Eisuke Kondo

TL;DR: Glycosylceramide-mediated proliferative responses of Valpha14 NKT cells were abrogated by treatment with chloroquine-concanamycin A or by monoclonal antibodies against CD1d/Vbeta8, CD40/CD40L, or B7/CTLA-4/CD28, but not by interference with the function of a transporter-associated protein.

TL;DR: The Vα14 NKT cell–deficient mice could no longer mediate the interleukin-12 (IL-12)–induced rejection of tumors, and they mediated their cytotoxicity by an NK-like effector mechanism after activation with IL-12.

TL;DR: The results suggest that the ligand-activated Valpha14 NKT cells kill tumor cells directly through a CD1d/Valpha14 T cell receptor-independent, NK-like mechanism.

TL;DR: It is found that a distinct subset of lymphocytes, Vα14 NKT cells expressing an invariant antigen receptor encoded by V α14/Jα281 and Vβ7 segments, accumulated in the decidua during pregnancy and provoked abortion upon stimulation with α-galactosylceramide (α-GalCer), a specific ligand for V β7 segments.

TL;DR: Expression of the invariant V alpha 14/J alpha 281, but not V alpha 1, TCR in transgenic mice lacking endogenous TCR alpha expression blocks the development of conventional T alpha beta cells and leads to the preferential development of Valpha 14 NK T cells, suggesting a prerequisite role of invariant T cell antigen receptor alpha chain (TCR alpha) in NK T cell development.