Author/Authors :
Tuovinen، نويسنده , , Heli and Pِntynen، نويسنده , , Nora and Gylling، نويسنده , , Mikhail and Kekنlنinen، نويسنده , , Eliisa and Perheentupa، نويسنده , , Jaakko and Miettinen، نويسنده , , Aaro and Arstila، نويسنده , , T. Petteri، نويسنده ,
Abstract :
Mutations in the transcriptional regulator Aire disrupt thymic αβ T cell selection, causing in humans Autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy (APECED). However, it is not known whether Aire is needed for normal γδ T cell development. We show that Aire−/− mice have a normal frequency of γδ T cells, with TCR repertoire comparable to that of wild-type mice, and normal amount of TCR Cδ mRNA in ileum and skin. γδ T cells did not express increased amounts of CD25 or display hyperproliferation, and were not involved in pathological salivary gland infiltrates. Lastly, the frequency of circulating γδ T cells was similar in APECED patients and healthy controls. These data indicate that γδ T cells develop independently of Aire and are unlikely to have a significant pathogenetic or protective role in APECED. The antigens responsible for γδ and αβ T cell selection are thus probably largely different.
Keywords :
APECED , APS-1 , Autoimmunity , T cell development