Electron-hole bilayers are expected to make a transition from a pair of weakly coupled two-dimensional systems to a strongly coupled exciton system as the barrier between the layers is reduced. ...Coulomb drag measurements on devices with a 30 nm barrier are consistent with two weakly coupled 2D Fermi systems where the drag decreases with temperature. For a 20 nm barrier, however, we observe an increase in the drag resistance as the temperature is reduced when a current is driven in the electron layer and voltage measured in the hole layer. These results indicate the onset of strong coupling possibly due to exciton formation or phenomena related to exciton condensation.
Summary
Patients with recurrent miscarriage (RM) show up‐regulated cytotoxic natural killer (NK) cells that are suspected to play a causal role in abortion. In the present study, we investigated ...counter‐regulating inhibitory mechanisms and compared the results in RM patients with those of healthy controls (HC), patients with end‐stage renal disease (ESRD) and kidney transplant recipients late post‐transplant (TX). NK, NK T and T cell subsets were analysed in the peripheral blood of 31 RM, 14 female ESRD and nine female TX patients as well as 21 female HC using eight‐colour fluorescence flow cytometry. Compared with HC, RM patients showed significantly higher absolute numbers of CD56+ NK cells co‐expressing the phenotype interferon (IFN)‐γR+, IL‐4+, transforming growth factor (TGF)‐β+, IL‐4+ human leucocyte antigen D‐related (HLA‐DR)+, TGF‐β+HLA‐DR+, IL‐4+TGF‐β+, IL‐4+TGF‐β–, IFN‐γ+ and/or IL‐10–IFN‐γ+ (all P ≤ 0·01), more IL‐17+CD56bright (P = 0·028) NK cells and more CD56dimCD16+ NK cells co‐expressing IFN‐γR, IFN‐γ, IL‐4 and/or TGF‐β (all P ≤ 0·01). When the same cell subsets were analysed in ESRD or TX patients, cytokine‐producing NK cell subsets were not significantly different from those of HC. RM patients showed significantly higher absolute numbers of CD158a+, CD158b+, CD158a–CD158e+ (all P < 0·05), NKG2D+NKG2A+, NKG2D +NKG2A–, NKG2D+ and/or NKG2A+ (all P ≤ 0·01) CD56+ NK cells and higher CD158a+, CD158b+ (all P < 0·05), NKG2D+ and/or NKG2A+ (all P < 0·01) CD56dim+CD16+ NK cells than HC. In contrast, ESRD patients had normal and TX recipients had lower CD158a+ and NKG2D+NKG2A–CD56+ NK cells and lower CD158a+CD56dim+CD16+ NK cells (all P < 0·05) than HC. RM patients have abnormally high circulating NK cells expressing inhibitory cytokines and inhibitory surface receptors which might contribute to the pathogenesis of RM.
Our data show that compared to female healthy controls, recurrent miscarriage patients have abnormally high NK, NKT and T cells in the blood which express inhibitory cytokines and inhibitory surface receptors. In contrast, dialysis and transplant patients had normal or even decreased levels of these cell subsets. We interpret these results as showing that the upregulation of inhibitory mechanisms in recurrent miscarriage patients represents a counter regulation to a strongly upregulated cytotoxic immune system, possibly the cause of recurrent miscarriage.
Little is known about a possible interaction of natural killer (NK) cells with regulatory T cells (T
) in long-term stable kidney transplant recipients. Absolute counts of lymphocyte and T
subsets ...were studied in whole blood samples of 136 long-term stable renal transplant recipients and 52 healthy controls using eight-colour fluorescence flow cytometry. Patients were 1946 ± 2201 days (153-10 268 days) post-transplant and showed a serum creatinine of 1·7 ± 0·7 mg/dl. Renal transplant recipients investigated > 1·5 years post-transplant showed higher total NK cell counts than recipients studied < 1·5 years after transplantation (P = 0·006). High NK cells were associated with high glomerular filtration rate (P = 0·002) and low serum creatinine (P = 0·005). Interestingly, high NK cells were associated with high CD4
CD25
CD127
forkhead box protein 3 (FoxP3
) T
that co-express the phenotype Helios
interferon (IFN)-γ
and appear to have stable FoxP3 expression and originate from the thymus. Furthermore, high total NK cells were associated with T
that co-express the phenotypes interleukin (IL)-10
transforming growth factor (TGF)-β
(P = 0·013), CD183
CD62L
(P = 0·003), CD183
CD62
(P = 0·001), CD183
CD62L
(P = 0·002), CD252
CD152
(P < 0·001), CD28
human leucocyte antigen D-related (HLA-DR
) (P = 0·002), CD28
HLA-DR
(P < 0·001), CD95
CD178
(P < 0·001) and CD279
CD152
(P < 0·001), suggesting that these activated T
home in peripheral tissues and suppress effector cells via TGF-β and cytotoxic T lymphocyte-associated protein 4 (CTLA-4). The higher numbers of NK and T
cell counts in patients with long-term good allograft function and the statistical association of these two lymphocyte subsets with each other suggest a direct or indirect (via DC) interaction of these cell subpopulations that contributes to good long-term allograft acceptance. Moreover, we speculate that regulatory NK cells are formed late post-transplant that are able to inhibit graft-reactive effector cells.
PDF
