ライフサイエンスコーパス: skin graft rejection

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

30 Furthermore, skin graft rejection remained significantly delayed in L

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

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

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

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

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

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

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

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

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

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