japan.ORCID 0000-0002-8088-5165
Tokyo Medical and Dental University · JPHeidelberg University · DEKeio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emergency myelopoiesis (EM) is a hematopoietic response against systemic infections that quickly supplies innate immune cells. As lymphopoiesis is strongly suppressed during EM, the role of lymphocytes in that process has not received much attention. Here, we found that myeloid-like B cells (M-B cells), which express myeloid markers, emerge in the bone marrow (BM) after the induction of EM. M-B cells were mainly derived from pre-B cells and preferentially expressed IL-10, which directly stimulates hematopoietic progenitors to enhance their survival and myeloid-biased differentiation. Indeed, lacking IL-10 in B cells, blocking IL-10 in the BM with a neutralizing antibody, and deleting the IL-10 receptor in hematopoietic progenitors significantly suppressed EM, which failed to clear microbes in a cecal ligation and puncture model. Thus, a distinct B cell subset generated during infection plays a pivotal role in boosting EM, which suggests the on-demand reinforcement of EM by adaptive immune cells.

Indexed as

B-LymphocytesInterleukin-10MyelopoiesisBone MarrowBone Marrow CellsHematopoiesisMyeloid CellsInterleukin-10

Identifiers

PMID36719648
PMCPMC9930167
OpenAlexW4318670722

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.