ArticleThe American journal of pathology2004
Effect of osteopontin alleles on beta-glucan-induced granuloma formation in the mouse liver.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 24 citations in OpenAlex.
- Fungal cell wall agents and bacterial lipopolysaccharide in organic dust as possible risk factors for pulmonary sarcoidosis.Journal of occupational medicine and toxicology (London, England) · 2016Article
- Osteopontin expression by CD103- dendritic cells drives intestinal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Osteopontin expression in the brain triggers localized inflammation and cell death when immune cells are activated by pertussis toxin.Mediators of inflammation · 2014Article
- Natural killer T cells suppress zymosan A-mediated granuloma formation in the liver by modulating interferon-γ and interleukin-10.Immunology · 2012Article
- Antigen-specific induction of osteopontin contributes to the chronification of allergic contact dermatitis.The American journal of pathology · 2010Article
- Regulated osteopontin expression by dendritic cells decisively affects their migratory capacity.The Journal of investigative dermatology · 2008Article
- In vivo osteopontin-induced macrophage accumulation is dependent on CD44 expression.Cellular immunology · 2008Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The granuloma formation is a host defense response against persistent irritants. Osteopontin is centrally involved in the formation of granulomas. Three osteopontin alleles, designated a, b, and c, have been found in mice. Here we used a murine model of zymosan (beta-glucan)-induced granuloma formation in the liver to determine possible functional differences between the osteopontin alleles in cell-mediated immunity. In contrast to mice with alleles a or c, mice with the allele b was defective in granuloma formation. As detected by mRNA expression, cytokines and chemokines known to be critically involved in granuloma formation were elicited in liver tissue, regardless of the osteopontin allele expressed. Alignment of the deduced amino acid sequences showed that unlike osteopontin c, b differs from a in 11 amino acids. All three osteopontin alleles had normal cell-binding properties. However, only the b allelic form was defective in the induction of cell migration as tested with dendritic cells. In conclusion, generation of a granulomatous response in mice depends critically on the presence of a functional osteopontin allele. Defective granuloma formation in mice with allele b is likely to be because of an impaired chemotactic function of the osteopontin b protein on immunocompetent cells.
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