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

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...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 2000-02, Vol.287 (5454), p.860-864
Main Authors: Ashkar, Samy, Weber, Georg F., Panoutsakopoulou, Vassiliki, Sanchirico, Marie E., Jansson, Marianne, Zawaideh, Samer, Rittling, Susan R., Denhardt, David T., Glimcher, Melvin J., Cantor, Harvey
Format: Article
Language:English
Subjects:
Animals
Antibodies
Bacteria
Biological and medical sciences
CD44 antigen
Cellular biology
Cytokines
Eta-1 protein
Feedback (Response)
Fundamental and applied biological sciences. Psychology
Fundamental immunology
g-Interferon
Genes
Genetics of the immune response
Granuloma
Granuloma - immunology
Herpes Simplex - immunology
Herpesvirus 1, Human - immunology
Human herpesvirus 1
Hyaluronan Receptors - metabolism
Hypersensitivity, Delayed
Immunity
Immunity (Disease)
Immunobiology
Infections
Interferon-gamma - biosynthesis
Interleukin-10 - biosynthesis
Interleukin-12 - biosynthesis
Keratitis, Herpetic - immunology
Listeriosis - immunology
Lymph nodes
Lymphocyte Activation
Macrophages
Macrophages - immunology
Mice
Mice, Inbred C3H
Mice, Inbred C57BL
Mice, Nude
Osteopontin
Phosphorylation
Receptors, Vitronectin - metabolism
Rodents
Sialoglycoproteins - immunology
Sialoglycoproteins - metabolism
Sialoglycoproteins - pharmacology
T lymphocytes
T-Lymphocytes - immunology
T-Lymphocytes - metabolism
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Description
Summary: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.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.287.5454.860