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.