Evidence map›Paper›PMID 25336168›Full record

ArticleMucosal immunology2015

Visualization of the entire differentiation process of murine M cells: suppression of their maturation in cecal patches.

S Kimura, M Yamakami-Kimura, Y Obata, K Hase, H Kitamura, H Ohno, T Iwanaga

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed, 71 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

7 authors at 5 institutions in 1 country.

S Kimura1] Laboratory of Histology and Cytology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan [2] Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Kanagawa, Japan.
M Yamakami-KimuraLaboratory of Histology and Cytology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Y Obata1] Laboratory for Immune Regulation, Graduate School of Medicine, Chiba University, Chiba, Japan [2] Division of Mucosal Barriology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
K Hase1] Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Kanagawa, Japan [2] Division of Mucosal Barriology, Institute of Medical Science, University of Tokyo, Tokyo, Japan [3] PRESTO, Japan Science and Technology Agency, Tokyo, Japan [4] Department of Biochemistry, Faculty of Pharmacy, Keio University, Tokyo, Japan.
H KitamuraDepartment of Veterinary Physiology, School of Veterinary Medicine, Rakuno Gakuen University, Hokkaido, Japan.
H Ohno1] Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Kanagawa, Japan [2] Division of Immunobiology, Department of Supramolecular Biology, Graduate School of Nanobioscience, Yokohama City University, Yokohama, Japan.
T IwanagaLaboratory of Histology and Cytology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Hokkaido University · JPChiba University · JPRakuno Gakuen University · JPRIKEN Center for Integrative Medical Sciences · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The microfold (M) cell residing in the follicle-associated epithelium is a specialized epithelial cell that initiates mucosal immune responses by sampling luminal antigens. The differentiation process of M cells remains unclear due to limitations of analytical methods. Here we found that M cells were classified into two functionally different subtypes based on the expression of Glycoprotein 2 (GP2) by newly developed image cytometric analysis. GP2-high M cells actively took up luminal microbeads, whereas GP2-negative or low cells scarcely ingested them, even though both subsets equally expressed the other M-cell signature genes, suggesting that GP2-high M cells represent functionally mature M cells. Further, the GP2-high mature M cells were abundant in Peyer's patch but sparse in the cecal patch: this was most likely due to a decrease in the nuclear translocation of RelB, a downstream transcription factor for the receptor activator of nuclear factor-κB signaling. Given that murine cecum contains a protrusion of beneficial commensals, the restriction of M-cell activity might contribute to preventing the onset of any excessive immune response to the commensals through decelerating the M-cell-dependent uptake of microorganisms.

Indexed as

Immunity, MucosalAnimalsCecumCell DifferentiationCell LineageChemokines, CCCytokinesEpithelial CellsGene Expression RegulationGPI-Linked ProteinsIntestinal MucosaMacrophage Inflammatory ProteinsMiceMice, Inbred BALB CMice, Inbred C57BLMicrobiotaCcl9 protein, mouseChemokines, CCCytokinesGp2 protein, mouseGPI-Linked ProteinsMacrophage Inflammatory ProteinsM-sec protein, mouseNF-kappa BPglyrp1 protein, mouseRANK LigandReceptor Activator of Nuclear Factor-kappa BRelb protein, mouseTnfrsf11a protein, mouseTnfsf11 protein, mouseTranscription Factor RelBTumor Necrosis Factors

Identifiers

PMID25336168
OpenAlexW2045802581

What OpenQuestion holds

Textmetadata
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.