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Resistance of novel mouse strains different in MHC class I and the NKC domain to the development of experimental tumors

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F16%3A00472126" target="_blank" >RIV/68378050:_____/16:00472126 - isvavai.cz</a>

  • Alternative codes found

    RIV/68407700:21460/16:00305826

  • Result on the web

    <a href="http://dx.doi.org/10.3892/ijo.2016.3561" target="_blank" >http://dx.doi.org/10.3892/ijo.2016.3561</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3892/ijo.2016.3561" target="_blank" >10.3892/ijo.2016.3561</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Resistance of novel mouse strains different in MHC class I and the NKC domain to the development of experimental tumors

  • Original language description

    To elucidate the immunological mechanisms critical for tumor progression, we bred novel mouse strains, different in the NKC and H-2D domains. We used inbreeding to generate hybrids of Balb/c and C57BL/6 of stable H-2Db+d-NK1.1neg and H-2Db-d+NK1.1high phenotypes. We analyzed the growth of three established MHC class I-deficient tumor cell lines: TC-1/A9 tumor (HPV-associated) and B16F10 melanoma, both syngeneic to C57BL/6, and the MCB8 (3-methycholanthreneinduced tumor) syngeneic to Balb/c. Furthermore, we induced colorectal carcinoma by azoxymethane-DSS treatment to test the susceptibility to chemically-induced primary cancer. We found that the novel strains spontaneously regressed the tumor transplants syngeneic to both Balb/c (MCB8) and C57BL/6 (B16F10 and TC-1/A9) mice. The H2-Db+d-NK1.1neg, but not the H2-Db-d+NK1.1high strain was also highly resistant to chemically-induced colorectal cancer in comparison to the parental mice. The immune changes during TC-1/A9 cancer development involved an increase of the NK cell distribution in the peripheral blood and spleen along with higher expression of NKG2D activation antigen; this was in correlation with the time-dependent rise of cytotoxic activity in comparison to C57BL/6 mice. The TC-1/A9 cancer regression was accompanied by higher proportion of B cells in the spleen and B220(+)/CD86(+) activated antigen-presenting B cells distributed in the lymphoid organs, as well as in the periphery. The changes in the T-cell population were represented mainly by the prevalence of T helper cells reflected by grown CD4/CD8 ratio, most prominent in the b+d-NK1.1neg strain. The results of the present study imply usefulness of the two novel mouse strains as an experimental model for further studies of tumor resistance mechanisms.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    EB - Genetics and molecular biology

  • OECD FORD branch

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2016

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    International Journal of Oncology

  • ISSN

    1019-6439

  • e-ISSN

  • Volume of the periodical

    49

  • Issue of the periodical within the volume

    2

  • Country of publishing house

    GR - GREECE

  • Number of pages

    10

  • Pages from-to

    763-772

  • UT code for WoS article

    000378263600034

  • EID of the result in the Scopus database