PT - JOURNAL ARTICLE AU - Olcese, L AU - Lang, P AU - Vély, F AU - Cambiaggi, A AU - Marguet, D AU - Bléry, M AU - Hippen, K L AU - Biassoni, R AU - Moretta, A AU - Moretta, L AU - Cambier, J C AU - Vivier, E TI - Human and mouse killer-cell inhibitory receptors recruit PTP1C and PTP1D protein tyrosine phosphatases. DP - 1996 Jun 15 TA - The Journal of Immunology PG - 4531--4534 VI - 156 IP - 12 4099 - http://www.jimmunol.org/content/156/12/4531.short 4100 - http://www.jimmunol.org/content/156/12/4531.full SO - J. Immunol.1996 Jun 15; 156 AB - NK cells express cell surface receptors for MHC class I proteins (KIR). Engagement of these receptors inhibits NK cell cytotoxic programs. KIR can be expressed on T cells, and their engagement also results in inhibition of effector functions initiated by the CD3/TCR complex. While human KIR genes belong to the Ig gene superfamily, mouse KIR belong to a family of dimeric lectins. Despite these distinct evolutionary origins, we show here that both HLA-Cw3-specific human p58.183 receptors and H-2D d/k-specific mouse Ly49A receptors recruit the same protein tyrosine phosphatases, PTP1C and PTP1D, upon phosphorylation of critical intracytoplasmic tyrosine residues. These results document a common pathway by which diverse KIR can down-regulate NK and T cell activation programs, and further define the sequence of the immunoreceptor tyrosine-based inhibitory motif (ITIM), initially described in FcgammaRIIB1, and expressed in both human and mouse KIR.