BIOLOGICAL ACTIVITY OF INTERLEUKIN-10 IN THE CENTRAL NERVOUS SYSTEM

Cytokines play a crucial role as mediators of inflammation. Astrocytes and microglia are the two major glial cells involved in the central nervous system immune responses. In this study we examined the effects of interleukin-10 (IL-10), one of the naturally occurring inhibitory cytokines, on differe...

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Published inNeurochemistry international Vol. 30; no. 4; pp. 433 - 439
Main Authors ZOCCHIA, CRISTINA, SPIGA, GIULIO, RABIN, STUART J, GREKOVA, MARIA, RICHERT, JOHN, CHERNYSHEV, OLGA, COLTON, CAROL, MOCCHETTI, ITALO
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.04.1997
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Summary:Cytokines play a crucial role as mediators of inflammation. Astrocytes and microglia are the two major glial cells involved in the central nervous system immune responses. In this study we examined the effects of interleukin-10 (IL-10), one of the naturally occurring inhibitory cytokines, on different types of glial cells in culture such as rat astrocytes, hamster microglia and C6-2B glioma cells. Phosphorylation of signal transducers and activators of transcription (STAT) proteins was used as a marker for IL-10 activity. Within minutes, IL-10 elicited a strong and weak increase in STAT3 and STAT1 phosphorylation, respectively, in human T lymphocytes, suggesting that STAT3 is a main IL-10 signaling event in these cells. In contrast, IL-10 failed to induce STAT3 in glial cells, but elicited a weak increase in STAT1 phosphorylation in microglia and C6-2B glioma cells only, suggesting that in some glial cell population(s) IL-10 may produce cellular responses via activation of the STAT1 pathway. Moreover, in C6-2B cells, IL-10 elicited a decrease in the level of basic fibroblast growth factor mRNA. A similar decrease was observed in adult rat hypothalamus, indicating that this cytokine may regulate glial production of trophic factors. Our data suggest that IL-10 may play a role in glial cell differentiation and proliferation. © 1997 Elsevier Science Ltd. All rights reserved
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ISSN:0197-0186
1872-9754
DOI:10.1016/S0197-0186(96)00079-4