The repertoire of killer cell Ig-like receptor and CD94 : NKG2A receptors in T cells: clones sharing identical alpha beta TCR rearrangement express highly diverse killer cell Ig-like receptor patterns

Citation
M. Uhrberg et al., The repertoire of killer cell Ig-like receptor and CD94 : NKG2A receptors in T cells: clones sharing identical alpha beta TCR rearrangement express highly diverse killer cell Ig-like receptor patterns, J IMMUNOL, 166(6), 2001, pp. 3923-3932
Citations number
58
Categorie Soggetti
Immunology
Journal title
JOURNAL OF IMMUNOLOGY
ISSN journal
00221767 → ACNP
Volume
166
Issue
6
Year of publication
2001
Pages
3923 - 3932
Database
ISI
SICI code
0022-1767(20010315)166:6<3923:TROKCI>2.0.ZU;2-Q
Abstract
Killer cell Ig-like receptor (KIR) and CD94:NKG2A molecules were first defi ned as human NK cell receptors (NKR), but now are known to be expressed and to function on subpopulations of T cells. Here the repertoires of KTR and CD94:NKG2A expression by T cells from two donors were examined and compared with their previously defined NK cell repertoires, T cell clones generated from peripheral blood of both donors expressed multiple NKR in different c ombinations and used the range of receptors expressed by NK cells. In both donors alpha beta T cells less frequently expressed the inhibitory receptor s CD94:NKG2A and KIR2DL1 than either gamma delta T cells or NK cells. In co ntrast to NK cells, not all NKR+ T cells expressed an inhibitory receptor f or autologous HLA class I. This lack of specific inhibitory NKR was especia lly apparent on cup T cells of one donor. Overall, alpha beta T cells exhib ited a distinct pattern of NKR expression different from that of gamma delt a T and NK cells, which expressed highly similar NKR repertoires, In one do nor, analysis of TCR rearrangement revealed a dominant subset of NKR+ T cel ls sharing identical TCR alpha- and beta -chains, Remarkably, among 55 T ce ll clones sharing the same TCR alpha beta rearrangement 18 different KIR ph enotypes were seen, suggesting that KIR expression was initiated subsequent ly to TCR rearrangement.