ArticleClinical immunology (Orlando, Fla.)2011
Islet allograft tolerance in the absence of invariant natural killer T cells.
Article in Clinical immunology (Orlando, Fla.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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7 authors at 2 institutions in 2 countries.
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Abstract
The invariant NKT cells are involved in both immunity and immune tolerance. However, their roles in transplant models remain controversial. We studied the role of NKT cells in the allograft response using two different strains of NKT deficient mice (CD1d-/- and Jα18-/- mice), and found that CD1d-/- and Jα18-/- mice rejected islet allografts with a similar kinetics as wild type B6 mice. Treatment of CD1d-/- and Jα18-/- mice with donor specific transfusion and anti-CD154 induced donor specific tolerance, which was identical to similarly treated wt B6 mice. The islet allograft tolerance requires Foxp3(+) Tregs. In the periphery, Foxp3(+) Tregs in CD1d-/-, Jα18-/-, and wt B6 mice were comparable both phenotypically and functionally. In addition, CD1d-/- and Jα18-/- CD4(+) T cells (non-Tregs) could be readily converted to Foxp3(+) Tregs by TGF-β in vitro. Our data suggest that islet allograft tolerance can be successfully established without invariant NKT cells.
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