ライフサイエンスコーパス: skin graft rejection

1 pairs both CD8 T cell infiltration and acute skin graft rejection.

2 nting CBK but not third-party B10.A (H2k+Dd) skin graft rejection.

3 - T cells, however, had no influence on male skin graft rejection.

4 skin grafts; T-cell recovery correlated with skin graft rejection.

5 imulatory blockade and to inhibit allogeneic skin graft rejection.

6 D8+ T cells produce RANTES during allogeneic skin graft rejection.

7 scular injury that resembles human first-set skin graft rejection.

8 fficient class I antigen expression to cause skin graft rejection.

9 d to the CD8+ T effector cells requisite for skin graft rejection.

10 ry mediators and accelerate T cell-meditated skin graft rejection.

11 for Parkin-dependent mitophagy in curtailing skin-graft rejection.

12 the impact of Parkin-dependent mitophagy on skin-graft rejection.

13 reviously recognized) features of allogeneic skin graft rejection: (1) that rejection can be initiate

14 Following the skin graft rejection, a rise in the MLR, development of

15 MHC genes would explain why cheetahs ablate skin graft rejection among unrelated individuals.

16 ed T cells in a SCID reconstitution model of skin graft rejection and are important in T cell accumul

17 plore the involvement of Langerhans cells in skin graft rejection and describe fascinating results.

18 H60 incompatibility does not result in skin graft rejection and only a minority of heart transp

19 nd endothelium was examined using allogeneic skin graft rejection as a model of cutaneous inflammatio

20 A model of HY-mediated skin graft rejection by athymic, TCD mice was used to sh

21 his cell line specifically induced a form of skin graft rejection characterized by the presence of TH

22 no inhibition or even acceleration of donor skin graft rejection compared with non-DST control (naiv

23 od subtly yet reproducibly decreases time to skin graft rejection elicited by central but not effecto

24 G-Neutrophils, were confirmed by third-party skin graft rejection; importantly, a graft-versus-leukem

25 n to donor cells is supported by accelerated skin graft rejection in mice transplanted with sca+ cell

26 r histocompatibility complex (MHC)-disparate skin graft rejection in mice.

27 ntigens via the indirect pathway can mediate skin graft rejection in the absence of IFN-gamma.

28 days postburn results in enhanced allogeneic skin graft rejection in unburned recipient mice.

29 drug-modified DCs prior to transplantation, skin graft rejection kinetics were similar to those in n

30 ored by mixed lymphocyte culture (MLC), CML, skin graft rejection, liver biopsies, and serial serum c

31 ates that subsequent to T cell initiation of skin graft rejection, platelets contribute to further T

32 Furthermore, skin graft rejection remained significantly delayed in L

33 OVA, exhibited a somewhat delayed first set skin graft rejection response with lower allo-specific C

34 dily mounted first and second set allogeneic skin graft rejection responses, and developed primary an

35 ly unreactive in certain other assays, e.g., skin graft rejection; responses to MHC alloantigens, by

36 allopeptide can mediate a form of allogeneic skin graft rejection that exhibits characteristics of a

37 administered systemically in mouse models of skin graft rejection, these nanosensors preferentially a

38 e the contribution of DNA-PKcs to allogeneic skin graft rejection to potentially highlight a novel st

39 Skin-graft rejection was seen in four of six animals rec

40 diac rejection, chronic renal rejection, and skin graft rejection were compared using CD20 or CD19 mA

41 umab (anti-CD3 mAb) and found it could delay skin graft rejection, whereas ipilimumab (anti-CTLA-4 [c

42 s was originally defined by the phenotype of skin graft rejection, which is a complex genetic trait.

43 pecific Treg cells significantly delayed CBK skin graft rejection without any other immunosuppression