HLA class I-specific inhibitory receptors in human T lymphocytes: Interleukin 15-induced expression of CD94/NKG2A in superantigen- or alloantigen-activated CD8<sup>+</sup> T cells

Mingari, Maria Cristina; Ponte, Marco; Bertone, Stefania; Schiavetti, Francesca; Vitale, Chiara; Fulle, Stefania; Moretta, Alessandro; Moretta, Lorenzo

doi:10.1073/pnas.95.3.1172

Cited by 215 publications

(182 citation statements)

References 34 publications

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“…This has been achieved upon antigenic stimulation, both in vitro and in vivo [13,14]. In vitro, this phenomenon is potentiated by cytokines, such as IL-2, IL-10, IL-12, IL-15 and TGFb [15][16][17][18]. These observations are consistent with the in vivo expression of NKR on antigen-experienced T cells.…”

Section: Introductionsupporting

confidence: 53%

Expression of inhibitory KIR is confined to CD8⁺ effector T cells and limits their proliferative capacity

et al. 2004

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A subset of effector/memory CD8 + T cells expresses natural killer cell receptors (NKR). Expression of inhibitory NKR at that stage of T cell differentiation is poorly understood. Interestingly, recent studies in mice indicated that transgenic expression of an inhibitory NKR induced the accumulation of memory T cells by inhibiting activation-induced cell death (AICD). To further understand the role of inhibitory NKR on T cells, we characterized the subset of human peripheral T cells expressing the inhibitory NKR, CD158b, and studied the modulation of antigen-driven T cell expansion by an endogenous inhibitory NKR. We found that CD158b expression was confined to a population of CD8 + TCRab + effector T cells as defined by a CD45RA + CCR7 -phenotype and high constitutive expression of granzyme B1. Few cells expressed the activating form CD158j in the absence of CD158b. Functionally, engagement of CD158b by MHC ligands diminished early TCR signaling, as well as AICD. However, the reduced AICD did not rescue cells for proliferation, since T cell expansion in the presence of CD158b triggering was impaired. Expression of inhibitory NKR on effector CD8 + T cells may explain in part the poor replicative capacity of T cells at that stage of differentiation.

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Section: Introductionsupporting

confidence: 53%

Expression of inhibitory KIR is confined to CD8⁺ effector T cells and limits their proliferative capacity

et al. 2004

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“…In the bone marrow of mice, expression of NK1.1 and Ly49 molecules have been shown to be associated with memory T cells (23). Studies performed in humans have described activated CD8 ϩ T cells that possess NKR-P1C (24) or inhibitory NK cell receptors such as p58.2 (25-27), NKB-1 (27,28), and CD94/NKG2A (25,29,30). Similar T cells have also been found in HIV-infected patients (31).…”

Section: Cd8␤ ϩ Nk11 ϩ Cells Are Not Conventional Nkt Cellsmentioning

confidence: 63%

Emergence of CD8+ T Cells Expressing NK Cell Receptors in Influenza A Virus-Infected Mice

Kambayashi

Assarsson

Michaëlsson

et al. 2000

The Journal of Immunology

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Both innate and adaptive immune responses play an important role in the recovery of the host from viral infections. In the present report, a subset of cells coexpressing CD8 and NKR-P1C (NK1.1) was found in the lungs of mice infected with influenza A virus. These cells were detected at low numbers in the lungs of uninfected mice, but represented up to 10% of the total CD8+ T cell population at day 10 postinfection. Almost all of the CD8+NK1.1+ cells were CD8αβ+CD3+TCRαβ+ and a proportion of these cells also expressed the NK cell-associated Ly49 receptors. Interestingly, up to 30% of these cells were virus-specific T cells as determined by MHC class I tetramer staining and by intracellular staining of IFN-γ after viral peptide stimulation. Moreover, these cells were distinct from conventional NKT cells as they were also found at increased numbers in influenza-infected CD1−/− mice. These results demonstrate that a significant proportion of CD8+ T cells acquire NK1.1 and other NK cell-associated molecules, and suggests that these receptors may possibly regulate CD8+ T cell effector functions during viral infection.

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“…Second stimulation of CMV-specific NKR Ϫ T cells with stimulatory cytokines and cognate peptide did not result in acquisition of KIR. Many other deliberate attempts to induce KIR expression in T cells in vitro have failed, although Mingari et al have reported the induction of CD94:NKG2A (50). Recently, down-regulation of KIR was reported on NKR ϩ T cell clones that were deprived of specific Ag (51).…”

Section: Discussionmentioning

confidence: 99%

The Repertoire of Killer Cell Ig-Like Receptor and CD94:NKG2A Receptors in T Cells: Clones Sharing Identical αβ TCR Rearrangement Express Highly Diverse Killer Cell Ig-Like Receptor Patterns

Uhrberg

Valiante

Young

et al. 2001

The Journal of Immunology

118

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Killer cell Ig-like receptor (KIR) and CD94:NKG2A molecules were first defined 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 KIR 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 combinations and used the range of receptors expressed by NK cells. In both donors αβ T cells less frequently expressed the inhibitory receptors CD94:NKG2A and KIR2DL1 than either γδ T cells or NK cells. In contrast to NK cells, not all NKR+ T cells expressed an inhibitory receptor for autologous HLA class I. This lack of specific inhibitory NKR was especially apparent on αβ T cells of one donor. Overall, αβ T cells exhibited a distinct pattern of NKR expression different from that of γδ T and NK cells, which expressed highly similar NKR repertoires. In one donor, analysis of TCR rearrangement revealed a dominant subset of NKR+ T cells sharing identical TCR α- and β-chains. Remarkably, among 55 T cell clones sharing the same TCRαβ rearrangement 18 different KIR phenotypes were seen, suggesting that KIR expression was initiated subsequently to TCR rearrangement.

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HLA class I-specific inhibitory receptors in human T lymphocytes: Interleukin 15-induced expression of CD94/NKG2A in superantigen- or alloantigen-activated CD8⁺ T cells

Cited by 215 publications

References 34 publications

Expression of inhibitory KIR is confined to CD8⁺ effector T cells and limits their proliferative capacity

Expression of inhibitory KIR is confined to CD8⁺ effector T cells and limits their proliferative capacity

Emergence of CD8+ T Cells Expressing NK Cell Receptors in Influenza A Virus-Infected Mice

The Repertoire of Killer Cell Ig-Like Receptor and CD94:NKG2A Receptors in T Cells: Clones Sharing Identical αβ TCR Rearrangement Express Highly Diverse Killer Cell Ig-Like Receptor Patterns

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HLA class I-specific inhibitory receptors in human T lymphocytes: Interleukin 15-induced expression of CD94/NKG2A in superantigen- or alloantigen-activated CD8+ T cells

Cited by 215 publications

References 34 publications

Expression of inhibitory KIR is confined to CD8+ effector T cells and limits their proliferative capacity

Expression of inhibitory KIR is confined to CD8+ effector T cells and limits their proliferative capacity

Emergence of CD8+ T Cells Expressing NK Cell Receptors in Influenza A Virus-Infected Mice

The Repertoire of Killer Cell Ig-Like Receptor and CD94:NKG2A Receptors in T Cells: Clones Sharing Identical αβ TCR Rearrangement Express Highly Diverse Killer Cell Ig-Like Receptor Patterns

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HLA class I-specific inhibitory receptors in human T lymphocytes: Interleukin 15-induced expression of CD94/NKG2A in superantigen- or alloantigen-activated CD8⁺ T cells

Expression of inhibitory KIR is confined to CD8⁺ effector T cells and limits their proliferative capacity

Expression of inhibitory KIR is confined to CD8⁺ effector T cells and limits their proliferative capacity