ライフサイエンスコーパス: splenic cell

1 esistant and could not be reconstituted with splenic cells.

2 proteins and is expressed at high levels in splenic cells.

3 leen as well as a reduction in the number of splenic cells.

4 e 129-145 bound in a population of nonimmune splenic cells.

5 levels of interleukin 4 compared with naive splenic cells.

6 ct of TNF for CTL generation by tumor bearer splenic cells.

7 i-MOPC-315 cytotoxicity by such tumor bearer splenic cells.

8 antitumor cytotoxicity by tumor-infiltrated splenic cells.

9 ty of TNF for CTL generation by tumor bearer splenic cells.

10 Conversely, GFP(+)HO-1(-/-) splenic cells also generated GFP(+)CD8(+) DCs in HO-1(+/

11 creased IFN-gamma production of autoreactive splenic cells and a decreased presence of regulatory CD4

12 at 2 days postburn in both Peyer's patch and splenic cells and a significant suppression in T-cell pr

13 and B6.Nba2-C) and lupus-prone (B6.Nba2-ABC) splenic cells and in a murine macrophage cell line that

14 of CD8+ T cells, reconstitution with CD8+ T splenic cells, and adoptive transfer of CD8+ CTL clones

15 pancreata, endotoxin, or anti-CD3-stimulated splenic cells, and T helper 1 lymphocytes, indicating th

16 -18 double knockout mice were protected from splenic cell apoptosis and sepsis-induced mortality by t

17 roles of T cells and IFN-gamma in mediating splenic cell apoptosis, parasitemia control, and host le

18 t via its ability to regulate sepsis-induced splenic cell apoptosis.

19 When these splenic cells are adoptively transferred to the peritone

20 n of CTLA-4Ig reduced BrdU incorporation for splenic cells by 70% with HD and LD stimulation, but had

21 odel, here we investigated the mechanisms of splenic cell death and their relationship to control of

22 f caspase 1 reduced levels of Il1beta/18 and splenic cell death, and prolonged survival in septic Sha

23 is was one of the major pathways involved in splenic cell death, which coincides with the peaks of pr

24 cannot be recapitulated in ex vivo-activated splenic cells, even though the latter express high level

25 Bone marrow and splenic cells extracted from tumor-bearing and control m

26 y-state levels of Ifi202 mRNA were higher in splenic cells from C57BL/6, B6.Nba2, NZB, and (NZB x NZW

27 However, splenic cells from CD154 knockout mice induced comparabl

28 determine the mechanism of TNF alpha action, splenic cells from control NOD and RIP-TNF alpha mice we

29 In contrast to the induction of diabetes by splenic cells from control NOD mice, splenic cells from

30 ice when CD8+ diabetogenic cloned T cells or splenic cells from diabetic NOD mice were adoptively tra

31 depletion shortly after transplantation with splenic cells from G-CSF-treated donors blocks suppressi

32 e expression of E2F1 and its target genes in splenic cells from lupus-prone B6.Nba2 congenic mice, wh

33 er of these Th2-deviated CD4(+) T cells with splenic cells from newly diabetic NOD mice into NOD.RAG(

34 etes by splenic cells from control NOD mice, splenic cells from RIP-TNF alpha transgenic mice did not

35 s and produced cytokines equivalent to naive splenic cells from Tg x RAG-1(+/+) mice.

36 expression on the PEC was up-regulated, but splenic cells had normal MHC class II expression.

37 iated with elevated STAT3 phosphorylation in splenic cells, IL-10 mRNA expression, and expansion of c

38 a significant increase in the proportion of splenic cells in S phase and an expansion of erythroid p

39 Moreover, culturing splenic cells in the presence of BAFF increased survival

40 reased erythroid differentiation of Vhl(R/R) splenic cells in vitro.

41 pression of v-rel in two B-cell lines and in splenic cells induced the expression of p75.

42 In contrast, IFN-gamma production by splenic cells isolated from treated IL-2-/- TNP-OVA-immu

43 d medium from PC-3M-IFN-beta cells augmented splenic cell-mediated cytolysis to control tumor cells,

44 ggregates, isolated from the bone marrow and splenic cells of aging mice and followed by biochemical

45 adoptive transfer into naive BF-F344 rats of splenic cells of naive CV-F344 rats (restimulated with B

46 rmore, Ifi202 mRNA levels were detectable in splenic cells of wild-type (Esr1(+/+)), but not null (Es

47 VIPR2 agonist or after adoptive transfer of splenic cell populations from agonist-treated mice admin

48 ve splenic damage with dramatic reduction of splenic cell populations.

49 tissue from the anterior stomach resulted in splenic cells randomly scattering suggesting a guidance

50 hat (i) regardless of route or mouse strain, splenic cells reactivated gammaHV68 less efficiently tha

51 on of TNF alpha in islets also downregulated splenic cell responses to autoantigens.

52 s, implicating the TALE homeoprotein Pbx1 in splenic cell specification.

53 timulation cultures of MOPC-315 tumor bearer splenic cell suspensions containing metastatic tumor cel

54 Moreover, splenic cell suspensions derived from alpha-asialo GM1-t

55 significantly higher in the Stat1-deficient splenic cells than in the wild-type cells.

56 hat TLR7.1 mice have a dramatic expansion of splenic cells that derive from granulocyte/macrophage pr

57 compared expression of IL-17A and IL-17F in splenic cells under different conditions.

58 Despite expression of IL-9 by DKO splenic cells upon in vitro mitogenic stimulation, IL-9

59 The phenotype of splenic cells was determined by flow cytometry.

60 ugh presented in vivo as well as in vitro by splenic cells, was unable to stimulate a specific T cell

61 reased steady-state levels of Ifi202 mRNA in splenic cells, whereas treatment with the male hormone d

62 own that supernatants from PTx-treated mouse splenic cells, which contained IL-6 and other proinflamm

63 itis was then used to show that treatment of splenic cells with ALF produced an 8.6-fold decrease in

64 The treatment of unfractionated splenic cells with ConA plus CT induced B-cell prolifera

65 The treatment of splenic cells with concanavalin A (ConA) plus CT enhance

66 The treatment of unfractionated splenic cells with CT, LT-IIa, or LT-IIb enhanced the pr

67 Treatment of splenic cells with IFN-alpha or -gamma reduced levels of