Activation of hepatic NKT cells and subsequent liver injury following administration of alpha-galactosylceramide.

Osman Y, Kawamura T, Naito T, Takeda K, Van Kaer L, Okumura K, Abo T
Eur J Immunol. 2000 30 (7): 1919-28

PMID: 10940881 · DOI:10.1002/1521-4141(200007)30:7<1919::AID-IMMU1919>3.0.CO;2-3

It has been established that alpha-galactosylceramide (alpha-GalCer), a glycolipid, is recognized by natural killer T (NKT) cells together with the monomorphic MHC-like antigen, CD1d, in mice and humans. In this study, we examined how NKT cells are modulated by in vivo administration of alpha-GalCer in mice. When 2 microg (or more)/mouse of alpha(-GalCer was injected i.p., the majority of NKT cells disappeared in the liver and spleen, possibly undergoing apoptosis, on day 1. At this time, NKT cytotoxicity seen in liver lymphocytes also disappeared. In parallel with this numerical and functional change of NKT cells, there was always concomitant hepatocyte damage, as shown by histology and elevated levels of transaminases. Subsequently, the number and function of NKT cells continued to increase from day 3 to day 7. The response seen in hepatic (and splenic) NKT cells did not occur in thymic NKT cells. All these phenomena induced in the liver did not appear in NKT-deficient mice such as beta2-microglobulin(-/-) and CD1d(-/-) mice. These results shed further light on the in vivo interaction between NKT cells and alpha-GalCer in mice.

MeSH Terms (26)

Aging Animals Antigens Antigens, CD1 Antigens, CD1d Antigens, Surface Apoptosis beta 2-Microglobulin Cell Count Cytotoxicity, Immunologic Galactosylceramides Immunophenotyping Injections, Intraperitoneal Killer Cells, Natural Kinetics Lectins, C-Type Liver Lymphocyte Activation Mice Mice, Inbred BALB C Mice, Knockout NK Cell Lectin-Like Receptor Subfamily B Proteins Spleen T-Lymphocytes Thymus Gland

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