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A comparative study of mRNA and protein expression of the autoimmune regulator gene ( Aire ) in embryonic and adult murine tissues
Author(s) -
Adamson KA,
Pearce SHS,
Lamb JR,
Seckl JR,
Howie SEM
Publication year - 2004
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1493
Subject(s) - autoimmune regulator , in situ hybridization , biology , messenger rna , immunohistochemistry , spleen , gene expression , gene , embryonic stem cell , lymphatic system , microbiology and biotechnology , pathology , immunology , antibody , autoimmune disease , medicine , genetics
Autoimmune polyendocrine syndrome type 1 (APS1) is a rare autosomal recessive human disorder caused by mutations in the autoimmune regulator gene ( AIRE ) and characterized by multiple autoimmune diseases. As reports of the tissue expression pattern of the murine Aire gene are discordant, a comprehensive survey of Aire expression was undertaken in adult and embryonic tissues at the mRNA and protein levels using real‐time RT‐PCR, in situ hybridization, and immunohistochemistry. In the adult, the highest Aire mRNA expression was in the thymus. All the other tissues investigated expressed Aire mRNA at low levels, but it was barely detectable in the adrenal gland. Aire protein expression was observed in the thymus, spleen, and lymph nodes. A common pattern was observed in other tissues, with staining in epithelial cells. An exception to this was the gut, where staining was seen in the mucin spaces. In embryonic tissue, Aire mRNA and protein expression was detected from E14.5 in the thymus. In the fetal liver, unlike the adult, staining was observed at E14.5 and decreased towards term. Thus, Aire is expressed in immunologically relevant tissues and in a restricted number of extra‐immunological tissues in the adult. Furthermore, the presence of Aire protein is reported in extra‐thymic tissues of the embryo. Copyright © 2004 John Wiley & Sons, Ltd.