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Eta-1 (Osteopontin): An Early Component of Type-1 (Cell-Mediated) Immunity

Science  04 Feb 2000:
Vol. 287, Issue 5454, pp. 860-864
DOI: 10.1126/science.287.5454.860

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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-γ 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.

  • * These authors contributed equally to this work.

  • Present address: Division of Radiation and Cancer Biology, New England Medical Center, 750 Washington Street, Boston, MA 02111, USA.

  • To whom correspondence should be addressed. E-mail: Harvey_Cantor{at}DFCI.harvard.edu

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