Naturally arising CD25(+)CD4(+) regulatory T (T(R)) cells can be exploited to establish immunologic tolerance to non-self antigens. In vivo exposure of CD25(+)CD4(+) T cells from normal naive mice to alloantigen in a T cell-deficient environment elicited spontaneous expansion of alloantigen-specific CD25(+)CD4(+) T(R) cells, which suppressed allograft rejection mediated by subsequently transferred naive T cells, leading to long-term graft tolerance. The expanded T(R) cells, which became CD25(low) in the absence of other T cells, stably sustained suppressive activity, maintained expression levels of other T(R) cell-associated molecules, including Foxp3, CTLA-4 and GITR, and could adoptively transfer tolerance to normal mice. Furthermore, specific removal of the T(R) cells derived from originally transferred CD25(+)CD4(+) T(R) cells evoked graft rejection in the long-term tolerant mice, indicating that any T(R) cells deriving from CD25(-)CD4(+) naive T cells minimally contribute to graft tolerance and that natural T(R) cells are unable to infectiously confer significant suppressive activity to other T cells. Similar antigen-specific expansion of T(R) cells can also be achieved in vitro by stimulating naturally present CD25(+)CD4(+) T cells with alloantigen in the presence of IL-2. The expanded CD25(+)CD4(+) T cells potently suppressed even secondary MLR in vitro and, by in vivo transfer, established antigen-specific long-term graft tolerance. Thus, in vivo or in vitro, direct or indirect ways of antigen-specific expansion of naturally arising Foxp3(+)CD25(+)CD4(+) T(R) cells can establish antigen-specific dominant tolerance to non-self antigens, and would also be instrumental in re-establishing self-tolerance in autoimmune disease and antigen-specific negative control of pathological immune responses.
Naturally arising CD4+CD25+ regulatory T (Treg) cells can be exploited to establish immunologic tolerance to allogeneic transplants. In vivo exposure of CD4+CD25+ T cells from normal naive mice to alloantigen in a T cell-deficient environment elicits spontaneous expansion of alloantigen-specific CD4+CD25+ natural Treg cells, which are able to suppress allograft rejection mediated by subsequently transferred naive T cells, leading to long-term graft tolerance. Similar antigen-specific expansion of natural Treg cells can also be achieved in vitro by stimulating CD4+CD25+ T cells from normal animals with alloantigen in the presence of high doses of interleukin-2. The expanded CD4+CD25+ Treg cells are even capable of suppressing secondary mixed leukocyte reaction in vitro and, by in vivo transfer, establishing antigen-specific long-term graft tolerance. Thus, in vivo or in vitro, direct or indirect ways of alloantigen-specific expansion of naturally arising CD4+CD25+ Treg cells can establish antigen-specific dominant tolerance to allogeneic transplants.
The hydrogenation of 1,3-butadiene on copper surfaces was studied in detail. A highly selective formation of 1-butene was observed in the range of temperatures from 27 to 76 °C; the initial rate of the formation was well expressed in terms of the partial pressures of hydrogen, ph and butadiene, ph, as v=kph⁄(1+Kpb)2 in the pressure range of 5–100 Torr. The reaction with D2 gave butene-d0 and -d1 as the main products, and the butadiene was partly exchanged with D2 during the hydrogenation. The microwave spectroscopic analysis revealed that the 1-butene produced consisted of CH2=CHCH2CH2D, CH2=CHCHDCH3, and CHD=CHCH2CH3, without even a trace of CH2=CDCH2CH3. Therefore, it was concluded that the reaction proceeds via the isobutenyl surface intermediate and that the dissociative adsorption of hydrogen is rate-determining. The structural analysis of the surface suggested that the stable lattice planes, such as (111), (100)3, and (110), are responsible for the reaction. The origin of the high 1-butene selectivity was discussed on the basis of the surface geometry and the proposed mechanism.
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