ライフサイエンスコーパス: red pulp

1 s were adjacent to Tcf21(+) stromal cells in red pulp.

2 nation revealed masses of hepatocytes in the red pulp.

3 , parasitized erythrocytes were found in the red pulp.

4 aught in fluid flow and are carried into the red pulp.

5 ked disorganization of the marginal zone and red pulp.

6 ife spans, were exclusively localized to the red pulp.

7 ne, whereas CD62L(-) cells were found in the red pulp.

8 on overload localized selectively to splenic red pulp.

9 ondary effector CD8 T cells are found in the red pulp.

10 h some XlAID(+) cells were also found in the red pulp.

11 lp, whereas Noxa and Bid were induced in the red pulp.

12 d in guiding T cell movements in the splenic red pulp.

13 gan T cell zones and by cells in the splenic red pulp.

14 ive splenic IgG AFC response, largely in the red pulp.

15 defined lymphoid follicles and expansion of red pulp, a greater than fourfold increase in splenic mo

16 Later, these cells were found in the red pulp and a disruption of all CD8 T cell zones was ob

17 in clusters in the cords of the subcapsular red pulp and are distinct from macrophages and DCs.

18 mouse models and a pathological reduction in red pulp and extramedullary hematopoiesis.

19 d a stellate shape and were localized to the red pulp and germinal centers, suggesting that they are

20 P-70(-/-) mice show more plasma cells in the red pulp and in the bone marrow, and increased NP-specif

21 ated IDO expression in the marginal zone and red pulp and inhibition of IDO markedly accelerated dise

22 ps anatomically to the splenic marginal zone/red pulp and is defined by prolonged motility paralysis

23 rate that CXCL12 is expressed within splenic red pulp and lymph node medullary cords as well as in bo

24 d redistribution of dendritic cells from the red pulp and marginal zone of the spleen into the T cell

25 he switched B cells transiently occupied the red pulp and marginal zone, whereas others persisted in

26 alized to Sn(+) Mphis and other cells in the red pulp and marginal zone.

27 IL-10 by splenic gamma delta+ T cells in the red pulp and marginal zones that coincided with maximal

28 f mice, effector CD8 T cells localize to the red pulp and memory CD8 T cells localize to the T cell z

29 The splenic red pulp and the luminal surface of high endothelial ven

30 ich is the interface between the nonlymphoid red pulp and the lymphoid white pulp, merged with compon

31 TNF production by spleen macrophages in the red pulp and the marginal zone.

32 ine splenic neutrophils that localize in the red pulp and the marginal zone.

33 Spleen tissue contained antigens in both the red pulp and the periartereolar region of the white pulp

34 owed disrupted follicular structure, loss of red pulp, and granulocyte and megakarocyte invasion.

35 r peripheral Ags: the splenic marginal zone, red pulp, and lymph node sinuses.

36 finity were mainly restricted to the splenic red pulp, and the host generated an effective CTL respon

37 of this redistribution of NA nerves into the red pulp are not known, it may be due to migration from

38 nd not in the T cell zone, marginal zone, or red pulp areas of the spleen.

39 lls appeared in follicles rather than in the red pulp, as was expected.

40 ls were distributed primarily in the splenic red pulp, between adjacent lobes in lymph node and rando

41 t active somatic hypermutation at the T zone-red pulp border rather than in GCs.

42 en sections, HCs adhered (via VCAM-1) to the red pulp, but not to other areas of normal spleen.

43 cells were observed as isolated cells in the red pulp by day 3 after immunization with Ars-keyhole li

44 enhanced phagocytosis of apoptotic cells by red pulp (CD68(+)F4/80(+)) macrophages, which expressed

45 to NOS-3 in the sinus-lining cells of spleen red pulp could explain the site-specific tyrosine nitrat

46 nding periarteriolar lymphatic sheaths and a red pulp depletion further complemented the Tg perinatal

47 ens exhibit indistinct lymphatic nodules and red pulp depletion; the latter correlates with erythrocy

48 are associated with viral replication in the red pulp, display minimal replication in CD11c(+) and DE

49 -/-) mice produced greater splenomegaly with red pulp expansion and obscured architecture.

50 n, initial splenic enlargement progressed to red pulp fibrosis, atrophy, and functional hyposplenism

51 mutant spleens displayed a severe defect in red pulp formation, including disruption of the sinusoid

52 ultivars (Yen 2 and Sayla) and less than the red pulp guava cultivar (Thai Maroon).

53 Large areas of the red pulp had low concentrations of S1P, while S1P was se

54 ntestine (mild inflammation) and the spleen (red pulp hypertrophy and white pulp activation); viral d

55 d in the white pulp but was increased in the red pulp in AA rats compared with non-AA rats.

56 gnal activated immune cells localized in the red pulp in AA.

57 d throughout white pulp, marginal zones, and red pulp in mice treated with rGM-CSF alone.

58 n liver sinusoids, the venous sinuses of the red pulp in spleen, and the medullary sinuses of lymph n

59 ly infected, which primarily occurred in the red pulp independent of T cells.

60 ls are nonrecirculatory and lodge in splenic red pulp, lymph node medullary cords, and bone marrow.

61 Thus, only red pulp M phi, and not other splenic or peritoneal M ph

62 This analysis revealed that repopulation by red pulp M phi, but not with other splenic M phi subsets

63 Splenic red pulp macrophages (RPM) degrade senescent erythrocyte

64 replication are detected in F4/80(+) splenic red pulp macrophages and in the bone marrow, lymph nodes

65 alphaDbeta2 is highly displayed on splenic red pulp macrophages and mediates their adhesion to loca

66 Red pulp macrophages are a distinct splenic subset invol

67 In the steady state, PPARgamma deficiency in red pulp macrophages did not induce overt inflammation i

68 Red pulp macrophages highly express genes involved in ca

69 Thus, Spi-C controls development of red pulp macrophages required for red blood cell recycli

70 cell-autonomous defect in the development of red pulp macrophages that is corrected by retroviral Spi

71 Additionally, red pulp macrophages, a discrete subset of yolk sac-deri

72 Spi-C is highly expressed in red pulp macrophages, but not monocytes, dendritic cells

73 endings were observed in close apposition to red pulp macrophages, but they do not express choline ac

74 e rim of SIGN-R1(+) macrophages and F4/80(+) red pulp macrophages.

75 peptide enabled their phagocytosis by human red pulp macrophages.

76 aly, be readily compensated for by activated red pulp macrophages.

77 is entirely due to the activity of SIGNR1(-) red pulp macrophages.

78 tor, selectively controls the development of red pulp macrophages.

79 idly cleared from the bloodstream by splenic red pulp macrophages.

80 The redistribution of NA nerves into the red pulp may be critical in modulating immune functions

81 haracterized cell that dominates the splenic red pulp of humans and closely related primates: the ven

82 ial cells associated with the arterioles and red pulp of normal spleen.

83 t may be due to migration from white pulp to red pulp of target immune cells that provide trophic sup

84 ration also occurs extrafollicularly, in the red pulp of the spleen and medullary cords in lymph node

85 ohort of B220(-)CD11b(+)NP(+) B cells in the red pulp of the spleen and not in the MZs.

86 of the marginal zone and infiltration of the red pulp of the spleen by macrophages, interstitial pneu

87 NK cells were localized consistently in red pulp of the spleen during induced NK-cell licensing,

88 mis, exocrine pancreas, renal glomeruli, the red pulp of the spleen, and within cellular compartments

89 an increase in the numbers of B cells in the red pulp of the spleen.

90 in the cytosol of sinus-lining cells in the red pulp of the spleen.

91 of marginal zone macrophages (MZMOs) to the red pulp of the spleen.

92 eraction with VN present in abundance in the red pulp of the spleen.

93 ey, and all three materials were seen in the red pulp of the spleen.

94 , in part, local accumulation in the splenic red pulp of typically rare extramedullary hematopoietic

95 CMV causes destruction of splenic white and red pulp pulp areas in the first few days of infection.

96 st, NK cells were found predominantly in the red pulp region of the spleen.

97 s-specific CD8(+) T cells within the splenic red pulp (RP) had higher two-dimensional (2D) effective

98 on of other splenic compartments such as the red pulp (RP) largely unexplored despite asplenic patien

99 lls patrol around the marginal zone (MZ) and red pulp (RP) of the spleen.

100 pansion and proliferation within the splenic red pulp (RP).

101 distribution of NA nerves from white pulp to red pulp suggests that these nerves signal activated imm

102 an induces F4-80+ macrophages in the splenic red pulp to secrete TGF-beta.

103 Here, we show that red pulp vascular cell adhesion molecule 1 (VCAM-1)(+) m

104 the white pulp and sinus-lining cells of the red pulp were reactive.

105 ated that podoplanin(+) stromal cells in the red pulp were the primary producers of CXCL12 after P. y

106 relocate from the bone marrow to the splenic red pulp, where they encounter granulocyte macrophage co

107 D8 T cells overexpressing T-bet homed to the red pulp, whereas those lacking B lymphocyte-induced mat

108 1(+) CD8(+) T cells in the marginal zone and red pulp, which ceases prior to the final KLRG1(Hi) CXCR

109 aureus, which induced MZMOs to move into the red pulp while MZBs migrated into the follicular zone.

110 mal cells, primarily around sinusoids in the red pulp, while Cxcl12 was expressed by a subset of Tcf2

111 EX-specific plasmablasts were located in the red pulp with persisting DEX-associated CD11c(+) dendrit

112 There was expansion of both white pulp and red pulp, with increased DN T cells.