ライフサイエンスコーパス: splenic

1 us laterality defects (heterotaxy) including splenic abnormalities and complex cardiac malformations-

2 BDs), in particular Crohn's Disease, aseptic splenic abscesses have been reported in patients with a

3 r-deficient) mice is substantially higher in splenic and aortic DCs compared with macrophages and is

4 Splenic and bone marrow neutrophils (Nphs) from BAFF-RFP

5 Using this tool, we found that splenic and bone marrow PC numbers remained constant ove

6 24 with OS was confirmed for the subgroup of splenic and extranodal MZLs.

7 h-1 resulted in a reduced proportion of both splenic and intragraft conventional T cells, while incre

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

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

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

11 vival was unclear, as complete blood counts, splenic and marrow cellularity, numbers and function of

12 Human splenic and peripheral blood IgD(low/-) B cells also exh

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

14 rose chow (HFS), multifunctionality of CD8 + splenic and tumor-infiltrating lymphocytes (TILs) was im

15 testinal mucosae, for example CCL25 enhanced splenic and vaginal Ag-specific T cell responses whereas

16 ary manifestations included hepatic, kidney, splenic, and bone marrow involvement, and microvascular

17 28-5,157.50 +/- 949.17, respectively; renal, splenic, and salivary retention).

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

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

20 Because splenic apoptosis was largely attributed to the apoptosi

21 ng in splenomegaly with disruption of normal splenic architecture and the presence of hemophagocytes,

22 matrix proteins that are exposed within the splenic architecture.

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

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

25 revents sympathetic hyperreflexia-associated splenic atrophy and loss of leukocytes to dramatically i

26 athetic hyperreflexia, to prevent associated splenic atrophy.

27 s of transcription factors known to regulate splenic B cell development, including NF-kappaB motifs.

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

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

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

31 es of serum antibodies as well as numbers of splenic B cells and bone marrow cells after different im

32 that CHIKV RNA was present preferentially in splenic B cells and follicular dendritic cells during th

33 ly, adoptive transfer of B-1a cells, but not splenic B cells from WT mice, restored MPL/TDCM-induced

34 comparing IgH.TEmu CLL cells with wild-type splenic B cells identified 96 differentially expressed p

35 r activated and proliferating intrarenal and splenic B cells in mice lacking IL-34, and with our nove

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

37 es, lipids, and metabolic enzymes of resting splenic B cells purified from young adult B cell-specifi

38 rogen peroxide generator Duox1 in stimulated splenic B cells under the influence of the T(H)2 cytokin

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

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

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

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

43 In vitro stimulation of splenic B lymphocytes demonstrated decreased IgA, IgG, a

44 medullary hematopoietic organs and that some splenic B lymphocytes express EdnrB.

45 Splenic B lymphocytes from EdnrB(NCC-/-) mice showed no

46 d that Sirt-1 deficiency in T cells enhanced splenic B-cell reconstitution and reduced follicular T h

47 C2.5 thymocytes possess higher affinity than splenic BDC2.5 T cells for all three epitopes, periphera

48 +)MHCII(hi) DCs, gene expression profiles of splenic C/EBPbeta(-/-) DCs showed a down-regulation of E

49 The splenic CD11c(+)MHCII(hi)CD64(+) DC compartment was also

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

51 ity but not Ig isotype production in primary splenic CD19(+) B cells.

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

53 c treatment of CDX-301 resulted in increased splenic CD3+ T cells, specifically CD4+T helper cells, c

54 Splenic CD4 T cell activation by particulate antigens is

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

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

57 Plasma viral RNA and splenic CD4(+) T cell viral DNA levels were measured imm

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

59 , both the absolute number and proportion of splenic CD4(+) T cells were reduced, while the proportio

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

61 uced robust CTL responses via Ag transfer to splenic CD8+ DCs in a manner independent of monocyte APC

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

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

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

65 Splenic cDC2s express high amounts of alpha4beta1 and al

66 terminal differentiation of NOTCH2-dependent splenic cDC2s.

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

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

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

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

71 ponsiveness to exogenous type I IFN, whereas splenic cells show a reduction in select ISGs in respons

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

73 ocytes accounted for the largest increase in splenic cellularity.

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

75 thelial binding capacity, allowing increased splenic clearance and enabling several months of subclin

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

77 impaired replication but rather to increased splenic clearance of longer-circulating infected erythro

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

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

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

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

82 Total splenic DC cell numbers were modestly increased but diff

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

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

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

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

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

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

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

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

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

92 ression of Th17 differentiation cytokines in splenic dendritic cells.

93 1.02; 95%CI: 1.0-1.04; p = 0.030); increased splenic diameter (OR:1.3; 95%CI:1.2-1.5; p < 0.001), inc

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

95 nate treatment, quantified as a reduction in splenic effector memory T cell frequencies and splenic T

96 Comparison of airway T(RM) cells and splenic effector-memory T cells transferred into the air

97 the most frequent applications of selective splenic embolization in patients with and without underl

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

99 In this study, we provide evidence that the splenic environment is of substantial importance in faci

100 Splenic erythroid progenitor cells and mesenchymal strom

101 o de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis.

102 of the erythroid progenitor pool and robust splenic erythropoiesis.

103 The loss of splenic ESAM(+) cDC2s was cell-intrinsic and could be re

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

105 arly accumulation of blood-borne prions upon splenic FDC or reduce susceptibility to IV prion infecti

106 s and antigen-containing immune complexes to splenic FDC.

107 Splenic ferroportin was increased probably to sustain he

108 d by recommending a withdrawal time from the splenic flexure of at least 3.25 min (ideally 3.5-4.0 mi

109 95; p<0.0001) and a withdrawal time from the splenic flexure of at least 3.25 min in negative procedu

110 Procedures not reaching the splenic flexure were associated with lower chance of ade

111 lected at weeks 0, 8, and 44 from the ileum, splenic flexure, and rectum (18 biopsy samples from each

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

113 less likely to have a procedure reaching the splenic flexure.

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

115 lized B cell trafficking into lymph node and splenic follicles.

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

117 ation compared with peritoneal B-2 cells and splenic follicular B cells, respectively.

118 ough mice continued to develop plasma cells, splenic follicular structure was restored, and renal pat

119 tibodies, splenocyte cytokine production and splenic forkhead box P3 (FOXP3)(+) regulatory T (Treg) c

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

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

122 We show that STm persists within splenic granulomas that are densely populated by CD11b(+

123 Tumor-derived secretory factors orchestrate splenic hematopoietic and stromal cells to fuel metastas

124 be more prone to develop splenic rupture, as splenic histiocytes engage in more robust erythrophagocy

125 LPS exposure caused splenic hypertrophy and platelet count suppression.

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

127 with altered immunophenotype with increased splenic IFN-gamma(+)CD4(+) T cells, effector memory CD4(

128 The extent of mobilization of splenic immune cells to peripheral tissues in health and

129 optogenetic tools to investigate whether the splenic immune response is directly controlled by descen

130 itability of peripheral blood as a proxy for splenic immune responses is however unknown.

131 tation accuracy and was compared against the splenic index equation.

132 eased levels of IFN-gamma in serum and lower splenic indexes were observed.

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

134 hemic attack without residual deficit, and 1 splenic infarct; all with no further complications.

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

136 cell deficiency alone enhanced resistance to splenic infection ~100-fold; however, combined B and T c

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

138 transplanted into syngeneic C57BL/6J mice by splenic injection.

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

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

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

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

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

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

145 95% confidence interval [CI], 0.84-1.16) or splenic injury (OR, 1.09; 95% CI, 0.62-1.90].

146 Secondary outcomes were splenic injury and aspiration pneumonia.

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

148 bowel perforation, aspiration pneumonia, and splenic injury.

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

150 intrinsic requirement for IL-18 signaling by splenic iNKT cells but not liver iNKT cells, suggesting

151 mour growth in the brain induced significant splenic involution, reductions in peripheral T cells, re

152 have end-organ dysfunction other than their splenic involvement.

153 howed defective iron recycling and increased splenic iron deposition.

154 reduced serum iron and increased hepatic and splenic iron storage.

155 HO-1 induction, while there was depletion of splenic iron stores.

156 lymphocyte sparing potential in cardiac and splenic irradiation models of lymphopenia and assessed t

157 9 lymphocyte populations in both cardiac and splenic irradiation models of lymphopenia.

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

159 e alters the gut microbe composition and the splenic leukocyte profile in acute heart failure (HF).

160 Thus, calorie-enriched OBD dysregulated splenic leukocytes by decreasing immune-responsive F4/80

161 Production of cytokines by splenic leukocytes were altered in EE-exposed mice.

162 ) T cell priming but, paradoxically, promote splenic Listeria monocytogenes infection.

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

164 ycytidylic acid increased BAFF expression in splenic Ly6C(hi) inflammatory MOs, CD11b(hi) activated N

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

166 ly, and production of signature cytokines in splenic lymphocytes and lung tissue on IL-33 injection.

167 -activated splenic lymphocytes as well as in splenic lymphocytes and macrophages stimulated with kill

168 on analysis of duck IL-23p19 (duIL-23p19) in splenic lymphocytes and macrophages stimulated with kill

169 ted in both spleens of RA-infected ducks and splenic lymphocytes and macrophages stimulated with kill

170 cks and was upregulated in mitogen-activated splenic lymphocytes as well as in splenic lymphocytes an

171 on during infection decreases the numbers of splenic lymphocytes.

172 ng epithelial lining fluid, within liver and splenic macrophages and in kidney distal tubules.

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

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

175 emistry revealed that nuclei of both BMD and splenic macrophages from wild type mice contain nBMP2, w

176 DCs) and macrophages and by ex vivo-isolated splenic macrophages in a CD169-dependent manner.

177 significantly differed from that observed in splenic macrophages in which inductive perforin-2 expres

178 ice and wild type mice, but are deficient in splenic macrophages isolated from mutant mice after seco

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

180 e, bone marrow derived (BMD) macrophages and splenic macrophages were isolated from wild type and nBm

181 Clodronate significantly reduced TAMs and splenic macrophages, resulting in reduced SCC volumes.

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

183 commonly referred to as the biliary atresia splenic malformation (BASM) syndrome.

184 For example, peritoneal B-1 cells and splenic marginal zone B cells exhibited significantly in

185 ost striking phenotypes-gender imbalance and splenic marginal zone B-cell lymphoma-emerged in combina

186 refine the catalogue of somatic variants in splenic marginal zone lymphoma (SMZL) and to provide a w

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

188 The splenic marginal zone macrophages (MZMs) are important f

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

190 etion in early hematopoietic progenitors and splenic mature B cells, respectively.

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

192 EV complicated by gastric, main portal vein, splenic mesenteric junction, and splenic vein occlusions

193 nt was also present in the main portal vein, splenic mesenteric junction, and splenic vein, causing a

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

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

196 Here we characterized the tumor and splenic microenvironment of two syngeneic subcutaneous (

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

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

199 Unlike implantation of splenic morsels in the great omentum, our approach uses

200 Pre-treating primary splenic mouse B-cells with proteasome inhibitors prevent

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

202 We analyzed intragraft and splenic MSC localization, graft survival, and alloimmune

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

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

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

206 one (MZ) B cell phenotypes and colonized the splenic MZ, revealing T-bet(+) MBC plasticity.

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

208 r mesenteric ganglia, significantly increase splenic nerve activity and inhibit TNF production.

209 f the vagus nerve inhibit vagus nerve-evoked splenic nerve responses.

210 vagus nerve evokes action potentials in the splenic nerve.

211 reticuloendothelial system via the vagus and splenic nerves.

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

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

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

215 te increase of heart and chronic increase of splenic neutrophils and monocytes.

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

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

218 We demonstrate that splenic neutrophils together with two macrophage populat

219 ferentiation by acting on macrophages in the splenic niche.

220 In parallel, we observed an increase in splenic NK and NKT cells expressing TLR3 in infected B6

221 Splenic nodules are uncommon entities that occur rarely

222 Hence, we presented the case of aseptic splenic nodules as a first manifestation of Crohn's Dise

223 usual onset of Crohn's disease with multiple splenic nodules is reported.

224 This case suggests that in light of splenic nodules of unknown etiology attention should be

225 bdominal computed tomography showed multiple splenic nodules of unknown origin.

226 intensity ES at the abdomen activates NPY(+) splenic noradrenergic neurons via the spinal-sympathetic

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

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

229 In direct contrast, the splenic PtC(+) B-1a cell population does not preserve it

230 Furthermore, splenic PtC(+) B-1a cells displayed more diverse variabl

231 V(H)12, and V(H)2 between the peritoneal and splenic PtC(+) populations with age.

232 of irradiation in our models of cardiac and splenic radiation-induced lymphopenia or gastrointestina

233 Hepatic and splenic radioactivity decreased over time.

234 IGF1 (insulin-like growth factor-1), and the splenic red pulp macrophage gene Spic.

235 Located within red pulp cords, splenic red pulp macrophages (RPMs) are constantly expos

236 Splenic red pulp macrophages (RPMs) contribute to erythr

237 atory hemophagocytes (iHPCs), which resemble splenic red pulp macrophages but are a distinct populati

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

239 ge to erythrocytes contributes to anemia and splenic retention of damaged cells in infected animals.

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

241 ea to identify 7 cases of babesiosis-related splenic rupture between 2014 and 2016.

242 Spontaneous splenic rupture is an increasingly reported complication

243 Splenic rupture occurred in approximately 1% of babesios

244 lthier patients may be more prone to develop splenic rupture, as splenic histiocytes engage in more r

245 Compared to cases without splenic rupture, these patients were younger (by >10 yea

246 fected mice and was accompanied by increased splenic sequestration of erythrocytes and fewer erythrop

247 Splenic sequestration of red blood cells, the appearance

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

249 try revealed significant tumor targeting and splenic sequestration.

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

251 onclusion: Testosterone treatment stimulates splenic stress erythropoiesis in iron-replete as well as

252 Splenic stress erythropoiesis was stimulated in iron-def

253 Infected splenic stromal cells produced IFN-I in a cGAS-STING-dep

254 ent for IL-17 in the proliferation of LN and splenic stromal cells, particularly fibroblastic reticul

255 ce results in increased frequency of Ccr4(+) splenic T cells and worsening of skin inflammation, as i

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

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

258 In CD8 + splenic T cells from the HFS mice, glycolysis/basal resp

259 Splenic T cells from these immunized mice produced simil

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

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

262 Adoptive transfer of splenic T cells into NOD.Rag1(-/-) mice demonstrated tha

263 5 T cells for all three epitopes, peripheral splenic T cells maintained high affinity only to the HIP

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

265 protein (Pmel)-Trx1 transgenic mouse-derived splenic T cells, flow cytometry, and gene expression ana

266 lenic effector memory T cell frequencies and splenic T helper 17 cells in both models, and a decrease

267 We identify dendritic cell-primed splenic T(reg) cells as the central arbiters of these th

268 lenectomized wild-type mice by transplanting splenic T(reg) cells from POL5551-treated infarcted DERE

269 KI) mice, but not March8 (-/-) mice, whereas splenic T(reg) were unaffected.

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

271 argeting HuR by its inhibitor DHTS inhibited splenic Th17 cell differentiation and reduced experiment

272 LA-4 on Th17 cells, knockout of HuR impaired splenic Th17 cell migration to the CNS and abolished the

273 mages to quantify T cell localization within splenic tissue by using a "signal absorption" strategy t

274 s of the malaria parasite, Plasmodium, human splenic tissue is not readily available in most cases.

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

276 Transcriptomic analysis of splenic tissues from imiquimod-treated autoimmune-prone

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

278 LL-CFA/I treatment suppressed splenic TNF-alpha(+)CD8(+) T cells 6-fold at 11 weeks (p

279 Lower frequencies of Sostdc1 (-/-) splenic tNKs express inhibitory Ly49G2 receptors, but hi

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

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

284 se incidence by 50% (p < 0.05) and increased splenic Tregs producing both IL-10 and IFN-gamma 8-fold

285 The exception was greater splenic uptake in the leukemia/MDS group than in the lym

286 Splenic uptake was higher in the AML/MDS group than in t

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

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

289 binding potential, particularly between the splenic vein and the entrance of the liver.

290 ortal vein, splenic mesenteric junction, and splenic vein occlusions; hence, it should be kept in min

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

292 was disseminated tuberculosis complicated by splenic vein thrombosis.

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

294 ortal vein, splenic mesenteric junction, and splenic vein, causing an engorged inferior mesenteric ve

295 Vascular resection (other than splenic vessels) was required in 19.1% of the converted

296 nied by loss of hepatic immune cells, higher splenic viral burden and reduction in global antiviral g

297 gorithm could aid a radiologist in assessing splenic volume change.

298 gists to detect abnormal splenic volumes and splenic volume changes.Supplemental material is availabl

299 and may help radiologists to detect abnormal splenic volumes and splenic volume changes.Supplemental

300 in CD8(+) T(M) accumulations in bone marrow, splenic white pulp, and, particularly, lymph nodes.