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1 d in guiding T cell movements in the splenic red pulp.
2 gan T cell zones and by cells in the splenic red pulp.
3 ive splenic IgG AFC response, largely in the red pulp.
4 nation revealed masses of hepatocytes in the red pulp.
5 , parasitized erythrocytes were found in the red pulp.
6 locytes in the cords and sinus lumens of the red pulp.
7 iently targeted myeloid cells in the splenic red pulp.
8 s were adjacent to Tcf21(+) stromal cells in red pulp.
9 aught in fluid flow and are carried into the red pulp.
10 ked disorganization of the marginal zone and red pulp.
11 ife spans, were exclusively localized to the red pulp.
12 ne, whereas CD62L(-) cells were found in the red pulp.
13 on overload localized selectively to splenic red pulp.
14 ondary effector CD8 T cells are found in the red pulp.
15 h some XlAID(+) cells were also found in the red pulp.
16 lp, whereas Noxa and Bid were induced in the red pulp.
17 th a loss of white pulp and grossly expanded red pulp, a deficit of Peyer patches, and small lymph no
18  defined lymphoid follicles and expansion of red pulp, a greater than fourfold increase in splenic mo
19         Later, these cells were found in the red pulp and a disruption of all CD8 T cell zones was ob
20  in clusters in the cords of the subcapsular red pulp and are distinct from macrophages and DCs.
21 mouse models and a pathological reduction in red pulp and extramedullary hematopoiesis.
22 d a stellate shape and were localized to the red pulp and germinal centers, suggesting that they are
23 P-70(-/-) mice show more plasma cells in the red pulp and in the bone marrow, and increased NP-specif
24 ated IDO expression in the marginal zone and red pulp and inhibition of IDO markedly accelerated dise
25 ps anatomically to the splenic marginal zone/red pulp and is defined by prolonged motility paralysis
26 rate that CXCL12 is expressed within splenic red pulp and lymph node medullary cords as well as in bo
27 d redistribution of dendritic cells from the red pulp and marginal zone of the spleen into the T cell
28 he switched B cells transiently occupied the red pulp and marginal zone, whereas others persisted in
29 alized to Sn(+) Mphis and other cells in the red pulp and marginal zone.
30 IL-10 by splenic gamma delta+ T cells in the red pulp and marginal zones that coincided with maximal
31 f mice, effector CD8 T cells localize to the red pulp and memory CD8 T cells localize to the T cell z
32 d pink skin), and H. polyrhizus (fruits with red pulp and pink skin) were investigated to develop the
33                                  The splenic red pulp and the luminal surface of high endothelial ven
34 ich is the interface between the nonlymphoid red pulp and the lymphoid white pulp, merged with compon
35 ine splenic neutrophils that localize in the red pulp and the marginal zone.
36  TNF production by spleen macrophages in the red pulp and the marginal zone.
37 Spleen tissue contained antigens in both the red pulp and the periartereolar region of the white pulp
38 owed disrupted follicular structure, loss of red pulp, and granulocyte and megakarocyte invasion.
39 r peripheral Ags: the splenic marginal zone, red pulp, and lymph node sinuses.
40 finity were mainly restricted to the splenic red pulp, and the host generated an effective CTL respon
41 of this redistribution of NA nerves into the red pulp are not known, it may be due to migration from
42 e treatment, as indicated by the increase in red pulp area, the number of nucleated erythroblasts, an
43 nd not in the T cell zone, marginal zone, or red pulp areas of the spleen.
44 lasmablasts in splenic bridging channels and red pulp as well as lymph node medullary cord areas.
45 lls appeared in follicles rather than in the red pulp, as was expected.
46 ls were distributed primarily in the splenic red pulp, between adjacent lobes in lymph node and rando
47 t active somatic hypermutation at the T zone-red pulp border rather than in GCs.
48 en sections, HCs adhered (via VCAM-1) to the red pulp, but not to other areas of normal spleen.
49 fection (dpi), and progresses throughout the red pulp by 4 dpi.
50 cells were observed as isolated cells in the red pulp by day 3 after immunization with Ars-keyhole li
51  enhanced phagocytosis of apoptotic cells by red pulp (CD68(+)F4/80(+)) macrophages, which expressed
52  undergo antigen-dependent arrest in splenic red pulp clusters of CCR2(+)Ly6C(+) monocytes to which t
53                               Located within red pulp cords, splenic red pulp macrophages (RPMs) are
54 to NOS-3 in the sinus-lining cells of spleen red pulp could explain the site-specific tyrosine nitrat
55 nding periarteriolar lymphatic sheaths and a red pulp depletion further complemented the Tg perinatal
56 ens exhibit indistinct lymphatic nodules and red pulp depletion; the latter correlates with erythrocy
57 are associated with viral replication in the red pulp, display minimal replication in CD11c(+) and DE
58 -/-) mice produced greater splenomegaly with red pulp expansion and obscured architecture.
59                                        Thus, red pulp fibroblasts anchor and nurture RPM, a function
60 RPMs are embedded in a reticular meshwork of red pulp fibroblasts characterized by the expression of
61                          Upon RPM depletion, red pulp fibroblasts transiently produced the monocyte c
62       Conditional deletion of Csf1 in WT1(+) red pulp fibroblasts, but not white pulp fibroblasts, dr
63 n, initial splenic enlargement progressed to red pulp fibrosis, atrophy, and functional hyposplenism
64  mutant spleens displayed a severe defect in red pulp formation, including disruption of the sinusoid
65 ultivars (Yen 2 and Sayla) and less than the red pulp guava cultivar (Thai Maroon).
66                           Large areas of the red pulp had low concentrations of S1P, while S1P was se
67 ntestine (mild inflammation) and the spleen (red pulp hypertrophy and white pulp activation); viral d
68 d in the white pulp but was increased in the red pulp in AA rats compared with non-AA rats.
69 gnal activated immune cells localized in the red pulp in AA.
70 d throughout white pulp, marginal zones, and red pulp in mice treated with rGM-CSF alone.
71 n liver sinusoids, the venous sinuses of the red pulp in spleen, and the medullary sinuses of lymph n
72 ly infected, which primarily occurred in the red pulp independent of T cells.
73  hand, KLRG1(+) MPs and TEs localized to the red pulp just as early, and they consistently localized
74 ls are nonrecirculatory and lodge in splenic red pulp, lymph node medullary cords, and bone marrow.
75                                   Thus, only red pulp M phi, and not other splenic or peritoneal M ph
76  This analysis revealed that repopulation by red pulp M phi, but not with other splenic M phi subsets
77 sulin-like growth factor-1), and the splenic red pulp macrophage gene Spic.
78 ast 2 dpi revealed substantial M.R2k/b F480+ red pulp macrophage loss along with buildup of oxidative
79 lyses revealed dramatic up-regulation of the red-pulp macrophage lineage-defining transcription facto
80                                      Splenic red pulp macrophages (RPM) degrade senescent erythrocyte
81  also by transcription factor SpiC-dependent red pulp macrophages (RPM) of the spleen.
82 ineage tracing, we find that tissue-resident red pulp macrophages (RPM), initially depleted by BCG ex
83  VCAM-1 expression of splenic iron-recycling red pulp macrophages (RPMs) and bone marrow erythroblast
84       Located within red pulp cords, splenic red pulp macrophages (RPMs) are constantly exposed to th
85                                      Splenic red pulp macrophages (RPMs) contribute to erythrocyte ho
86                                              Red pulp macrophages (RPMs) of the spleen mediate turnov
87 BCs), a task chiefly accomplished by splenic red pulp macrophages (RPMs) via erythrophagocytosis.
88 replication are detected in F4/80(+) splenic red pulp macrophages and in the bone marrow, lymph nodes
89 rophages were most closely related to spleen red pulp macrophages and Kupffer cells and shared the ex
90   alphaDbeta2 is highly displayed on splenic red pulp macrophages and mediates their adhesion to loca
91                                              Red pulp macrophages are a distinct splenic subset invol
92 mophagocytes (iHPCs), which resemble splenic red pulp macrophages but are a distinct population deriv
93 In the steady state, PPARgamma deficiency in red pulp macrophages did not induce overt inflammation i
94                                              Red pulp macrophages highly express genes involved in ca
95  could quickly attenuate the function of the red pulp macrophages on detaining aged or diseased RBCs,
96          Thus, Spi-C controls development of red pulp macrophages required for red blood cell recycli
97 cell-autonomous defect in the development of red pulp macrophages that is corrected by retroviral Spi
98                                Additionally, red pulp macrophages, a discrete subset of yolk sac-deri
99                 Spi-C is highly expressed in red pulp macrophages, but not monocytes, dendritic cells
100 endings were observed in close apposition to red pulp macrophages, but they do not express choline ac
101 idly cleared from the bloodstream by splenic red pulp macrophages.
102 nts, namely interendothelial slits (IES) and red pulp macrophages.
103 e rim of SIGN-R1(+) macrophages and F4/80(+) red pulp macrophages.
104  peptide enabled their phagocytosis by human red pulp macrophages.
105 aly, be readily compensated for by activated red pulp macrophages.
106 is entirely due to the activity of SIGNR1(-) red pulp macrophages.
107 tor, selectively controls the development of red pulp macrophages.
108     The redistribution of NA nerves into the red pulp may be critical in modulating immune functions
109 rier with splenic avidity and propensity for red pulp myeloid cell uptake.
110 haracterized cell that dominates the splenic red pulp of humans and closely related primates: the ven
111 ial cells associated with the arterioles and red pulp of normal spleen.
112 t may be due to migration from white pulp to red pulp of target immune cells that provide trophic sup
113 ration also occurs extrafollicularly, in the red pulp of the spleen and medullary cords in lymph node
114 ohort of B220(-)CD11b(+)NP(+) B cells in the red pulp of the spleen and not in the MZs.
115 of the marginal zone and infiltration of the red pulp of the spleen by macrophages, interstitial pneu
116      NK cells were localized consistently in red pulp of the spleen during induced NK-cell licensing,
117 mis, exocrine pancreas, renal glomeruli, the red pulp of the spleen, and within cellular compartments
118 an increase in the numbers of B cells in the red pulp of the spleen.
119 ey, and all three materials were seen in the red pulp of the spleen.
120  in the cytosol of sinus-lining cells in the red pulp of the spleen.
121  of marginal zone macrophages (MZMOs) to the red pulp of the spleen.
122 eraction with VN present in abundance in the red pulp of the spleen.
123 , in part, local accumulation in the splenic red pulp of typically rare extramedullary hematopoietic
124  CMV causes destruction of splenic white and red pulp pulp areas in the first few days of infection.
125 st, NK cells were found predominantly in the red pulp region of the spleen.
126 s-specific CD8(+) T cells within the splenic red pulp (RP) had higher two-dimensional (2D) effective
127 on of other splenic compartments such as the red pulp (RP) largely unexplored despite asplenic patien
128 lls patrol around the marginal zone (MZ) and red pulp (RP) of the spleen.
129 pansion and proliferation within the splenic red pulp (RP).
130   Degeneration and necrosis in the white and red pulps, scattered lymphocytes, and increased collagen
131        Upon release from arterioles into the red pulp sinuses, T cells latched onto perivascular stro
132                    Here, we have uncovered a red-pulp-specific, myofibroblastic niche that supports m
133                               In the splenic red pulp, subpopulations of CSF1R+/F4/80+/Mac3+cells wer
134 eal that the NPSCs primarily localize in the red pulp, suggesting that the observed changes in lipid
135 distribution of NA nerves from white pulp to red pulp suggests that these nerves signal activated imm
136 arly, and they consistently localized to the red pulp thereafter.
137 an induces F4-80+ macrophages in the splenic red pulp to secrete TGF-beta.
138                           Here, we show that red pulp vascular cell adhesion molecule 1 (VCAM-1)(+) m
139 the white pulp and sinus-lining cells of the red pulp were reactive.
140 ated that podoplanin(+) stromal cells in the red pulp were the primary producers of CXCL12 after P. y
141 ted their spread to the erythroblasts in the red pulp where FVC manifests its pathogenesis.
142 ory monocytes and fibroblasts of the splenic red pulp, where it grants stem-like cells access to sign
143 relocate from the bone marrow to the splenic red pulp, where they encounter granulocyte macrophage co
144 D8 T cells overexpressing T-bet homed to the red pulp, whereas those lacking B lymphocyte-induced mat
145 1(+) CD8(+) T cells in the marginal zone and red pulp, which ceases prior to the final KLRG1(Hi) CXCR
146 aureus, which induced MZMOs to move into the red pulp while MZBs migrated into the follicular zone.
147 mal cells, primarily around sinusoids in the red pulp, while Cxcl12 was expressed by a subset of Tcf2
148 EX-specific plasmablasts were located in the red pulp with persisting DEX-associated CD11c(+) dendrit
149   There was expansion of both white pulp and red pulp, with increased DN T cells.

 
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