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Erschienen in: Pediatric Surgery International 1/2023

01.12.2023 | Original Article

Expression of programmed cell death-1 on neuroblastoma cells in TH-MYCN transgenic mice

verfasst von: Yuta Takeuchi, Seiichiro Inoue, Akio Odaka

Erschienen in: Pediatric Surgery International | Ausgabe 1/2023

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Abstract

Background

Immunotherapy may improve the poor prognosis of high-risk neuroblastoma. Programmed cell death-1 (PD-1) is expressed in several cancers. The tyrosine hydroxylase MYCN (TH-MYCN) transgenic mouse model is widely used in neuroblastoma research, but detailed information on its immunological background is lacking. Therefore, we studied the immunological tumor microenvironment and tumor cell surface antigen expression in homozygote and hemizygote mice and effects of antibody therapy against PD-1.

Methods

CD4, CD8, CD11b, and CD11c expression in immune cells from retroperitoneal lymph nodes and spleen was analyzed by flow cytometry. Tumor cell surface antigen expression was confirmed, and data from homozygote and hemizygote mice were compared. Effects of anti-PD-1 antibody were evaluated.

Results

CD4-, CD8-, CD11b-, and CD11c-positive cells were not significantly different in homozygote and hemizygote mice, and CD11b- and CD11c-positive cells were identified in the tumor microenvironment in both. Tumor cells expressed PD-1, and anti-PD-1 antibody had anti-tumor effects and significantly reduced the percentage of living tumor cells in cultures after 2 h.

Conclusion

The immunological background is similar in homozygote and hemizygote TH-MYCN transgenic mice, and both have PD-1–positive tumor cells. Anti-PD-1 antibody suppresses tumor growth. This mouse model may be a useful for studying immunotherapy of neuroblastoma.
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Metadaten
Titel
Expression of programmed cell death-1 on neuroblastoma cells in TH-MYCN transgenic mice
verfasst von
Yuta Takeuchi
Seiichiro Inoue
Akio Odaka
Publikationsdatum
01.12.2023
Verlag
Springer Berlin Heidelberg
Erschienen in
Pediatric Surgery International / Ausgabe 1/2023
Print ISSN: 0179-0358
Elektronische ISSN: 1437-9813
DOI
https://doi.org/10.1007/s00383-022-05292-y

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