Interleukin-1β decreases HLA class II expression on a glioblastoma multiforme cell line

Cowan, Elliot P.; Pierce, Michael L.; Dhib‐Jalbut, Suhayl

doi:10.1016/0165-5728(91)90030-b

Cited by 18 publications

(5 citation statements)

References 45 publications

(35 reference statements)

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“…RNA isolation and analysis. Total cellular RNA was isolated by the acidified guanidinium phenol-chloroform method (4) and analyzed by Northern (RNA) blotting as previously described (6). The probes used were as follows: pHLA-2a.1, an HLA-A locus-specific fragment (a gift from Harry Orr, University of Minnesota, Minneapolis) (21); HLA-DRA, a 600-bp 3' PstI fragment of HLA-DRA-10 (a gift from Eric Long, National Institutes of Health, Bethesda, Md.…”

Section: Methodsmentioning

confidence: 99%

Induction of HLA class I and class II expression in human T-lymphotropic virus type I-infected neuroblastoma cells

Lehky

Cowan

Lampson

et al. 1994

J Virol

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Human T-lymphotropic virus type I (HTLV-I) is associated with a neurologic disease, HTLV-I-associated myelopathy-tropical spastic paraparesis, in which both pathological and immunological changes are observed within the central nervous system. The pathogenesis of infection in HTLV-I-associated myopathy-tropical spastic paraparesis is not well understood with respect to the cell tropism of HTLV-I and its relationship to the destruction of neural elements. In this study, neuroblastoma cells were infected with HTLV-I by coculturing with HUT-102 cells to demonstrate that cells of neuronal origin are susceptible to this retroviral infection. HTLV-I infection of the neuroblastoma cells was confirmed by verifying the presence of HTLV-I gp46 surface antigens by flow cytometry and by verifying the presence of HTLV-I pX RNA by Northern (RNA) blotting and in situ hybridization techniques. To determine whether HTLV-I infection could potentially lead to changes in cell surface recognition by the immune system, the infected neuroblastoma cells were analyzed for altered HLA expression. The HTLV-I-infected, cocultured neuroblastoma cells were shown, through cell surface antigen expression and RNA transcripts, to express HLA classes I and II. In contrast, cocultured neuroblastoma cells that did not become infected with HTLV-I expressed only HLA class I. HLA class I expression was enhanced by the cytokines tumor necrosis factor a and gamma interferon and in the presence of HUT-102 supernatant. In this system, expression of HLA class I and II molecules appeared to be regulated by different mechanisms. HLA class I expression was probably induced by cytokines present in the HUT-102 supernatant and was not dependent on HTLV-I infection. HLA class II expression required HTLV-I infection of the cells. The observation of HTLV-I infection leading to HLA induction in these neuroblastoma cells provides a possible mechanism for immunologic recognition of infected neuronal cells.

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Section: Methodsmentioning

confidence: 99%

Induction of HLA class I and class II expression in human T-lymphotropic virus type I-infected neuroblastoma cells

Lehky

Cowan

Lampson

et al. 1994

J Virol

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“…GBM cells also secrete interleukin-1α and -1β (IL-1 α and β) ( 96 ). The down regulation of HLA class II expression on the U-105 MG GBM cell line by IL-1β suggests that this could be another mechanism which reduces immune recognition by CD4 + T cells ( 97 ).…”

Section: Immune Inhibitory Proteins Expressed By Gbm Tumorsmentioning

confidence: 99%

Immune Escape in Glioblastoma Multiforme and the Adaptation of Immunotherapies for Treatment

et al. 2020

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Glioblastoma multiforme (GBM) is the most frequently occurring primary brain tumor and has a very poor prognosis, with only around 5% of patients surviving for a period of 5 years or more after diagnosis. Despite aggressive multimodal therapy, consisting mostly of a combination of surgery, radiotherapy, and temozolomide chemotherapy, tumors nearly always recur close to the site of resection. For the past 15 years, very little progress has been made with regards to improving patient survival. Although immunotherapy represents an attractive therapy modality due to the promising pre-clinical results observed, many of these potential immunotherapeutic approaches fail during clinical trials, and to date no immunotherapeutic treatments for GBM have been approved. As for many other difficult to treat cancers, GBM combines a lack of immunogenicity with few mutations and a highly immunosuppressive tumor microenvironment (TME). Unfortunately, both tumor and immune cells have been shown to contribute towards this immunosuppressive phenotype. In addition, current therapeutics also exacerbate this immunosuppression which might explain the failure of immunotherapy-based clinical trials in the GBM setting. Understanding how these mechanisms interact with one another, as well as how one can increase the anti-tumor immune response by addressing local immunosuppression will lead to better clinical results for immune-based therapeutics. Improving therapeutic delivery across the blood brain barrier also presents a challenge for immunotherapy and future therapies will need to consider this. This review highlights the immunosuppressive mechanisms employed by GBM cancers and examines potential immunotherapeutic treatments that can overcome these significant immunosuppressive hurdles.

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“…Whereas TAMs do not show many traditional immunocyte properties, they can interfere with the functions of other immune cells to help GBM tumor progression. TAMs produce interleukin-1 (IL-1), an immunoregulatory polypeptide, to decrease the expression of cell surface antigen HLA class II in glioblastoma cancer cells, partially through impairing the cell response to IFN-gamma [ 60 ]. Thereby, macrophages help GBM cancer cells to escape from being targeted by T cells.…”

Section: Tams Support Gbm Tumor Progressionmentioning

confidence: 99%

Reciprocal Supportive Interplay between Glioblastoma and Tumor-Associated Macrophages

Zhou

Bao

2014

Cancers

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Glioblastoma multiforme (GBM) is the most lethal and aggressive type of primary brain malignancy. Failures of the traditional therapies in treating GBMs raise the urgent requirement to develop new approaches with more responsive targets. The phenomenon of the high infiltration of tumor-associated macrophages (TAMs) into GBMs has been observed for a long time. Regardless of the limited knowledge about TAMs, the high percentage of supportive TAM in GBM tumor mass makes it possible to be a good target for GBM treatment. In this review, we discussed the unique features of TAMs in GBMs, including their origin, the tumor-supportive properties, the secreted cytokines, and the relevant mechanisms. In addition, we tried to interpret the current understandings about the interplay between GBM cancer cells and TAMs. Finally, the translational studies of targeting TAMs were also described.

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Interleukin-1β decreases HLA class II expression on a glioblastoma multiforme cell line

Cited by 18 publications

References 45 publications

Induction of HLA class I and class II expression in human T-lymphotropic virus type I-infected neuroblastoma cells

Induction of HLA class I and class II expression in human T-lymphotropic virus type I-infected neuroblastoma cells

Immune Escape in Glioblastoma Multiforme and the Adaptation of Immunotherapies for Treatment

Reciprocal Supportive Interplay between Glioblastoma and Tumor-Associated Macrophages

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