
Mutations in the transcriptional regulator Aire disrupt thymic alphabeta T cell selection, causing in humans Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED). However, it is not known whether Aire is needed for normal gammadelta T cell development. We show that Aire(-/-) mice have a normal frequency of gammadelta T cells, with TCR repertoire comparable to that of wild-type mice, and normal amount of TCR Cdelta mRNA in ileum and skin. gammadelta 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 gammadelta T cells was similar in APECED patients and healthy controls. These data indicate that gammadelta T cells develop independently of Aire and are unlikely to have a significant pathogenetic or protective role in APECED. The antigens responsible for gammadelta and alphabeta T cell selection are thus probably largely different.
Adult, Male, Mice, Knockout, T-Lymphocytes, AIRE Protein, Receptors, Antigen, T-Cell, gamma-delta, Middle Aged, Mice, Inbred C57BL, Mice, Animals, Humans, Female, Polyendocrinopathies, Autoimmune, Transcription Factors
Adult, Male, Mice, Knockout, T-Lymphocytes, AIRE Protein, Receptors, Antigen, T-Cell, gamma-delta, Middle Aged, Mice, Inbred C57BL, Mice, Animals, Humans, Female, Polyendocrinopathies, Autoimmune, Transcription Factors
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