The role of immune cell subpopulations in the growth and rejection of TC-1/A9 tumors in novel mouse strains differing in the H2-D haplotype and NKC domain

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388971%3A_____%2F18%3A00494099" target="_blank" >RIV/61388971:_____/18:00494099 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68378050:_____/18:00494099 RIV/68407700:21460/18:00328915

Výsledek na webu

<a href="http://dx.doi.org/10.3892/ol.2018.7763" target="_blank" >http://dx.doi.org/10.3892/ol.2018.7763</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3892/ol.2018.7763" target="_blank" >10.3892/ol.2018.7763</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The role of immune cell subpopulations in the growth and rejection of TC-1/A9 tumors in novel mouse strains differing in the H2-D haplotype and NKC domain

Popis výsledku v původním jazyce

The present study aimed to elucidate the role of cluster of differentiation (CD)8+,CD4+, natural killer (NK), and myeloid (CD11b+) cells in the course of the growth and rejection of experimental major histocompatibility complex (MHC) class I-deficient, HPV16 E6/E7-associated TC-1/A9 tumors in mice. Stable mouse lines (F-30) generated by inbreeding of Balb/c and C57BL/6 strains, which were characterized by H-2Db+d-NK1.1neg (B6-neg) and H-2Db-d+NK1.1high (Balb-high) phenotypes, were used for the present study. The novel strains spontaneously regressed tumors in 70-90% of cases. Ex vivo histological analysis of the tumor microenvironment in cryosections showed an indirect correlation between the growth of the transplanted tumor (progressor vs. regressor mice) and the proportion of immunocompetent cell infiltration in the tumors. The regressor mice exhibited a higher infiltration of tumors with CD4(+) and CD8(+) cells, and in Balb-high with NK cells as well, compared with the progressors. All tumor transplants also indicated a huge infiltration of CD11b(+) cells, but this infiltration was not dependent on the stage of the TC-1/A9 tumor development. Depletion of individual cell subpopulations in vivo exhibited different effects on the tumor development in the two strains. Elimination of CD8-positive cells enhanced growth of TC-1/A9 tumor transplants in both hybrid stains, whereas CD4(+) cell depletion affected rejection of TC-1/A9 tumors in the B6-neg mice only. Depletion of NK cells with anti-asialo GM1 antibody in the Balb-high strain led to enhancement of tumor growth, which was more pronounced after depletion of the NK1.1(+) subpopulation. On the other hand, depletion of NK cells with anti-asialo GM1 in B6-neg mice did not affect the regression of TC-1/A9 tumor transplants, but increased the CD11b(+) cell infiltration. In summary, these results indicate that co-operation of particular subsets of immunocompetent cells is essential for the rejection of TC-1/A9 tumor transplants. In B6-neg mice, the co-operative action of CD8(+) and CD4(+) cells is required, whereas in Balb-high mice, the synergy of CD8(+) and NK1.1(+) cells is of major importance.

Název v anglickém jazyce

The role of immune cell subpopulations in the growth and rejection of TC-1/A9 tumors in novel mouse strains differing in the H2-D haplotype and NKC domain

Popis výsledku anglicky

The present study aimed to elucidate the role of cluster of differentiation (CD)8+,CD4+, natural killer (NK), and myeloid (CD11b+) cells in the course of the growth and rejection of experimental major histocompatibility complex (MHC) class I-deficient, HPV16 E6/E7-associated TC-1/A9 tumors in mice. Stable mouse lines (F-30) generated by inbreeding of Balb/c and C57BL/6 strains, which were characterized by H-2Db+d-NK1.1neg (B6-neg) and H-2Db-d+NK1.1high (Balb-high) phenotypes, were used for the present study. The novel strains spontaneously regressed tumors in 70-90% of cases. Ex vivo histological analysis of the tumor microenvironment in cryosections showed an indirect correlation between the growth of the transplanted tumor (progressor vs. regressor mice) and the proportion of immunocompetent cell infiltration in the tumors. The regressor mice exhibited a higher infiltration of tumors with CD4(+) and CD8(+) cells, and in Balb-high with NK cells as well, compared with the progressors. All tumor transplants also indicated a huge infiltration of CD11b(+) cells, but this infiltration was not dependent on the stage of the TC-1/A9 tumor development. Depletion of individual cell subpopulations in vivo exhibited different effects on the tumor development in the two strains. Elimination of CD8-positive cells enhanced growth of TC-1/A9 tumor transplants in both hybrid stains, whereas CD4(+) cell depletion affected rejection of TC-1/A9 tumors in the B6-neg mice only. Depletion of NK cells with anti-asialo GM1 antibody in the Balb-high strain led to enhancement of tumor growth, which was more pronounced after depletion of the NK1.1(+) subpopulation. On the other hand, depletion of NK cells with anti-asialo GM1 in B6-neg mice did not affect the regression of TC-1/A9 tumor transplants, but increased the CD11b(+) cell infiltration. In summary, these results indicate that co-operation of particular subsets of immunocompetent cells is essential for the rejection of TC-1/A9 tumor transplants. In B6-neg mice, the co-operative action of CD8(+) and CD4(+) cells is required, whereas in Balb-high mice, the synergy of CD8(+) and NK1.1(+) cells is of major importance.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10606 - Microbiology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2018

Kód důvěrnosti údajů

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

Název periodika

Oncology Letters

ISSN

1792-1074

e-ISSN

—

Svazek periodika

15

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

GR - Řecká republika

Počet stran výsledku

8

Strana od-do

3594-3601

Kód UT WoS článku

000430818300123

EID výsledku v databázi Scopus

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