The ice reservoir that served as the source for the meltwater pulse IA remains enigmatic and controversial. We show that each of the melting scenarios that have been proposed for the event produces a distinct variation, or fingerprint, in the global distribution of meltwater. We compare sea-level fingerprints associated with various melting scenarios to existing sea-level records from Barbados and the Sunda Shelf and conclude that the southern Laurentide Ice Sheet could not have been the sole source of the meltwater pulse, whereas a substantial contribution from the Antarctic Ice Sheet is consistent with these records.

To define the phenotype and T cell receptor (TCR) repertoire of CD1d-dependent T cells, we compared the populations of T cells that persisted in major histocompatibility complex (MHC)-deficient mice, which lack mainstream T cells, with those from MHC/CD1d doubly deficient mice, which lack both mainstream and CD1d-dependent T cells. Surprisingly, up to 80% of the CD1d-dependent T cells were stained by tetramers of CD1d/α-galactosylceramide, which specifically identify the previously described CD1d autoreactive Vα14-Jα18/Vβ8 natural killer (NK) T cells. Furthermore, zooming in on the CD1d-dependent non-Vα14 T cells, we found that, like Vα14 NK T cells, they mainly expressed recurrent, CD1d autoreactive TCR families and had a natural memory phenotype. Thus, CD1d-restricted T cells differ profoundly from MHC-peptide–specific T cells by their predominant use of autoreactive and semiinvariant, rather than naive and diverse, TCRs. They more closely resemble other lineages of innate lymphocytes such as B-1 B cells, γδ T cells, and NK cells, which express invariant or semiinvariant autoreactive receptors. Finally, we demonstrate that the MHC-restricted TCR repertoire is essentially non–cross-reactive to CD1d. Altogether, these findings imply that lipid recognition by CD1d-restricted T cells may have largely evolved as an innate rather than an adaptive arm of the mouse immune system.

No abstract

IL-12 is a potent cytokine that impairs the growth of several tumors in vivo in natural as well as in therapeutic conditions. Although IL-12 can enhance a number of immunological antitumor mechanisms, including those mediated by NK cells and CTL, recent reports have suggested that the mouse CD1d-restricted Vα14-Jα18 NKT cell was the essential cell type recruited in most, if not all tumor rejection models, including the B16 melanoma. In this study, we have examined and compared the role of NKT cells, T cells, NK cells, and other non-T non-B cells in the rejection of B16 melanoma cells after exogenous administration of IL-12. Surprisingly, our results failed to confirm a necessary role for NKT cells in this model. Instead, we found that NK cells mediated the rejection of liver metastases, whereas other γc-dependent non-T non-B cells, possibly lymphoid dendritic cells, were required for rejection of skin tumors. These findings challenge the view that NKT cells are systematically required for IL-12-mediated rejection of tumors, and instead reveal that a variety of effector pathways can be recruited depending on the tumor microenvironment.

Young and adult chickens exhibit substantial inner-ear damage and post-exposure deterioration in cochlear nerve activity following exposure to intense sound. Both the structural and functional losses largely recover in both age groups within 2–4 weeks after exposure. However, some aspects of acoustic trauma differ between the young and adult chicken ear. Overstimulation in the young chick causes considerable post-exposure loss and then recovery of the steady-state endocochlear potential, while in the adult animal there is little post-exposure effect on this potential. Moreover, in adults there is post-exposure loss but little recovery in the distortion product otoacoustic emission (DPOAE). The present study explores the possibility of an age difference in the effects of overstimulation on the DPOAE by examining these emissions in young chicks following exposure to an intense pure tone. Chicks exposed to intense sound were formed into groups at 0 and 12 days of recovery, and these were complemented by two additional groups of age-matched controls. The cubic difference tone emission (the 2f₁–f₂ DPOAE component) was measured at 9 levels for 13 frequencies in all groups. Shortly after the exposure, the DPOAE reliably declined with the maximum loss at or above the exposure tone frequency. The exposed chicks examined 12 days after exposure showed complete recovery of the DPOAE. It would appear that 12 days of recovery sufficiently repaired inner ear damage to completely restore DPOAE production. This result is different from that in adult chicken and may be related to the greater severity of acoustic damage in the adult ear, a reduced susceptibility of the young ear to acoustic trauma, or the ability of the young animal to more successfully repair the inner ear.