engleski

Liver regeneration in MHC clas I deficient mice

Major histocompatibility antigens (MHC) class I-encoded molecules are known to play a major role in processes of presentation of endogenously synthesized antigens and those of negative and positive selection of T cells in the thymus to self antigens. Owing to the possibility that some autoreactive clones of lymphocytes perform morphogenetic function and participate in the control of normal growth, in this work we analyzed the dynamics of liver regeneration after 1/3 partial hepatectomy (pHx) in mice which are defective in b2 microglobulin (b2-m) due to the mutation in the b2-m gene. Since they do not express correctly folded MHC class I trimolecular complexes and lack CD8+ T cells, it was hypotethesized that changes in liver regeneration might be seen, if MHC antigen and T-cell restricted mechanisms are involved in the regulation of liver growth. Phenotype of locally activated lymphoid cells and intensity of liver regeneration after pHx were estimated by cytofluorometric screening of intrahepatic lymphatic cells and hepatic cell cycle analysis. The data have shown that S phase of hepatocytes in regenerating liver of mice homozygous for b2-m -/- genotype is initially significantly reduced (at 24th hour) and then markedly increased (at 48h and 7 days after pHx) in comparison with their heterozygous littermates. In both groups an early (at 24th) peak of intrahepatic NK1.1.+ and CD5+ cells was seen, which disappeared on the second postoperative day. The data suggest that MHC class I antigens owing to their modulatory activity on NK and CD8+ cells are involved in regulation of liver regeneration.

liver regeneration; beta2-microglobulin deficient mice; MHC class I antigens; intrahepatic NK; CD8+ and CD5+ cells

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