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 their exposure to pro-survival niches in the white pulp.

3 ent against a small Salmonella subset in the white pulp.

4 recruitment of NK cells into the spleen and white pulp.

5 ium, terminal respiratory tract, and splenic white pulp.

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

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

8 with transitional B cells excluded from the white pulp.

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

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

11 ng in a 3-way interaction profile within the white pulp.

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

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

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

15 and the maintenance of an organized splenic white pulp.

16 ermal Langerhans cells do not access splenic white pulp.

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

18 mononuclear cells cross to enter the splenic white pulp.

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

20 ers throughout diseased nodes and in splenic white pulp.

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

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

23 (DCs), and iNKT cells recruited outside the white pulp; 2) followed by long-lasting contacts (12 to

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

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

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

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

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

29 nt support for Salmonella clearance from the white pulp and eradication failure.

30 ow IgD(+) cells, splenomegaly with a loss of white pulp and grossly expanded red pulp, a deficit of P

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

32 (Hylocereus) species H. undatus (fruits with white pulp and pink skin), and H. polyrhizus (fruits wit

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

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

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

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

37 extramedullary hematopoiesis (EH), depleted white pulp, and absence of germinal centers.

38 cytokines, a significant reduction in spleen white pulp, and lymphocyte infiltration in the liver.

39 ) T(M) accumulations in bone marrow, splenic white pulp, and, particularly, lymph nodes.

40 This also led to a decrease in the white pulp area with a significant decline in the B cell

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

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

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

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

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

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

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

48 at MPs became preferentially enriched in the white pulp as early as 1 to 2 weeks postinfection, and t

49 lization in blood-exposed regions around the white pulp augments cDC2 capture of particulate antigens

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

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

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

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

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

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

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

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

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

59 may be crucial for memory formation and that white pulp-derived signals may contribute to long-term m

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

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

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

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

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

65 Csf1 in WT1(+) red pulp fibroblasts, but not white pulp fibroblasts, drastically altered the RPM netw

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

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

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

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

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

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

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

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

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

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

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

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

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

79 1P, while S1P was sensed by cells inside the white pulp near the marginal sinus.

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

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

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

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

84 firm that CXCR3 re-positions NK cells in the white pulp of the spleen after infection, which is vital

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 NA cause changes to the lipid composition in white pulp regions of the spleen, as anticipated, based

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

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

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

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

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

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

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

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

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

109 d the density of such cells was lower in the white pulp than in other spleen compartments containing

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

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

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

113 hich, in turn, transported Listeria into the white pulp to prime CD8(+) T cells.

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

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

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

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

118 Control of white pulp viral replication is associated with migratio

119 postinfection, and their predominance in the white pulp was maintained throughout the course of a yea

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

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

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

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

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

125 2D) effective affinity than those within the white pulp (WP).

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

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