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Retracted: Dissociated expression of natural killer 1.1 and T‐cell receptor by invariant natural killer T cells after interleukin‐12 receptor and T‐cell receptor signalling
Author(s) -
Emoto Masashi,
Shimizu Takamitsu,
Koike Hiromi,
Yoshizawa Izumi,
Hurwitz Robert,
Kaufmann Stefan H. E.,
Emoto Yoshiko
Publication year - 2010
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2009.03148.x
Subject(s) - stimulation , receptor , biology , t cell receptor , microbiology and biotechnology , endocrinology , medicine , immune system , t cell , immunology , biochemistry
Summary Invariant (i) natural killer T (NKT) cells become undetectable after stimulation with α‐galactosylceramide (α‐GalCer) or interleukin (IL)‐12. Although down‐modulation of surface T‐cell receptor (TCR)/NKR‐P1C (NK1.1) expression has been shown convincingly after stimulation with α‐GalCer, it is unclear whether this also holds true for IL‐12 stimulation. To determine whether failure to detect iNKT cells after IL‐12 stimulation is caused by dissociation/internalization of TCR and/or NKR‐P1C, or by block of de novo synthesis of these molecules, and to examine the role of IL‐12 in the disappearance of iNKT cells after stimulation with α‐GalCer, surface (s)/cytoplasmic (c) protein expression, as well as messenger RNA (mRNA) expression of TCR/NKR‐P1C by iNKT cells after stimulation with α‐GalCer or IL‐12, and the influence of IL‐12 neutralization on the down‐modulation of sTCR/sNKR‐P1C expression by iNKT cells after stimulation with α‐GalCer were examined. The s/cTCR +  s/cNKR‐P1C + iNKT cells became undetectable after in vivo administration of α‐GalCer, which was partially prevented by IL‐12 neutralization. Whereas s/cNKR‐P1C + iNKT cells became undetectable after in vivo administration of IL‐12, s/cTCR + iNKT cells were only marginally affected. mRNA expression of TCR/NKR‐P1C remained unaffected by α‐GalCer or IL‐12 treatment, despite the down‐modulation of cTCR and/or cNKR‐P1C protein expression. By contrast, cTCR +  cNKR‐P1C +  sTCR −  sNKR‐P1C − iNKT cells and cNKR‐P1C +  sNKR‐P1C −  iNKT cells were detectable after in vitro stimulation with α‐GalCer and IL‐12, respectively. Our results indicate that TCR and NKR‐P1C expression by iNKT cells is differentially regulated by signalling through TCR and IL‐12R. They also suggest that IL‐12 participates, in part, in the disappearance of iNKT cells after stimulation with α‐GalCer by down‐modulating not only sNKR‐P1C, but also sTCR.

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