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The function of the Fc receptors gamma chain (FcR gamma) for the expression of the T cell receptor (TCR) complex and for T cell development, especially for T cells localized in epithelia, was investigated by analyzing FcR gamma-deficient mice. In wild-type mice, CD8 alpha alpha + beta -TCR alpha beta + T cells of intestinal intraepithelial lymphocytes (i-IEL) utilized CD3 zeta homodimers and zeta-FcR gamma heterodimers, whereas CD8 alpha alpha + beta -TCR gamma delta + i-IEL used zeta-FcR gamma and FcR gamma homodimers in the TCR complex. On the other hand, these T cells in FcR gamma-deficient mice contained only zeta homodimers. The surface expression of the TCR complex was reduced in CD8 alpha alpha + beta -i-IEL and dendritic epidermal T cells (DETC) in these mice, whereas the development of these T cells was normal. The degree of reduction appeared to depend on the expression level of FcR gamma. In contrast to these populations, TCR gamma delta + intraepithelial T cells in reproductive organs (r-IEL) were dramatically decreased, suggesting that the development of r-IEL is FcR gamma-dependent, probably due to the predominant usage of FcR gamma homodimers in the TCR complex. These results indicate that the FcR gamma chain contributes differently to the TCR expression and to the development of T cells localized in epithelia.

The high-affinity receptor for IgE (FcepsilonRI) that is expressed on the surface of mast cells plays an important role in antigen/IgE-mediated allergic reactions. We have previously found that critical elements in the promoter of the FcepsilonRI alpha- and beta-chain genes are recognized by the transcription factor GATA-1 in electrophoretic mobility shift assays coupled with a transient expression system for the alpha- and beta-chain promoters. To confirm that GATA-1 is involved in the expression of FcepsilonRI definitively, we generated bone marrow-derived mast cells from GATA-1 knockdown (KD) heterozygous mice. FACS analysis showed that the frequency of FcepsilonRI-positive cells was significantly decreased in mast cells derived from bone marrow of GATA-1 KD mice. Reverse transcription-PCR analysis showed that the level of transcripts not only for GATA-1 but also for both the alpha- and beta-chains was significantly lower in KD mast cells, whereas that of the FcepsilonRI gamma-chain was not affected. Degranulation caused by cross-linking of FcepsilonRI on mast cells prepared from KD mice was markedly repressed in comparison with that of wild-type mast cells. We concluded that the transcription factor GATA-1 positively regulates FcepsilonRI alpha- and beta-chain expression and therefore is involved in mast cell development.