Tumor Immunoediting, from T Cell-Mediated Immune Surveillance to Tumor-Escape of Uterine Leiomyosarcoma
The majority of smooth muscle tumors found in the uterus are benign, but uterine leiomyosarcomas (LMSs) are extremely malignant, with high rates of recurrence and metastasis. The development of gynecologic tumors is often correlated with female hormone secretion; however, the development of uterine...
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OMICS Publishing Group
2018
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Online Access: | http://hdl.handle.net/1721.1/116887 https://orcid.org/0000-0003-2839-8228 |
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author | Hayashi, Takuma Horiuchi, Akiko Sano, Kenji Hiraoka, Nobuyoshi Ichimura, Tomoyuki Ishiko, Osamu Kanai, Yae Yaegashi, Nobuo Aburatani, Hiroyuki Shiozawa, Tanri Tonegawa, Susumu Konishi, Ikuo |
author2 | Massachusetts Institute of Technology. Department of Biology |
author_facet | Massachusetts Institute of Technology. Department of Biology Hayashi, Takuma Horiuchi, Akiko Sano, Kenji Hiraoka, Nobuyoshi Ichimura, Tomoyuki Ishiko, Osamu Kanai, Yae Yaegashi, Nobuo Aburatani, Hiroyuki Shiozawa, Tanri Tonegawa, Susumu Konishi, Ikuo |
author_sort | Hayashi, Takuma |
collection | MIT |
description | The majority of smooth muscle tumors found in the uterus are benign, but uterine leiomyosarcomas (LMSs) are extremely malignant, with high rates of recurrence and metastasis. The development of gynecologic tumors is often correlated with female hormone secretion; however, the development of uterine LMS is not substantially correlated with hormonal conditions, and the risk factors are not clearly understood. The presentation of antigenic peptides by major histocompatibility complex (MHC) class I molecules is important for tumor rejection by cytotoxic T-lymphocytes (CTLs). Such antigenic peptides are generated as a result of the degradation of intracellular proteins by the proteasome pathway, a process that is influenced by the interferon (IFN)-γ-inducible low molecular mass polypeptide-2 (LMP2) subunit of the 20S proteasome. Homozygous deficient mice for LMP2 are now known to spontaneously develop uterine LMS. LMP2 expression is reportedly absent in human uterine LMS, but present in human myometrium. Further studies revealed a few infiltrating CD56+ NK cells in human uterine LMS tissues. This review aims at summarizing recent insights into the regulation of NK cell function and the T cell-mediated immune system as tumor immune surveillance, first attempts to exploit NK cell activation to improve immunity to tumors. |
first_indexed | 2024-09-23T09:02:26Z |
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institution | Massachusetts Institute of Technology |
last_indexed | 2024-09-23T09:02:26Z |
publishDate | 2018 |
publisher | OMICS Publishing Group |
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spelling | mit-1721.1/1168872022-09-30T13:01:05Z Tumor Immunoediting, from T Cell-Mediated Immune Surveillance to Tumor-Escape of Uterine Leiomyosarcoma Hayashi, Takuma Horiuchi, Akiko Sano, Kenji Hiraoka, Nobuyoshi Ichimura, Tomoyuki Ishiko, Osamu Kanai, Yae Yaegashi, Nobuo Aburatani, Hiroyuki Shiozawa, Tanri Tonegawa, Susumu Konishi, Ikuo Massachusetts Institute of Technology. Department of Biology Picower Institute for Learning and Memory Tonegawa, Susumu The majority of smooth muscle tumors found in the uterus are benign, but uterine leiomyosarcomas (LMSs) are extremely malignant, with high rates of recurrence and metastasis. The development of gynecologic tumors is often correlated with female hormone secretion; however, the development of uterine LMS is not substantially correlated with hormonal conditions, and the risk factors are not clearly understood. The presentation of antigenic peptides by major histocompatibility complex (MHC) class I molecules is important for tumor rejection by cytotoxic T-lymphocytes (CTLs). Such antigenic peptides are generated as a result of the degradation of intracellular proteins by the proteasome pathway, a process that is influenced by the interferon (IFN)-γ-inducible low molecular mass polypeptide-2 (LMP2) subunit of the 20S proteasome. Homozygous deficient mice for LMP2 are now known to spontaneously develop uterine LMS. LMP2 expression is reportedly absent in human uterine LMS, but present in human myometrium. Further studies revealed a few infiltrating CD56+ NK cells in human uterine LMS tissues. This review aims at summarizing recent insights into the regulation of NK cell function and the T cell-mediated immune system as tumor immune surveillance, first attempts to exploit NK cell activation to improve immunity to tumors. 2018-07-11T14:39:55Z 2018-07-11T14:39:55Z 2012-02 2011-10 2018-07-10T18:27:42Z Article http://purl.org/eprint/type/JournalArticle 2157-7560 http://hdl.handle.net/1721.1/116887 Hayashi, Takuma. “Tumor Immunoediting, from T Cell-Mediated Immune Surveillance to Tumor-Escape of Uterine Leiomyosarcoma.” Journal of Vaccines & Vaccination (2012) © 2012 Hayashi T, et al https://orcid.org/0000-0003-2839-8228 http://dx.doi.org/10.4172/2157-7560.S1-002 Journal of Vaccines & Vaccination Creative Commons Attribution 4.0 International License http://creativecommons.org/licenses/by/4.0/ application/pdf OMICS Publishing Group Journal of Vaccines & Vaccination |
spellingShingle | Hayashi, Takuma Horiuchi, Akiko Sano, Kenji Hiraoka, Nobuyoshi Ichimura, Tomoyuki Ishiko, Osamu Kanai, Yae Yaegashi, Nobuo Aburatani, Hiroyuki Shiozawa, Tanri Tonegawa, Susumu Konishi, Ikuo Tumor Immunoediting, from T Cell-Mediated Immune Surveillance to Tumor-Escape of Uterine Leiomyosarcoma |
title | Tumor Immunoediting, from T Cell-Mediated Immune Surveillance to Tumor-Escape of Uterine Leiomyosarcoma |
title_full | Tumor Immunoediting, from T Cell-Mediated Immune Surveillance to Tumor-Escape of Uterine Leiomyosarcoma |
title_fullStr | Tumor Immunoediting, from T Cell-Mediated Immune Surveillance to Tumor-Escape of Uterine Leiomyosarcoma |
title_full_unstemmed | Tumor Immunoediting, from T Cell-Mediated Immune Surveillance to Tumor-Escape of Uterine Leiomyosarcoma |
title_short | Tumor Immunoediting, from T Cell-Mediated Immune Surveillance to Tumor-Escape of Uterine Leiomyosarcoma |
title_sort | tumor immunoediting from t cell mediated immune surveillance to tumor escape of uterine leiomyosarcoma |
url | http://hdl.handle.net/1721.1/116887 https://orcid.org/0000-0003-2839-8228 |
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