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

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-γ (IFN-γ). Other cytokines released during an inflammatory process can potentially influence MHC expression as well. One...

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Detalles Bibliográficos
Autores principales: Cowan, Elliot P., Pierce, Michael L., Dhib-Jalbut, Suhayl
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Published by Elsevier B.V. 1991
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7119491/
https://www.ncbi.nlm.nih.gov/pubmed/1711536
http://dx.doi.org/10.1016/0165-5728(91)90030-B
Descripción
Sumario: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-γ (IFN-γ). 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 effedt of IL-1β 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-1β/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-γ. This effect was also observed on steady-state levels of class II RNA and could be neutralized with antibodies to IL-1β. All class II transcripts examined (HLA-DR, -DQ, and -DP α and β) were affected. Class I expression was only marginally changed by IL-1β treatment. A minimal concentration of 1 U IL-1β/ml was required to reduce class II expression and a kinetics experiment indicated that U-105MG must be treated for at least 4 days with IL-1β 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.