We have identified two human C-type lectin-like receptors, CLEC-1 and CLEC-2. Both display a single carbohydrate recognition domain and a cytoplasmic tyrosine-based motif. They are homologous to the NK cell receptors NKG2s and CD94 and also to the oxidized low-density lipoprotein receptor 1.
View Article and Find Full Text PDFIg-like transcripts (ILTs) encode cell surface receptors expressed on myeloid and lymphoid cells that are structurally and functionally related to killer cell inhibitory receptors. One ILT, designated ILT1, contains a short cytoplasmic domain that lacks sequence motifs implicated in signal transduction. Its function is unknown.
View Article and Find Full Text PDFLeukocyte activation can be negatively regulated by inhibitory receptors specific for MHC class I molecules. While one inhibitory receptor, Ig-like transcript 2 (ILT2), is expressed by all lymphoid and myelomonocytic cell types, other receptors display a more selective tissue distribution. Here we characterize an inhibitory receptor, termed ILT4, which is selectively expressed in monocytes, macrophages, and dendritic cells (DCs), binds classical class I molecules and the nonclassical class I molecules HLA-G, and transduces negative signals that can inhibit early signaling events triggered by stimulatory receptors.
View Article and Find Full Text PDFNatural killer (NK) cell-mediated lysis is negatively regulated by killer cell inhibitory receptors specific for major histocompatibility complex (MHC) class I molecules. In this study, we characterize a novel inhibitory MHC class I receptor of the immunoglobulin-superfamily, expressed not only by subsets of NK and T cells, but also by B cells, monocytes, macrophages, and dendritic cells. This receptor, called Ig-like transcript (ILT)2, binds MHC class I molecules and delivers a negative signal that inhibits killing by NK and T cells, as well as Ca2+ mobilization in B cells and myelomonocytic cells triggered through the B cell antigen receptor and human histocompatibility leukocyte antigens (HLA)-DR, respectively.
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