ライフサイエンスコーパス: white pulp

1 id white pulp, merged with components of the white pulp.

2 es and in lymphocyte-containing areas of the white pulp.

3 tween MZ and follicular areas of the splenic white pulp.

4 with transitional B cells excluded from the white pulp.

5 e to chemokines and cannot enter the splenic white pulp.

6 ne of the spleen into the T cell area of the white pulp.

7 s and a gateway for lymphocytes entering the white pulp.

8 ) and S1P(3) and to migrate into the splenic white pulp.

9 ation in the peripheral areas of the splenic white pulp.

10 and the maintenance of an organized splenic white pulp.

11 ermal Langerhans cells do not access splenic white pulp.

12 B cells at the T/B interface of the splenic white pulp.

13 mononuclear cells cross to enter the splenic white pulp.

14 l sinus lining cells at the periphery of the white pulp.

15 ers throughout diseased nodes and in splenic white pulp.

16 lieved to reside in the marginal zone of the white pulp.

17 ed pulp and the periartereolar region of the white pulp.

18 ort a decline in NA nerve density in splenic white pulp (45%) at 15 months of age compared with 8-mon

19 on) and the spleen (red pulp hypertrophy and white pulp activation); viral dissemination to the splee

20 e highly concentrated in the T-cell areas of white pulp after rGM-CSF/IL-4 administration, whereas th

21 Relocation of MZ B cells to the white pulp allowed virus transfer to follicular dendriti

22 cluded extensive depletion of lymphocytes in white pulp and a marked lymphocytopenia in 15 of 19 pati

23 o expressed as a meshlike network in splenic white pulp and in the medullary region of the lymph node

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

25 Splenic dendritic cells of the white pulp and sinus-lining cells of the red pulp were r

26 along with lymphoid depletion in the splenic white pulp and thymus.

27 to reduce B cell accumulation in the splenic white pulp and to promote egress of activated T cells fr

28 plain how NK cells protect the lymphoid-rich white pulp areas from CMV, allowing protective adaptive

29 was MOMA-2+ macrophages localized within the white pulp areas of the spleen.

30 The splenic white pulp areas show loss of discrete T and B lymphocyt

31 ghly organized lymphotoxin dependent B and T white pulp areas within which CD4-dependent memory Ab re

32 of murine CMV-specific activated NK cells to white pulp areas, where they associate directly with pod

33 ccumulations of lymphocytes in their splenic white pulp areas, with no evidence of focal aggregation

34 s associated with B/T segregation of splenic white pulp areas.

35 ressed on marginal sinus lining cells at the white pulp border.

36 However, NA nerve density was reduced in the white pulp but was increased in the red pulp in AA rats

37 Lymphocytes enter the splenic white pulp by crossing the poorly characterized boundary

38 ce have a small and partially differentiated white pulp containing marginal zone and interdigitating

39 e steps involved in lymphocyte homing to the white pulp cords of the spleen are poorly understood.

40 nished homing to Peyer's patches and splenic white pulp cords.

41 mphocyte transit from the marginal zone into white pulp cords.

42 ibutions necessary for B cell migration into white pulp cords.

43 in the study showed higher activity than the white pulp cultivars (Yen 2 and Sayla) and less than the

44 ns, small proportions of cells along red and white pulp divisions expressed high levels of IFN-gamma

45 IV-infected T cells were numerous within the white pulp during acute infection, but were rarely obser

46 to altered spatial rearrangement of both the white pulp endothelial cells and the smooth muscle actin

47 nlarged spleens with abnormal B cell-derived white pulp enlargement.

48 re splenomegaly with abnormal B-cell-derived white pulp expansion and enlarged lymph nodes.

49 phages that are uniquely arrayed outside the white pulp follicles to screen the blood for bacterial a

50 4) profound splenic remodeling with abundant white pulp follicles, markedly increased size of the mar

51 lls promotes migration of these cells to the white pulp, followed by CR2 proteolysis, which allows tr

52 Nonetheless, these mice display mild splenic white pulp hypoplasia and blunted primary serum Ab respo

53 t anti-PtC B-1 cells first appear within the white pulp in neonates, expand in association with folli

54 RNA in radiation sensitive tissues analysed (white pulp in the spleen and bases of crypts in small in

55 Here we report that the white pulp in the spleens of patients dying from malaria

56 T cell entry to the white pulp is also reduced by blockade of LFA-1 and alph

57 nal consequence, lymphocyte traffic into the white pulp is impaired during chronic leishmaniasis.

58 ng this were enlarged spleens with prominent white-pulp macrophage infiltration.

59 ce have an irregularly shaped, discontinuous white pulp margin.

60 s they were diffusely distributed throughout white pulp, marginal zones, and red pulp in mice treated

61 en the nonlymphoid red pulp and the lymphoid white pulp, merged with components of the white pulp.

62 1P, while S1P was sensed by cells inside the white pulp near the marginal sinus.

63 s were in marginal zones surrounding splenic white pulp nodules, and only smaller numbers were in T c

64 appropriate compartmentalization within the white pulp of lymphocyte-deficient mice despite an unusu

65 the normal lymphofollicular structure in the white pulp of SCD mice without distinct B, T, and margin

66 cells being positive focally in the splenic white pulp of six septic but in no nonseptic patients.

67 s that accumulated at the T/B borders in the white pulp of the spleen and that OX40-dependent signals

68 es caused marked lymphocyte apoptosis in the white pulp of the spleen on day 2 postinfection.

69 We show that T0 cells cannot enter the white pulp of the spleen until they mature into the T1 a

70 ell zones around the germinal centers of the white pulp of the spleen within 6 h of trauma and lasted

71 o the marginal zone to those adherent to the white pulp of the spleen, an increase in the number of C

72 Spi-B mRNA in the medulla of the thymus, the white pulp of the spleen, and the germinal centers of ly

73 d in the crypt cells of the small intestine, white pulp of the spleen, bronchiolar epithelium of the

74 me very inefficiently to lymph nodes and the white pulp of the spleen, show reduced interstitial migr

75 lls in lymph nodes, Peyer's patches, and the white pulp of the spleen.

76 s in the area of MZ and follicles within the white pulp of the spleen.

77 endothelium, as well as discrete defects in white pulp organization during postnatal development.

78 -expressing DC were both observed in splenic white pulp, p40(+) DC rarely colocalized with bacilli.

79 n of non-T/non-B cells along splenic red and white pulp region borders characteristic of marginal zon

80 ion, frequently involving more than a single white pulp region.

81 NA nerves distributed to central arterioles, white pulp regions, trabeculae, and capsule.

82 T/B cell-dependent leukocyte migration into white pulp regions.

83 ed and germinal centers appear in 55% of the white pulp regions.

84 elocalization of nucleated cells from red to white pulp regions.

85 and T2 stages, and that this entry into the white pulp requires integrin and chemokine receptor sign

86 are associated with virus replication in the white pulp, show preferential replication in a majority

87 vidence that the virus replicates in red and white pulp stroma in vivo and in vitro.

88 Thus, splenic white pulp structure, which depends on the expression of

89 correlated with an ability to infiltrate the white pulp (T-dependent) area of the spleen, cause ablat

90 In the splenic white pulp, this compartmentalization is also thought to

91 s that LT induces the differentiation of the white pulp to create sites for lymphocyte segregation.

92 cellular bacteria to the T cell areas of the white pulp to initiate CD8(+) T cell responses.

93 ransitional B cells need to migrate into the white pulp to receive survival signals.

94 e not known, it may be due to migration from white pulp to red pulp of target immune cells that provi

95 The redistribution of NA nerves from white pulp to red pulp suggests that these nerves signal

96 otoxin-deficient mice, the developing Flk-1+ white pulp vessels failed to organize or upregulate MAdC

97 Control of white pulp viral replication is associated with migratio

98 nt induction of Puma occurred in the splenic white pulp, whereas Noxa and Bid were induced in the red

99 D and E residing in the T cell areas of the white pulp, while DC within population C localize in the

100 cterized by the abnormal infiltration of the white pulp with cells expressing the plasma cell marker

101 small proportion of NKT cells located in the white pulp (WP) exhibit limited activation.

102 y of the spleen's lymphoid architecture, the white pulp (WP), is the accumulation of B cells around s

103 d about how T lymphocytes access the splenic white pulp (WP).

104 2D) effective affinity than those within the white pulp (WP).

105 l compartmentalization remained abnormal and white pulp zones were small.