Literature DB >> 1711536

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

E P Cowan1, M L Pierce, S Dhib-Jalbut.   

Abstract

Antigens encoded within the major histocompatibility complex (MHC) are not normally expressed in the central nervous system (CNS), but can be induced by treatment with interferon-gamma (IFN-gamma). Other cytokines released during an inflammatory process can potentially influence MHC expression as well. One cytokine of interest is interleukin-1 (IL-1), an immunoregulatory polypeptide that is produced by macrophages and also by cells in the CNS. In this study, the effect of IL-1 beta on MHC expression in a human glioblastoma multiforme cell line, U-105 MG, has been examined. Treatment of U-105 MG with 10 U IL-1 beta/ml for a period of 5 days resulted in a decrease in constitutive cell surface HLA class II expression and limited the induction of class II by IFN-gamma. This effect was also observed on steady-state levels of class II RNA and could be neutralized with antibodies to IL-1 beta. All class II transcripts examined (HLA-DR, -DQ, and -DP alpha and beta) were affected. Class I expression was only marginally changed by IL-1 beta treatment. A minimal concentration of 1 U IL-1 beta/ml was required to reduce class II expression and a kinetics experiment indicated that U-105 MG must be treated for at least 4 days with IL-1 beta for a decrease in class II expression to be observed. This study suggests that IL-1 may play a role in limiting immunoreactivity in the CNS by limiting class II induction.

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Year:  1991        PMID: 1711536      PMCID: PMC7119491          DOI: 10.1016/0165-5728(91)90030-b

Source DB:  PubMed          Journal:  J Neuroimmunol        ISSN: 0165-5728            Impact factor:   3.478


  44 in total

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Journal:  J Neuroimmunol       Date:  1990-05       Impact factor: 3.478

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Journal:  J Exp Med       Date:  1987-07-01       Impact factor: 14.307

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Journal:  J Neuroimmunol       Date:  1987-01       Impact factor: 3.478

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Review 4.  Immune Escape in Glioblastoma Multiforme and the Adaptation of Immunotherapies for Treatment.

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