Evidence map›Paper›PMID 35960733›Full record

ArticlePloS one2022

A high-quality severe combined immunodeficiency (SCID) rat bioresource.

Yoshiki Miyasaka, Jinxi Wang, Kosuke Hattori, Yuko Yamauchi, Miho Hoshi, Kazuto Yoshimi, Saeko Ishida, Tomoji Mashimo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Mammalian genome research resources available from the National BioResource Project in Japan.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
    Review
  9. Review
  10. Article
  11. Frontiers in cardiovascular medicine · 2023
    Article
  12. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Yoshiki MiyasakaInstitute of Experimental Animal Sciences, Graduate School of Medicine, Osaka University, Suita City, Osaka, Japan.ORCID 0000-0003-4020-9290
Jinxi WangInstitute of Experimental Animal Sciences, Graduate School of Medicine, Osaka University, Suita City, Osaka, Japan.
Kosuke HattoriInstitute of Experimental Animal Sciences, Graduate School of Medicine, Osaka University, Suita City, Osaka, Japan.
Yuko YamauchiInstitute of Experimental Animal Sciences, Graduate School of Medicine, Osaka University, Suita City, Osaka, Japan.
Miho HoshiDivision of Animal Genetics, Laboratory Animal Research Center, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Kazuto YoshimiInstitute of Experimental Animal Sciences, Graduate School of Medicine, Osaka University, Suita City, Osaka, Japan.
Saeko IshidaDivision of Animal Genetics, Laboratory Animal Research Center, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Tomoji MashimoInstitute of Experimental Animal Sciences, Graduate School of Medicine, Osaka University, Suita City, Osaka, Japan.ORCID 0000-0001-7543-7301
The University of Tokyo · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunodeficient animals are valuable models for the engraftment of exogenous tissues; they are widely used in many fields, including the creation of humanized animal models, as well as regenerative medicine and oncology. Compared with mice, laboratory rats have a larger body size and can more easily undergo transplantation of various tissues and organs. Considering the absence of high-quality resources of immunodeficient rats, we used the CRISPR/Cas9 genome editing system to knock out the interleukin-2 receptor gamma chain gene (Il2rg) in F344/Jcl rats-alone or together with recombination activating gene 2 (Rag2)-to create a high-quality bioresource that researchers can freely use: severe combined immunodeficiency (SCID) rats. We selected one founder rat with frame-shift mutations in both Il2rg (5-bp del) and Rag2 ([1-bp del+2-bp ins]/[7-bp del+2-bp ins]), then conducted mating to establish a line of immunodeficient rats. The immunodeficiency phenotype was preliminarily confirmed by the presence of severe thymic hypoplasia in Il2rg-single knockout (sKO) and Il2rg/Rag2-double knockout (dKO) rats. Assessment of blood cell counts in peripheral blood showed that the white blood cell count was significantly decreased in sKO and dKO rats, while the red blood cell count was unaffected. The decrease in white blood cell count was mainly caused by a decrease in lymphocytes. Furthermore, analyses of lymphocyte populations via flow cytometry showed that the numbers of B cells (CD3- CD45+) and natural killer cells (CD3- CD161+) were markedly reduced in both knockout rats. In contrast, T cells were markedly reduced but showed slightly different results between sKO and dKO rats. Notably, our immunodeficient rats do not exhibit growth retardation or gametogenesis defects. This high-quality SCID rat resource is now managed by the National BioResource Project in Japan. Our SCID rat model has been used in various research fields, demonstrating its importance as a bioresource.

Indexed as

Severe Combined ImmunodeficiencyAnimalsGene EditingInterleukin Receptor Common gamma SubunitMiceMice, SCIDRatsRats, Inbred F344T-LymphocytesInterleukin Receptor Common gamma Subunit

Identifiers

PMID35960733
PMCPMC9374221
OpenAlexW4290851846

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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.