Introduction Asymmetrical dimethyl arginine (ADMA) is an endogenous non-selective inhibitor of nitric oxide synthase that may influence the severity of organ failure and the occurrence of shock secondary to an infectious insult. Levels may be genetically determined by a promoter polymorphism in a regulatory gene encoding dimethylarginine dimethylaminohydrolase II (DDAH II), which functions by metabolising ADMA to citrulline. The aim of this study was to examine the association between ADMA levels and the severity of organ failure and shock in severe sepsis and also to assess the influence of a promoter polymorphism in DDAH II on ADMA levels.

Little is known about hepatic T lymphocyte subpopulations in the human liver. The aim of this study was to document the various subpopulations present in the liver and compare them to peripheral T lymphocytes in the same patients. Normal hepatic tissue was obained at time of transplant from five patients, and a single cell suspension of lymphocytes were prepared by standard methods. Ceils were stained with monoclonal antibodies specific for CD8ct and CD8B chains, CD4, CD8, CD3, o~BTCR, and ySTCR, and analyzed by two and three colour flow cytometry. Of the hepatic CD3+ cells, 71% were CD8+ and 25% were CD4+, with a CD4/CD8 ratio of 1:3 in contrast to the peripheral CD4/CD8 ratio of 2:1.18% of the hepatic CD3+ cells expressed ySTCR. Significantly, CD8~ct accounted for 27% [mean] of the total hepatic CD8+ population. Conclusion: There is now evidence that the adult human gut can support extrathymic T cell differentation. A significant population of hepatic CD8txct cells would suggest that the liver is also a site of extrathymic differentiation, which may have important implications for the understanding of autoimmunity and graft tolerance.

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