RESEARCH Greater frequency of CD5- e

Selective recognition of peptides within particular major histocompatibility complex (MHC) molecules by clono-typic T cell receptors (TCR) underlies both the specifi-city and mechanics of T cell activation. While the overall strength or avidity of the cognate TCR/peptide/MHC interaction must itself exceed a certain threshold, non-polymorphic accessory, co-receptor and other molecules can modulate the tenor of signal transduction and sway the outcome of antigen-specific recognition. The group B cysteine-rich scavenger receptor CD5 modulates antigen-specific signaling on virtually all T cells in a ligand-independent manner [1-5]. When T cells form conjugates with antigen-presenting cells, CD5 colocal-izes with TCRs engaging cognate MHC/peptide com-plexes within the immunological synapse and recruits SHP phosphatases to the area through its cytoplasmic tyrosine inhibitory motif (ITIM), [3,6]. Thus, localized antagonism of phosphorylation events by CD5 dimin-ishes TCR-derived activation signals [7]. With highe