The Susceptibility to Cytotoxic T Lymphocyte Mediated Lysis of Chemically Induced Sarcomas from Immunodeficient and Normal Mice

Svane, Inge Marie; Engel, Anne-Marie; Thomsen, Allan Randrup; Werdelin, Ole

doi:10.1046/j.1365-3083.1997.d01-369.x

Cited by 8 publications

(3 citation statements)

References 36 publications

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“…36 Selective presentation of virus-specific peptides by the L d molecule, and a positive correlation between the sensitivity to CTL-mediated lysis and surface expression of the L d antigen of tumor cells have also been described. 37,38 Therefore, loss of L d expression may play a major role in tumor cell escape from the immune system. The L d molecule may present a potent fibrosarcoma tumor antigen, and loss of L d expression may be a necessary event for tumor progression in immunocompetent mice.…”

Section: Discussionmentioning

confidence: 99%

“…This second molecular lesion was present in 83% of the autologous metastases. 37,38 Therefore, loss of L d expression may play a major role in tumor cell escape from the immune system. In connection with these results, we recently obtained similar findings in patients with melanoma in which the same HLA class I-altered phenotype was found in different metastases that appeared in different sites and at different times in the same patient (Mendez et al, unpublished data).…”

Section: Mhc Class I Expression Of Metastatic Colonies From Nude Micementioning

confidence: 99%

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Immunoselection by T lymphocytes generates repeated MHC class I-deficient metastatic tumor variants

et al. 2000

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Alteration of MHC class I molecule expression is a widespread mechanism used by tumor cells to evade T cell responses. It has long been proposed that the origin of these MHC class I-negative or -deficient tumor variants is T cell immune selection. However, there are no experimental or clinical data to substantiate this hypothesis, and this issue is currently the subject of debate. Here we report that an H-2 class I-negative fibrosarcoma tumor clone generated MHC class I-negative spontaneous lung metastases in immunocompetent syngeneic BALB/c mice. Interestingly, the same B9 clone generated MHC class I-positive metastatic nodes, under basal conditions, in athymic nu/nu BALB/c mice. This phenomenon was observed in the metastatic nodules generated after a period of in vivo growth but not in the primary tumors growing locally in the footpad. These findings support the hypothesis that the H-2 phenotype of metastatic nodes is influenced by the T cell repertoire of the host, since in the absence of this T cell pressure (i.e., in nude mice) the metastatic nodes 'recovered' H-2 class I expression. In addition, 2 different phenotypes were found when the metastatic nodules obtained from immunocompetent mice were treated with IFN-␥. One phenotype, present in 83% of the colonies, was characterized by resistance of the L d molecule to IFN-␥ induction, due to a deletion involving the L d gene. The second phenotype (17% of the colonies) was similar to the original B9 clone and was characterized by the response of K, D and L class I genes to IFN-␥. These data provide evidence that the changes in MHC class I expression during tumor development might not be random but could be predictable.

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Section: Discussionmentioning

confidence: 99%

Section: Mhc Class I Expression Of Metastatic Colonies From Nude Micementioning

confidence: 99%

Immunoselection by T lymphocytes generates repeated MHC class I-deficient metastatic tumor variants

et al. 2000

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“…The paradigm of cancer immunoediting reconciles the mechanisms of tumor surveillance with the presence of clinically evident cancers. Tumors derived from mutagenesis in immunodeficient mice are more immunogenic compared to those from immunocompetent mice [4,5]. This phenomenon indicates that tumors develop differently in the presence of immune system.…”

Section: Introductionmentioning

confidence: 99%

Immunosurveillance and Immunoediting of Lung Cancer: Current Perspectives and Challenges

Kunimasa

Goto

2020

IJMS

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The immune system plays a dual role in tumor evolution—it can identify and control nascent tumor cells in a process called immunosurveillance and can promote tumor progression through immunosuppression via various mechanisms. Thus, bilateral host-protective and tumor-promoting actions of immunity are integrated as cancer immunoediting. In this decade, immune checkpoint inhibitors, specifically programmed cell death 1 (PD-1) pathway inhibitors, have changed the treatment paradigm of advanced non-small cell lung cancer (NSCLC). These agents are approved for the treatment of patients with NSCLC and demonstrate impressive clinical activity and durable responses in some patients. However, for many NSCLC patients, the efficacy of immune checkpoint inhibitors is limited. To optimize the full utility of the immune system for eradicating cancer, a broader understanding of cancer immunosurveillance and immunoediting is essential. In this review, we discuss the fundamental knowledge of the phenomena and provide an overview of the next-generation immunotherapies in the pipeline.

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Recent Advances of RNA m6A Modifications in Cancer Immunoediting and Immunotherapy

Ma,

Barr,

2023

Cancer Treatment and Research

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The Susceptibility to Cytotoxic T Lymphocyte Mediated Lysis of Chemically Induced Sarcomas from Immunodeficient and Normal Mice

Abstract: presentation of viral antigen to specific cytotoxic T cells originated from tumours known from previous experiments to be readily accepted after transplantation to immunocompetent, histocompatible recipients.

Cited by 8 publications

References 36 publications

Immunoselection by T lymphocytes generates repeated MHC class I-deficient metastatic tumor variants

Immunoselection by T lymphocytes generates repeated MHC class I-deficient metastatic tumor variants

Immunosurveillance and Immunoediting of Lung Cancer: Current Perspectives and Challenges

Recent Advances of RNA m6A Modifications in Cancer Immunoediting and Immunotherapy

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