ライフサイエンスコーパス: splenic

1 ls (BMDCs), and restrains Ag presentation in splenic and BMDCs.

2 xhibit specific and significant increases in splenic and bone marrow B1 cell numbers, and that the B1

3 ation, polarization and homing of B cells to splenic and extranodal tissues, eventually driving malig

4 We found that splenic and hepatic NK cells from SHIV(SF162P3)-infected

5 Furthermore, when splenic and intrahepatic lymphocytes from IFN-alpha- and

6 score of 0-1), and left postceliac arteries (splenic and left gastroepiploic arteries, score of 0-1)

7 days and displayed >91 and >93% clearance of splenic and liver parasitic burden, respectively.

8 a), and interleukin-2 (IL-2) (P < 0.001) and splenic and lung CD8(+) T cells expressing IFN-gamma (P

9 antigen-specific T-cell responses, including splenic and lung polyfunctional CD4(+) T cells expressin

10 ivo, accompanied by significant increases in splenic and lymph node CD4(+) and CD8(+) T cells and pro

11 In this report, we show that although both splenic and peripheral blood MF CD34(+) cells expressed

12 y shown, acutely infected mice, with ongoing splenic and systemic inflammatory responses, controlled

13 Apparent differences between splenic and tumor polymorphonuclear cells/granulocytic m

14 studies have demonstrated the importance of splenic and vagus nerve functions in the inflammatory pr

15 r LRT + SBN (6 vs 0, P = 0.03; 2 vascular, 2 splenic, and 1 liver injury; 1 reexploration to adjust g

16 model, loss of Tlx1 during formation of the splenic anlage increased RA signaling by regulating seve

17 d mediastinal lymph nodes, with expansion of splenic antigen-experienced effector and memory CD4(+) T

18 HFD altered the composition and phenotype of splenic antigen-presenting cells that led to their enhan

19 -mediated Ag targeting system that uptake by splenic APC subsets is severely hampered in mice lacking

20 Burn injury induced significant splenic apoptosis and systemic cytokine production.

21 atocytic cells and delivered to the liver by splenic application.

22 The aim was to preserve the main splenic artery and avoid the complications of splenic ar

23 Although splenic artery aneurysms (SAAs) are common, their giant

24 ific IgM and IgG production in vivo, whereas splenic artery delivery of PD-L1-deficient HSCs failed t

25 We report a case of pseudo aneurysm of splenic artery developed after an episode of acute on ch

26 plenic artery and avoid the complications of splenic artery embolization like infarcts and abscess.

27 Portal inflow modification (splenic artery ligation, hemiportocaval shunt, or splene

28 urysm of the pancreatic tail, diagnosed as a splenic artery pseudoaneurysm by CT.

29 UGI hemorrhage from splenic artery pseudoaneurysm can have a relapsing cours

30 essential in the management of patients with splenic artery pseudoaneurysm.

31 The preaneurysmal part of splenic artery was occluded completely with exclusion of

32 hypothalamic-pituitary-adrenal axis leads to splenic atrophy and contraction of NK cell numbers in th

33 IgM (sIgM (-/-)) antibodies display abnormal splenic B cell development, which results in increased m

34 gM (-/-) mice, suggesting that sIgM regulate splenic B cell differentiation by decreasing BCR signali

35 hibited a clear reduction in total blood and splenic B cells and a further pronounced one in transiti

36 f GL transcription in developing and resting splenic B cells and altered CSR in activated B cells.

37 In mice, this leads to a loss of splenic B cells beyond the transitional stage 1.

38 or antibody production in the LPS-stimulated splenic B cells from Sil1Gt mice.

39 Adoptive transfer of splenic B cells into B cell-deficient mice revealed that

40 n this study, we show that ATM expression by splenic B cells is required for efficient establishment

41 onstrate that enforced expression of Sox2 in splenic B cells severely inhibits AID expression and CSR

42 plus thymic or splenic DC, whereas thymic or splenic B cells were poor donors.

43 xpression of endogenous Ig H and L chains in splenic B cells, upregulation of RAG, and serological po

44 en examined following ex vivo stimulation of splenic B cells, where Atad5(+/m) cells accumulated in t

45 a slight decrease in the fraction of mature splenic B cells, whereas deletion of nfkb2 caused a mark

46 immunoglobulin M (sIgM) expression on murine splenic B cells.

47 on or oligomerization both compromise CSR in splenic B cells.

48 ficant reduction in CSR in ex vivo activated splenic B cells.

49 on were depleted by 70% in ex vivo activated splenic B cells.

50 Engrafted splenic B-1 cells exhibited a mature phenotype, as evide

51 als treated with anti-CD71 Ab showed reduced splenic bacterial load following bacterial challenge com

52 LL xenografts, with marked reduction in mean splenic blast counts (P < .01) in 6 of 6 samples.

53 uteri also decreased the relative numbers of splenic CD11b(+)Gr-1(+) immature myeloid cells.

54 Type 1 IFN expression in splenic CD11c DC of stress-treated mice demonstrated a s

55 inal kinase, and gene expression analysis of splenic CD19(+) B cells demonstrated induction of Hes1 a

56 Splenic CD3(+) alphabeta TCR(+) cells and Foxp3(+) T reg

57 tivation and inflammatory gene expression in splenic CD4 T cells, including IFN-regulated genes, incr

58 the Notch2- and LTbetaR-dependent subset of splenic CD4(+) cDC2s.

59 nd hypertrophy, whereas adoptive transfer of splenic CD4(+) T cells (and, to a lesser extent, cardiac

60 c cells pretreated with vehicle or PAHSA and splenic CD4(+) T cells from syngeneic mice were co-cultu

61 The 9142-primed mice had elevated splenic CD4(+) T cells producing gamma interferon and in

62 ted in an increased frequency of PLN but not splenic CD4(+) T cells that exhibited a polarized morpho

63 eractions within the spleen and expansion of splenic CD4(+)Foxp3(+) T(REG)s.

64 crophage-derived chemokine CCL22 to increase splenic CD4(+)Foxp3(+) T(REG)s.

65 reflected two intrinsic defects observed in splenic CD8(+) DCs in vitro, namely antigen cross-presen

66 Adoptive transfer of splenic CD8(+) T cells from OVA-sensitized WT mice suppr

67 therapy resulted in significantly decreased splenic CD8(+) T-cell proliferation in vitro that could

68 rface expression was strongly upregulated on splenic CD8alpha(+) conventional dendritic cells (DCs) a

69 d a defect in the homeostatic maintenance of splenic CD8alpha(+) DCs and in the capacity of these cel

70 ) mice lacked lung-resident CD103(+) DCs and splenic CD8alpha(+) DCs, yet harbored increased IRF4-dep

71 available for adaptive immunity induction by splenic CD8alpha(+) dendritic cells.

72 ibits IL-27 production in macrophages and in splenic cDC, and we identify a novel pathway consisting

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

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

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

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

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

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

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

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

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

82 n vivo, CLP led to a significant increase in splenic cfB expression that correlated with the plasma R

83 nuate AKI and prevent CKD by stimulating the splenic cholinergic anti-inflammatory pathway.

84 es have implicated vagus nerve regulation of splenic cholinergic nicotinic acetylcholine receptor alp

85 This prevents their destruction by splenic clearance and allows increased parasitaemia.

86 nduced increases in red blood cell lysis and splenic clearance may be a significant factor in the une

87 r drug effect is likely to cause accelerated splenic clearance of the rheologically impaired Plasmodi

88 ies in vivo, where a clear difference in the splenic clearance of transfected tumor cells was observe

89 ility to tether to the endothelium and avoid splenic clearance.

90 sion and ligand interaction of Nkrp1g in the splenic compartment, and found an exclusive expression o

91 ) B cells, leaving the contribution of other splenic compartments such as the red pulp (RP) largely u

92 , and significant and selective expansion of splenic CXCR2(+) neutrophils in chGRKO arthritic compare

93 a, TNF-alpha, CXCL1, and CCL2) and extensive splenic damage with dramatic reduction of splenic cell p

94 gin influenced cross-dressing; thymic versus splenic DC exhibited an increased capacity to capture TE

95 inhibition of il27p28 expression in vivo in splenic DC following administration of dimethyl PGE2 in

96 data indicate that Smad7 expression governs splenic DC subset differentiation and is critical for th

97 inhibitory Fcgamma receptors (FcgammaRs) on splenic DC subsets in vivo and how they contribute to th

98 xpression of FcgammaRIV on both conventional splenic DC subsets, the induction of CD8(+) T cell respo

99 which expresses the highest GILZ level among splenic DC subsets.

100 readily acquired MHC from TEC plus thymic or splenic DC, whereas thymic or splenic B cells were poor

101 lls (DC), as we observed high IgM binding to splenic DC.

102 In this study, we show that murine ex vivo splenic DCs are unresponsive to TSLP, as they fail to ph

103 otes stable interactions between T cells and splenic DCs or BMDCs.

104 (+) cDCs but not pulmonary CD103(+) cDCs and splenic DCs were tdTomato-C3aR(+) Surprisingly, neither

105 ctivation in murine bone marrow-derived DCs, splenic DCs, and human blood-derived DCs.

106 Numbers of CD11b(+)CD4(+) splenic DCs, but not CD11b(+) dermal DCs, were reduced,

107 -KO(DC)), which presented a 20% reduction of splenic DCs, partially explained by enhanced apoptosis.

108 hange in expression of TSLPR or of gammac In splenic DCs, the induction of IL-7Ralpha occurs mainly i

109 rleukin (IL)-1alpha, IL-1beta, and IL-6 from splenic DCs.

110 0 and OX40L by matrix metalloproteinase-2 on splenic dendritic cells.

111 ression of Th17 differentiation cytokines in splenic dendritic cells.

112 Splenic denervation interrupts the anti-inflammatory neu

113 Deletion of Tff2 recapitulates splenic denervation to promote carcinogenesis.

114 Calculated peak splenic divided by myocardial signal intensity (peak spl

115 Adoptive transfer of splenic DN cells gives rise to CD8alphaalpha cells in th

116 indings suggest potential involvement of the splenic dysfunction in AD and the importance of biomarke

117 that inflammatory cytokines associated with splenic dysfunction were altered in the plasma of these

118 o-positive [tdT+] BM cells), circulating and splenic EC-CFUs were BM-derived (tdT+), whereas cells po

119 Paternal exposure to dLAN decreased splenic endocrine receptor expression and global methyla

120 Indeed, treatment to reduce splenic erythroblasts and mature red blood cells correla

121 e was associated with a higher percentage of splenic F4/80(+) cells, and these cells had a higher per

122 at 16:4(n-3) exerts its effect by activating splenic F4/80(+)/CD11b(low) macrophages, which results i

123 Splenic ferroportin was increased probably to sustain he

124 s feasible and safe for patients affected by splenic flexure cancer.

125 4-3.82); patients with SSA/P proximal to the splenic flexure had the highest risk for CRC (OR, 12.42;

126 owed parietal thickening of the colon at the splenic flexure with pneumatosis and signs of perforatio

127 ncer was defined as any tumor arising in the splenic flexure, descending colon, sigmoid colon, or rec

128 , as patients whose tumors originated in the splenic flexure, descending colon, sigmoid colon, or rec

129 , as patients whose tumors originated in the splenic flexure, descending colon, sigmoid colon, or rec

130 Prospects of vesiculation occurring during splenic flow of erythrocytes are addressed via model sim

131 tely fivefold and a proportional decrease in splenic follicular B cells (CD21/35(int)CD23(+)) at 1, 2

132 els, cytokine production by splenocytes, and splenic forkhead box P3 (FOXP3)(+) regulatory T (Treg) c

133 gic responses and increases the frequency of splenic FOXP3(+) Treg cells.

134 Alterations in splenic function were identified through the investigati

135 educed proinflammatory mediators assessed in splenic gene expression and serum proteins.

136 Additionally, two distinct in vivo splenic gene-expression signatures were induced.

137 Pirfenidone dampened splenic germinal center B-cell and T-follicular helper c

138 tory disease and the level of destruction of splenic germinal centers.

139 y that G-CSF treatment generates low-density splenic granulocytes that inhibit experimental aGVHD.

140 opoietic progenitors suggests that increased splenic hematopoiesis results from increased stem and pr

141 ministration, with a concomitant increase in splenic hemoglobin content.

142 Most splenic HSCs were adjacent to Tcf21(+) stromal cells in

143 ons, IL-22 deficiency resulted in thymic and splenic hypertrophy, while excessive IL-22 induced atrop

144 CNV resulted in an increase in splenic IL-17-producing gammadeltaT- and Th17-cells; yet

145 nces in either serum levels of antibodies or splenic immune cell subsets.

146 lly internalized by T lymphocytes over other splenic immune cells.

147 f the abdomen also showed a small peripheral splenic infarct, while CECT of the chest revealed bilate

148 ysms of the right hepatic artery and massive splenic infarction as rare complications of Streptococcu

149 Here we show that during mouse malaria, splenic inflammatory monocytes differentiate into monocy

150 cells from DPPIV+ rats were transplanted via splenic injection into partial hepatectomized DPPIV- rat

151 lenic nAChRa7 receptors, we demonstrate that splenic injection of the nicotinic receptor blocker alph

152 Adult patients with isolated splenic injuries admitted from January 1 through June 30

153 was used to identify patients with isolated splenic injuries and the procedures that they received.

154 valuation of the natural history of isolated splenic injuries from index admission through 6 months f

155 Options for managing splenic injuries have evolved with a focus on nonoperati

156 To describe the natural history of isolated splenic injuries in the United States and determine whet

157 rent management strategies used for isolated splenic injuries in the United States are well matched t

158 95% confidence interval [CI], 0.84-1.16) or splenic injury (OR, 1.09; 95% CI, 0.62-1.90].

159 Secondary outcomes were splenic injury and aspiration pneumonia.

160 Esophageal cancer surgery carries a risk of splenic injury, which may require splenectomy, but predi

161 tion pneumonia, but not bowel perforation or splenic injury.

162 thin 6 months of discharge after an isolated splenic injury.

163 bowel perforation, aspiration pneumonia, and splenic injury.

164 We determined that both circulating and splenic iNKT cell frequencies were markedly decreased in

165 selection of patients for observation versus splenic intervention.

166 , use of any prior chemotherapy (P= .04) and splenic involvement (P= .03) were significantly associat

167 stic for OS (P = .036), whereas male sex and splenic involvement were adversely prognostic for PFS (P

168 We demonstrate a quantitative decrease in splenic iron following infection despite increased numbe

169 ransferrin receptor expression and increased splenic iron/hemosiderin deposition.

170 n host MHC class I, with a critical role for splenic langerin(+) CD8alpha(+) dendritic cells (DCs) in

171 vely on generation of bone marrow as well as splenic LLPCs.

172 The mechanism of splenic lymphocyte accumulation involved reduced sphingo

173 We have previously observed alterations in splenic lymphocyte subsets in animals with defective mig

174 ment significantly reduced EMMPRIN levels on splenic lymphocytes at the presymptomatic (day 7) phase,

175 influenza- or FVIII-stimulated lymph node or splenic lymphocytes, naive CD4(+) lymphocytes preferenti

176 ging features is essential as in our case of splenic lysis.

177 Liver and splenic macrophages also express high levels of ferropor

178 axis led to enhanced cPLA2 activity in these splenic macrophages and secretion of the resistance-indu

179 etin [Epo]) treatment, only native CD11b(lo) splenic macrophages expand dramatically post-stress in n

180 Similarly, parasitized splenic macrophages from live attenuated parasite-infect

181 Our work also indicated that splenic macrophages from PBA-dosed mice exhibited the lo

182 ulates a GPR120-induced signaling cascade in splenic macrophages to promote chemotherapy resistance.

183 ith administered PEGylated quantum dots, but splenic macrophages took up less material (25.4 +/- 10.1

184 A subpopulation of DHRS9-expressing human splenic macrophages was identified by immunohistochemist

185 nicotinic acetylcholine receptor-expressing splenic macrophages.

186 ic acetylcholine receptors (alpha7nAChRs) on splenic macrophages.

187 th split dose regimens it was concluded that splenic malaria parasite clearance capacity was readily

188 Splenic marginal zone (MZ) B cells are innate-like lymph

189 In this study, we found binding of PTX3 to splenic marginal zone (MZ) B cells, an innate-like subse

190 Splenic marginal zone B (MZB) cells, positioned at the i

191 compromise bone marrow B lymphopoiesis, but splenic marginal zone B cell development failed, and B c

192 lent B-cell tumor that is distinguished from splenic marginal zone lymphoma (SMZL) by the different p

193 Splenic marginal zone lymphoma (SMZL) is a rare B-cell m

194 Exposure of splenic marginal zone lymphoma cell lines to a demethyla

195 re different treatments (eg, HCL-variant and splenic marginal zone lymphoma).

196 pite colocalization of virus and pDCs to the splenic marginal zone.

197 apparent in the form of multiple hepatic and splenic masses mimicking malignancy.

198 Splenic mature neutrophils mediated pneumococcal clearan

199 nogenetic profile was identified for primary splenic MCL, which was enriched for DBA.44-positive case

200 abolic tumor volume) and increase in healthy splenic metabolism at 3 mo were observed in responders (

201 others (eg, alpha = .08 for intraparenchymal splenic metastases).

202 We propose that malaria-induced splenic MO-DCs take a reverse migratory route.

203 t, beta-adrenergic antagonism also prevented splenic monocyte egress after acute stress.

204 yses were measured in spinal cord microglia, splenic monocytes, and spinal cord tissue from SOD1 mice

205 thrombosis clotting times; and percentage of splenic monocytes, neutrophils, and CD4 T cells were exa

206 ed only residual Clr-g surface expression on splenic monocytes, whereas many hematopoietic cell lines

207 e a rapid, GCN2-dependent stress response in splenic MPhis with increased IL-10 and TGF-beta producti

208 kin and spleen, and substantial decreases in splenic mRNA expression of both inflammasome components

209 divided by myocardial signal intensity (peak splenic/myocardial signal intensity) differed between st

210 a subset of neutrophils that surrounded the splenic MZ and expressed an immune activation-related ge

211 Marginal zone (MZ) B cells reside in the splenic MZ and play important roles in T cell-independen

212 Ly9 to wild-type mice selectively eliminated splenic MZ B cells and significantly reduced the numbers

213 mice had an increase in CD21/35(high)CD23(-) splenic MZ B cells of approximately fivefold and a propo

214 m after experimental stroke prevents loss of splenic MZ B cells, preserves IgM levels, and reduces ba

215 (n = 151), extranodal (n = 28), and primary splenic (n = 27) MCL cases.

216 Supporting a role for splenic nAChRa7 receptors, we demonstrate that splenic i

217 Splenic NCC display markers indicating a glial lineage a

218 reticuloendothelial system via the vagus and splenic nerves.

219 hages and a protective role for two distinct splenic neutrophil populations (Ly6G(hi) and Ly6G(interm

220 RNA sequencing reveals that the splenic neutrophil transcriptional program changes signi

221 in skin inflammation paralleled decreases in splenic neutrophils (CD11b(+)Ly6G(+)) but not monocytes

222 . pneumoniae infection, these populations of splenic neutrophils act in concert with specialized macr

223 d the localization and cell-cell contacts of splenic neutrophils at several stages in the progression

224 authors identify novel populations of murine splenic neutrophils that localize in the red pulp and th

225 We demonstrate that splenic neutrophils together with two macrophage populat

226 Notably, in progressive CLL, splenic neutrophils were observed to differentiate towar

227 cy proliferation and mobilization from their splenic niche after pneumococcal stimulation to increase

228 Further ex-vivo analysis of splenic NK cells exposed to DFMO, Rosuvastatin or combin

229 Here we show that splenic or, unexpectedly, blood-borne MDSC execute far-r

230 of specific macrophage subsets that mediate splenic organization.

231 Splenic parasite burdens correlated positively with Leis

232 finding in that case was destruction of the splenic parenchyma with protrusion of the remaining tiss

233 ed for Sendai virus immune complex uptake by splenic pDCs in vitro, and internalization via FcgammaRI

234 Aggregation of plasmacytoid DCs in the splenic perifollicular region, follicular translocation

235 owing infection despite increased numbers of splenic phagocytes.

236 capillaries, microcirculation inflammation, splenic plasma cells, circulating B cell activating fact

237 significantly increased PC-specific CD138(+) splenic plasmablasts bearing a B-1a phenotype, and produ

238 evealed that rCl-13(GPC/VGKS) infected fewer splenic plasmacytoid dendritic cells than rCl-13, yet th

239 ymal cells and reduced vasculogenesis of the splenic primordium.

240 anscription of these enzymes correlated with splenic pro-inflammatory gene expression when treatment

241 HMGB1-release induced bone marrow egress and splenic proliferation of bone marrow-derived suppressor

242 hat virus-specific CD8(+) T cells within the splenic red pulp (RP) had higher two-dimensional (2D) ef

243 Portal blood flow and renal and splenic resistive indexes were calculated through echogr

244 long with host phospholipids involved in the splenic response in murine tissues.

245 , higher interferon gamma and interleukin 17 splenic responses, and more multifunctional CD4(+) T cel

246 The impairments in splenic retention and cardiac infiltration of leukocytes

247 Splenic retention of the leukocytes was associated with

248 ion of leukocytes with reciprocally enhanced splenic retention of the same immune cell populations.

249 found to be a more important determinant of splenic retention than its membrane stiffness.

250 (hi) and Ly6G(intermediate)) residing in the splenic RP.

251 ul crisis, dactylitis, acute chest syndrome, splenic sequestration, or blood transfusion) was less fr

252 acute chest syndrome, hepatic sequestration, splenic sequestration, or priapism) and the acute chest

253 try revealed significant tumor targeting and splenic sequestration.

254 ted in bone marrow LLPCs compared with their splenic short-lived counterparts (SLPCs).

255 us avoiding clearance during passage through splenic sinuses.

256 Moreover, primary splenic stromal cells grown in the presence of IL-17 enh

257 he MZ of Notch2HCS mice occupied most of the splenic structure.

258 epeat examination of individuals with failed splenic switch-off may significantly improve test sensit

259 Splenic switch-off was assessed in perfusion cardiac MR

260 In Neil3-/- mice, splenic T and B cells as well as germinal center B cells

261 Here, TMEV infection induced splenic T cell depletion, which was associated with lowe

262 erated large numbers of Th1 CD4(+) ESAT-6(+) splenic T cells compared to those of mice infected with

263 by transcriptome analysis to be elevated in splenic T cells from germfree and antibiotic-treated mic

264 Splenic T cells from untreated Sphk2(-/-) mice were hype

265 Cardiac and splenic T cells in HF are primed to induce cardiac injur

266 ind a population of constitutively activated splenic T cells in naive mice and further that most bone

267 The protection was reproduced by injecting splenic T cells that had been preincubated with noradren

268 tissue pathology, 9142-primed mice also had splenic T regulatory cells with greater suppressive acti

269 ted mice had significantly higher numbers of splenic T(REG)s compared with NC and WT BMDC-pretreated

270 evels of Erdr1, germfree mice have increased splenic T-cell apoptosis.

271 of the mast cell protease MCPT1, as well as splenic T-helper-2 cell-derived cytokine production.

272 Here we show that splenic TFF2, a secreted anti-inflammatory peptide, is r

273 tinfection, Icos(-/-) mice accumulated fewer splenic TFHs compared with Icos(+/+) mice, leading to su

274 bodies blunted the CNV-induced production of splenic Th17- and gammadeltaT-cells, reduced CNV size an

275 Splenic Th9 and Th17 cells, plasma concentrations and li

276 osition were observed in renal, hepatic, and splenic tissues at much higher tissue concentrations (P

277 Rat brain and renal, hepatic, and splenic tissues were harvested 7 days after final inject

278 t TTP deficiency has profound effects on the splenic transcriptome, even in the absence of secondary

279 provide evidence that in Ly9-deficient mice splenic transitional 1, MZ, and B1a B cells are markedly

280 Flow cytometry analysis of the splenic transitional B cell subsets demonstrated that MZ

281 n is precisely downmodulated upon culture of splenic transitional B cells in the presence of BAFF.

282 s, serum cytokine levels, and S. typhimurium splenic translocation were measured.

283 Diminished splenic Treg frequency in LPS-exposed fetuses was associ

284 Moreover, IL233-treated mice had fewer splenic Tregs and more Tregs in kidneys after IRI.

285 In vitro, splenic Tregs from IL233-treated mice suppressed CD4(+)

286 eg generation in the thymus with a switch of splenic Tregs toward an inflammatory phenotype.

287 tenuation was associated with an increase in splenic type 1 regulatory T cells.

288 F-FLT PET clearly showed an intense abnormal splenic uptake, whereas spleen uptake was inconclusive w

289 elial cells (ECs) within the bone marrow and splenic vascular niche play an essential role in modulat

290 reas central marrow remains vascularized and splenic vascular niches expand.

291 ained in the superior mesenteric vein (SMV), splenic vein (SV), portal vein (PV), and the TIPS.

292 inically unsuspected partial thrombus in the splenic vein on imaging.

293 reatment led to a complete resolution of the splenic vein thrombosis.

294 was disseminated tuberculosis complicated by splenic vein thrombosis.

295 ssociation with transplant failure than does splenic vein thrombus or edema.

296 Splenic vein thrombus was identified in 10 of 20 failed

297 of intraparenchymal forward diastole flow), splenic vein thrombus, and edema.

298 An increased calibre of the splenic vein with a hyperechogenicity within it raised t

299 operating characteristic curve, 0.929) than splenic volume (area under the receiver operating charac

300 LSN scores, splenic volume, and the ratio of left lateral segment (L