Figure 1.

Summary of known and novel aspects of γδ IEL biology revealed through gene-expression studies. DNA-microarray [14] and SAGE [16] analysis provide concordant information, showing the expression of a broad range of proteins required by activated-yet-resting' γδ IELs for activation, function, and survival within epithelia. When a γδ IEL (shown in red) has its TCR stimulated by antigen presented on the cell surface of a stressed, transformed or infected epithelial cell (shown in blue), a signaling cascade is triggered, involving the signal transducer and activator of transcription 3 (STAT3), the tyrosine kinases Jak3 and Lck, and the regulator of G-protein signaling-1 (RGS-1). The downstream activation of various transcription factors leads to expression of proteins with diverse function. Illustrated on the figure going clockwise from top left: BY55, 4-1BB (CD137 ligand) and 2B4, co-stimulatory and accessory receptors; FcεRIγ, a receptor for the immunoglobulin E (IgE) molecule; CD3, a complex of multiple signaling chains associated with the TCR; KGF, keratinocyte growth factor; MIP-1, macrophage inflammatory protein-1; IL-17, interleukin-17; TGFβ, transforming growth factor β; INF-γ, interferon-γ; Flt3L, the ligand for the receptor tyrosine kinase Flt3; LDLR, the low-density lipoprotein receptor (LDLR). Details of other molecules mentioned in the figure are discussed in the text.