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From the * Department of Molecular and Experimental Medicine and Immunology, The Scripps
Research Institute, La Jolla, California 92037; and HLA-G is the only class I determinant of the major histocompatibility complex (MHC) expressed by the trophoblasts, the fetal cells invading the maternal decidua during pregnancy. A
unique feature of this nonclassical HLA molecule is its low polymorphism, a property that has
been postulated to play an important role in preventing local activation of maternal alloreactive
T and natural killer cells against the fetus. Yet, the mechanisms by which fetal HLA-G can be
recognized as a self-MHC molecule by the maternal immune system remain unclear. Here we
report the novel observation that HLA-G is expressed in the human thymus. Expression is targeted to the cell surface of thymic medullary and subcapsular epithelium. Thymic epithelial cell
lines were generated and shown to express three alternatively spliced HLA-G transcripts, previously identified in human trophoblasts. Sequencing of HLA-G1 transcripts revealed a few nucleotide changes resulting in amino acid substitutions, all clustered within exon 3 of HLA-G, encoding for the 
Department of Stomatology, University of
California San Francisco, San Francisco, California 94143
2 domain of the molecule. Our findings raise the possibility that maternal
unresponsiveness to HLA-G-expressing fetal tissues may be shaped in the thymus by a previously unrecognized central presentation of this MHC molecule on the medullary epithelium.
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