| Literature DB >> 10657301 |
S Ashkar1, G F Weber, V Panoutsakopoulou, M E Sanchirico, M Jansson, S Zawaideh, S R Rittling, D T Denhardt, M J Glimcher, H Cantor.
Abstract
Cell-mediated (type-1) immunity is necessary for immune protection against most intracellular pathogens and, when excessive, can mediate organ-specific autoimmune destruction. Mice deficient in Eta-1 (also called osteopontin) gene expression have severely impaired type-1 immunity to viral infection [herpes simplex virus-type 1 (KOS strain)] and bacterial infection (Listeria monocytogenes) and do not develop sarcoid-type granulomas. Interleukin-12 (IL-12) and interferon-gamma production is diminished, and IL-10 production is increased. A phosphorylation-dependent interaction between the amino-terminal portion of Eta-1 and its integrin receptor stimulated IL-12 expression, whereas a phosphorylation-independent interaction with CD44 inhibited IL-10 expression. These findings identify Eta-1 as a key cytokine that sets the stage for efficient type-1 immune responses through differential regulation of macrophage IL-12 and IL-10 cytokine expression.Entities:
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Year: 2000 PMID： 10657301 DOI： 10.1126/science.287.5454.860
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728