ライフサイエンスコーパス: spleen

1 te counts, and similar diffuse uptake in the spleen.

2 were the urinary bladder wall, kidneys, and spleen.

3 he ability to migrate to the lymph nodes and spleen.

4 ve increased mature B cells in the MZ of the spleen.

5 the intestine to the cells of the liver and spleen.

6 ost bone marrow to the pleural space via the spleen.

7 a direct cellular contribution of NCC to the spleen.

8 and with expansion of memory T cells in the spleen.

9 infiltrating the lung or mobilized from the spleen.

10 of CD11b(+) Gr1(+) MDSCs in bone marrow and spleen.

11 me are found in other tissues, including the spleen.

12 assage of erythrocytes through an artificial spleen.

13 BED-CC-PSMA except for reduced uptake in the spleen.

14 sed frequencies of CD8(+)CD103(+) DCs in the spleen.

15 ne-NICC xenografts, draining lymph node, and spleen.

16 reduction in parasite loads in the liver and spleen.

17 pact of murine anti-CD20 Ab in the blood and spleen.

18 discrete checkpoints in the bone marrow and spleen.

19 naive T-cell trafficking to lymph nodes and spleen.

20 lesion size and GAS burden in the liver and spleen.

21 y Streptococcus pneumoniae is cleared by the spleen.

22 rkedly accelerated platelet clearance in the spleen.

23 C flow through the venous slits of the human spleen.

24 d reduced bacterial burdens in the liver and spleen.

25 creased Samd14 expression in bone marrow and spleen.

26 mechanistic parameters were analysed in the spleen.

27 -1) in the brain to 12.7 muGy.MBq(-1) in the spleen.

28 phagocyte system (MPS) such as the liver and spleen.

29 tate of CD4 and CD8 T cells in the liver and spleen.

30 , including 1 with visceral extension to the spleen.

31 opoietic organs, such as the BM, thymus, and spleen.

32 ergen recall response in the lymph nodes and spleen.

33 omposition and bacterial burden in lungs and spleens.

34 Sv/MBq), liver (8.94 +/- 1.67 muSv/MBq), and spleen (9.49 +/- 3.89 muSv/MBq).

35 Lymphopenia did not parallel the observed spleen alteration.

36 resulted in a lack of mature B cells in the spleen and a block in B cell development in the bone mar

37 y a reduced mycobacterial burden in lung and spleen and a prolonged overall survival in animals that

38 ifferentiation of B cells in bone marrow and spleen and analyzed their endosomal morphology, BCR expr

39 and embryonic day 18.5 fetal liver and adult spleen and bone marrow cells, respectively.

40 ls early after infection and developed fewer spleen and bone marrow IgG plasma cells and memory B cel

41 mation but also increased tumor dispersal to spleen and bone marrow.

42 ated by using real-time PCR in the liver and spleen and by means of ELISA in plasma.

43 bound specifically to GPR44 in pancreas and spleen and could be competed away dose-dependently in no

44 system is comprised in SMA, we analyzed the spleen and immunological components in SMA mice.

45 ctivator of transcription 1 in the liver and spleen and increased expression of the IFN-gamma-inducib

46 ressed on several CD4 Th cell subsets in the spleen and kidney of diseased mice, and expression corre

47 various organs and tissues, including liver, spleen and kidneys.

48 gamma/IL10 dual producer CD4+ T cells in the spleen and leads to a significant reduction in parasite

49 hi) iMOs are continuously recruited into the spleen and liver during L. donovani infection and they a

50 Mononuclear cells were isolated from spleen and liver for analysis by flow cytometry.

51 latum, correlating with a reduction in lung, spleen and liver fungal burdens.

52 In the spleen and liver of infected CB17 SCID mice, the bacteri

53 8 T cells, have dramatically high ROS in the spleen and liver of mice but not in the thymus or adipos

54 evere inflammatory lesions were found in the spleen and liver samples of SFTSV-infected hamsters.

55 emoglobin concentration, platelet count, and spleen and liver volumes remained stable for up to 4 yea

56 were associated with allometries of kidney, spleen and liver weights to body weight, 36 of which wer

57 parable levels of early viral replication in spleen and liver were observed in MCMV-infected Ebi3(-/-

58 nted QTNs responsible for relative growth of spleen and liver were verified by genome-wide test.

59 also affected the immune cell content of the spleen and liver, enhancing NK, NKT, and CD8(+) T cell a

60 and affected the immune cell content of the spleen and liver.

61 x1 cKO mice lack iNKT17 cells in the thymus, spleen and liver.

62 ) mice provided equivalent protection in the spleen and liver.

63 decrease in iNKT cell numbers in the thymus, spleen and liver.

64 Similar cells were identified in the spleen and lung of MO-treated mice and also were induced

65 d networks-one spans the blood, bone marrow, spleen and lung, while the other is restricted to tissue

66 At 24 h, the PD-L1-rich spleen and lungs demonstrated decreasing uptake with inc

67 Flow cytometry of both spleen and lymph node samples revealed higher frequencie

68 T cells subsets in blood, spleen and lymph nodes were detected dynamically by flow

69 ain- and PMCAb-derived PrP(Sc) were found in spleen and lymph nodes, whereas dsPMCAb-derived PrP(Sc)

70 ased Th1, Th2, Th17 cells, and Tregs, in the spleen and mediastinal lymph nodes, with expansion of sp

71 Spleen and mesenteric lymph node were collected, process

72 reased natural killer cells in the heart and spleen and neutrophils in the heart.

73 s with the highest uptake on images were the spleen and pancreas.

74 Ang II-induced T-cell activation in the spleen and perivascular adipose tissue was blunted in Tc

75 We found higher expression of Gal-1 in the spleen and Peyer's patches of mice infected orogastrical

76 id progenitor population that expands in the spleen and preferentially differentiates into mature B c

77 t increased the number of Tregs in blood and spleen and prevented IRI more efficiently than a mixture

78 e, Lactobacillus spp. can translocate to the spleen and prime the innate immune system for enhanced r

79 ad a greater number of maternal cells in the spleen and thymus but a much larger percentage was Foxp3

80 LR7 responses of transitional B cells in the spleen and was overexpressed in T1 B cells from BXD2 lup

81 eased numbers of CD4(+) T and B cells in the spleens and bronchoalveolar lavage (BAL) were also obser

82 i colonies grew from 68% of lungs and 36% of spleens and cervical lymph nodes but fewer than 20% of a

83 known neoantigens simultaneously in tumours, spleens and lymph nodes in tumour-bearing mice.

84 n was analysed in CD4+ T cells isolated from spleens and lymph nodes of arthritic mice treated with C

85 on, RhB was detected in the livers, kidneys, spleens and superficial parotid lymph nodes of the mice.

86 38 (2.3%) in the pancreas, 109 (6.7%) in the spleen, and 305 (18.8%) with multiple sites.

87 ) and/or Ly6c(lo) monocyte subsets in blood, spleen, and bone marrow were not altered.

88 fection, an altered cytokine response in the spleen, and enhanced bacterial clearance in multiple per

89 iched in SIV DNA in blood, lymph nodes (LN), spleen, and gut, and contained replication-competent and

90 ression was examined in the serum (protein), spleen, and hypothalamus (mRNA).

91 n macrophage-rich tissues such as the liver, spleen, and in particular bone marrow.

92 inish the cholesterol pool within the liver, spleen, and kidney at molar concentrations 10-to-100-fol

93 nt contrast enhancement on the heart, liver, spleen, and kidney, and sustain for more than 1 h, about

94 yde, to determine their toxicities in liver, spleen, and kidney, with and without the addition of Int

95 s in multiple organs, including liver, lung, spleen, and kidney.

96 cular helper T cells and plasmablasts in the spleen, and led to elevated levels of serum IgM and enha

97 impairment of bacterial clearance in blood, spleen, and liver and an exaggerated systemic inflammato

98 acterial burden in the draining lymph nodes, spleen, and liver were observed.

99 in peripheral tissues (including the heart, spleen, and liver) under Cu deficiency and that subcutan

100 olony-forming units were found in the lungs, spleen, and liver.

101 o, they migrated simultaneously to the lung, spleen, and other tested organs.

102 nduced myeloid expansion in the bone marrow, spleen, and peripheral blood.

103 alysis of human DC subsets in blood, tonsil, spleen, and skin.

104 loid inflammatory infiltrate in the skin and spleen, and substantial decreases in splenic mRNA expres

105 , visceral adipose tissue, bone marrow (BM), spleen, and the circulation.

106 inished (68)Ga-DOTATATE uptake in the liver, spleen, and thyroid but did not compromise tracer uptake

107 2%) for livers, +8% (range, +2% to +20%) for spleens, and +6% (range, -11% to +16%) for NET lesions.

108 o measured data in 54 kidneys, 25 livers, 27 spleens, and 30 NET lesions.

109 is rapidly cleared from the serum by liver-, spleen-, and bone marrow-resident phagocytic cells.

110 Recent studies have implicated the spleen as an anatomic site for integration of inflammato

111 healthy nude mice using the left kidney and spleen as reference organs.

112 d Th17- or IFNgamma-producing T cells in the spleen as well as regulatory T cell suppression.

113 mmatory M2 macrophage responses in liver and spleen, as associated with increased expression of argin

114 rly defenses against L. monocytogenes in the spleen, as well as a decrease in the tissue density of i

115 chemokines Cxcl9 and Cxcl10 in the liver and spleen, as well as in plasma.

116 7 member A (CLEC7A or DECTIN1) signaling via spleen-associated tyrosine kinase (SYK), a SYK inhibitor

117 d low nonspecific retention in the liver and spleen at 24 h after probe administration.

118 ore, the total numbers of donor cells in the spleen at their peaks were 10- to 100-fold larger in the

119 experimental periodontitis in vivo Purified spleen B cells from C57BL/6J mice (8 to 10 weeks old) we

120 Spleen B cells isolated from C57BL/6J mice were cultured

121 Thus, during positive selection in the spleen, BCR signaling causes immature T1 B cells to beco

122 st physiologic uptake to be in the liver and spleen (besides the red marrow).

123 n of HMGCS2 was also different in kidney and spleen between control and STZ treated mice.

124 adipose tissue, whereas it was minor in the spleen, blood, BM, and the airways.

125 e detected predominantly in lung and also in spleen, BM, blood and LN.

126 les were detectable in the liver, kidney and spleen but no other sites within 24 hours.

127 ll subtype distribution was disrupted in the spleen, but adoptive transfer studies indicated that the

128 to replicate in macrophages and colonize the spleens, but not the livers, of infected mice.

129 phils mediated pneumococcal clearance in the spleen by plucking bacteria off the surface of RP macrop

130 In this study, we show that SDR increases spleen CD11b(+)Ly6C(interm)Ly6G(+) neutrophil and CD11b(

131 In spleen, CD4(+) cells formed large clusters surrounded by

132 tometry was used to evaluate bone marrow and spleen cells from mice infected with P. gingivalis and c

133 GFP-specific restimulation of spleen cells from R. typhi(GFPuv)-infected BALB/c mice e

134 Injection of naive mice with apoptotic spleen cells generated by irradiation led to DC changes

135 ecific (P25 CD4(+) TCR transgenic) wild-type spleen cells into sanroqueRag1(-/-) mice actually led to

136 lr-d and Clr-f are virtually absent from the spleen, Clr-g transcripts were abundantly detected throu

137 gher numbers of erythroid progenitors in the spleen compared with wild-type mice.

138 metabolic rate organs (heart, liver, kidney, spleen) compared with SM was found.

139 scriptome and immune cell composition of the spleen, consistent with reduced inflammation.

140 r population, which is enriched in the mouse spleen, defined by cKit(+)CD71(low)CD24(high) expression

141 of cultured endothelial progenitor cells or spleen-derived endothelial cells with inflammatory cytok

142 ults demonstrate that SMN deficiency impacts spleen development and suggests a potential role for imm

143 rriers typically accumulate in the liver and spleen due to resident macrophages that form the mononuc

144 ls are preferentially recruited to lung over spleen due to robust expression in the lung of the Th17

145 ay that supports lymphoid development in the spleen during acute Plasmodium infection.

146 Here, we demonstrate that NCC colonize the spleen during embryogenesis and persist into adulthood.

147 ruitment of Ly6C(hi) iMOs into the liver and spleen during L. donovani infection using a CCR2 antagon

148 macrophages, were found to be altered in SMA spleens even in pre-symptomatic post-natal day 2 animals

149 bladder (critical organ), liver, kidney, and spleen exhibited the highest uptake.

150 Here, we report NECD behavior from horse spleen ferritin, a approximately 490 kDa protein complex

151 The T cells then exit the spleen for the CNS where they first roll and crawl along

152 At day 21, we harvested blood and spleens for fluorescence-activated cell sorting and hear

153 rythrocytic parasites in bone marrow and the spleen has been reported in cases of Plasmodium vivax ma

154 i) iMOs isolated from the infected liver and spleen have distinct phenotypic and activation profiles.

155 0.97-0.99; Delta = 0.44), and reference SUV (spleen: ICC, 0.81; Delta = 1.10; liver: ICC, 0.79; Delta

156 megaly were observed in the heart, liver and spleen in betaT.

157 cell migration between the intestine and the spleen in EAU Kaede mice.

158 g periods of time within lymph nodes and the spleen in the steady state.

159 d identified organs, including the liver and spleen, in which these changes originated.

160 cted in cell suspensions of murine lungs and spleens indicating successful humanization.

161 lturable bacteria in their lungs, livers, or spleens, indicating that the vaccine formulation had gen

162 (S1P1R) directs the exit of T cells from the spleen into blood, and from lymph nodes and Peyer's patc

163 higher TMTV (P = .0055) and higher levels of spleen involvement (P < .0001).

164 in expression per million B cells within the spleen is described.

165 ariation in different regions (aorta, liver, spleen, kidney, small bowel, lumbar vertebra, psoas musc

166 e observed a similar metallocluster in horse spleen L-ferritin, indicating that it represents a commo

167 The increased spleen levels of Lactobacillus 16S rRNA in SDR mice posi

168 us induced cytokines in the heart, pancreas, spleen, liver, and jejunum.

169 esulted in robust engraftment of CMML in BM, spleen, liver, and lung of recipients (n = 82 total mice

170 se in radiation dose delivered to the heart, spleen, liver, kidneys, stomach, colon, small intestine,

171 iple innate and adaptive immune cells in the spleen, liver, lung and bone marrow, often leading to ch

172 n and experimental infections, as well as in spleen, lung, and brain tissues of infected mice.

173 n among secondary lymphoid organs, including spleen, lymph nodes and Peyer's patches, where T cells s

174 components in blood, lymphoid (bone marrow, spleen, lymph nodes), and mucosal (lungs, intestines) si

175 antibodies recognized native Siglec-E within spleen lysates.

176 Liver and spleen masses decreased in the ILI group (-0.12 +/- 0.02

177 Leukocytes in murine hearts, pericardial AT, spleen, mediastinal lymph nodes, and bone marrow were qu

178 ceptor-dense organs such as the pancreas and spleen, moderate uptake in the brain and myocardium, and

179 cillus RNA in the spleen, which localized in spleen monocytes.

180 These multipotent progenitors of the spleen (MPPS) develop from MPP2, a myeloid-biased subset

181 LSIRS were observed in spleen (n = 14), liver (n = 3), and nodal (n = 8) lesion

182 alyzed iNKT cells in both blood (n = 26) and spleen (n = 9) samples from 32 patients with HHV-8 MCD a

183 e, different to the intestinal tract, in the spleen, Nkrp1g is selectively expressed by a subset of N

184 histology and microstructural changes in the spleen of adult male and female CD-1 mice exposed to 4 t

185 bleeding at grade 3 or worse, with palpable spleen of at least 5 cm and without grade 2 or greater p

186 DC numbers were restored in the spleen of C57BL/6 and peripheral blood of SJL/J mice alo

187 Furthermore, eosinophils from the lungs and spleen of fungal allergen-challenged wild-type mice are

188 FVIII localizes in the marginal sinus of the spleen of FVIII-deficient mice shortly after injection,

189 in the small vessels of the bone marrow and spleen of patients with primary myelofibrosis have a mes

190 lar endothelial cells in the bone marrow and spleen of patients with primary myelofibrosis show funct

191 versed the altered B cell development in the spleen of sIgM (-/-) mice, suggesting that sIgM regulate

192 pie, as no PrP(Sc) was detected in brains or spleen of these animals by either Western blotting or af

193 CD4(+)PD-1(+)CXCR5(+/-) cells resided in the spleen of these mice likely due to a loss of regulatory

194 changed miRNAs and deregulated genes in the spleen of three groups of broilers: nonchallenged (NC),

195 Proliferation of CD4+ cells from spleens of healthy mice was not affected by CM-MSC but r

196 Eosinophils from the spleens of IL-5 transgenic mice, fluorescently labeled e

197 only PA14 was recovered from the livers and spleens of infected mice.

198 only PA14 was recovered from the livers and spleens of infected mice.

199 miR-718 expression was also induced in the spleens of mice upon LPS injection.

200 l12b expression was also found in livers and spleens of mice with MAS.

201 11 fibrosarcoma cells were injected into the spleens of syngeneic mice to isolate tumour sub-populati

202 ted decrease in the B-cell population of the spleens of these animals.

203 Foxp3Treg cell from spleens of treated BALB/c mice (tolerant Treg cell), and

204 ulocytic myeloid-derived suppressor cells in spleens of tumor-bearing mice and ex vivo.

205 pic (non-mac-tropic) Envs recovered from the spleen or brain, (iii) the evidence was consistent with

206 known as conventional NK cells in the mouse spleen or human peripheral blood.

207 ucing B cells within pericardial AT, but not spleen or lymph nodes.

208 or reduced TB dissemination to other lobes, spleen, or liver/kidney; in contrast, the controls showe

209 f severe BCG disease and maintained lung and spleen organ integrity, which was accompanied by a reduc

210 nificantly higher in the thyroid, liver, and spleen (P < 0.05) than the values measured after the adm

211 muscle, submandibular and sublingual gland, spleen, pancreas, liver, and gallbladder was observed.

212 nd IFN-gamma in CD4(+) and CD8(+) T cells in spleens, pancreatic lymph nodes (pLN) and other lymph no

213 point, inflammatory monocytes infiltrate the spleen parenchyma but remain mainly intravascular in the

214 The spleen plays an integral protective role against encapsu

215 te their differentiation into B cells in the spleen postinfection are not defined.

216 gradable micron-sized particles in liver and spleen precludes their clinical use and limits the trans

217 To avoid clearance by the spleen, red blood cells infected with the human malaria

218 The primary endpoint was spleen response (defined as the proportion of patients w

219 patients, 46 (55%, 95% CI 44-66) achieved a spleen response.

220 , which inhibits both JAK2 and FLT3, induced spleen responses with limited myelosuppression in phase

221 extramedullary hematopoiesis occurred in the spleen, resulting in a four-fold increase in megakaryocy

222 of tumor metastases to the liver, lungs, and spleen revealed that sunitinib administration enhances m

223 ET of spleen revealed thousands of virions released by individ

224 This effect is specific to the spleen, revealing a unique molecular pathway that regula

225 n sample (0.07 x 10(-5) %ID/g), one juvenile spleen sample (0.039 x 10(-5) %ID/g), and one juvenile b

226 Spleen samples were collected at 40 days post injection

227 marrow neutrophils by flow cytometry and on spleen sections by immunohistochemistry.

228 Immunohistochemical analysis of spleen sections from wild-type and bumble mice revealed

229 ells in both the avian and non-human primate spleen, showing evolutionary conservation of these cells

230 innervation and the HPA axis, which modulate spleen shrinkage and cellular immunity.

231 We observed increased capillary exchange and spleen shrinkage by d 3 post-ICH, with recovery by d 14.

232 Finally, in mouse models of ICH, spleen shrinkage could be related to innervations from a

233 The extent of spleen shrinkage was associated with brain hematoma size

234 edema was observed in the presence of severe spleen shrinkage.

235 was not superior to BAT for the reduction of spleen size by at least 35% compared with baseline.

236 ort, we identify: a significant reduction in spleen size in multiple SMA mouse models and a pathologi

237 orrelated with higher Sokal score, increased spleen size, and high leukocyte and peripheral-blood bla

238 EBOV replication in the liver but not in the spleen, suggesting that in this model, efficiency of vir

239 = 0.016) and a greater decrease in the lung/spleen SUVmax index (not reached vs. 7.1; P = 0.043) wer

240 ulated more monocytes and neutrophils in the spleen than did WT mice during Listeria monocytogenes in

241 eir peaks were 10- to 100-fold larger in the spleen than in the lung, contradicting the notion that t

242 nd progenitor cell populations in the BM and spleen that are hypersensitive to granulocyte macrophage

243 llular and microanatomical structures of the spleens that reveal minor alterations in immunomodulator

244 In the mutant spleen, the characteristic perifollicular rim marking th

245 ZEV NPs rapidly accumulated in the liver and spleen, the target organs of intracellular infection.

246 rythropoiesis at all erythroid stages in the spleen thereby excluding erythroid differentiation defec

247 of several pro-inflammatory genes within the spleen; this was not evident among mice treated at ZT14.

248 tion in the bone marrow that persists in the spleen, thymus and blood.

249 f 521 small regulatory microRNAs (miRNAs) in spleen tissue from young and old animals of 6 mouse stra

250 dy and accumulated the greatest in liver and spleen tissues.

251 m that can encapsulate mRNA, navigate to the spleen, transfect B lymphocytes, and induce more than 60

252 ton's tyrosine kinase (pBtk), phosphorylated Spleen tyrosine kinase (pSyk), and nuclear receptor Nur7

253 Antibody-mediated TREM2 stimulation enhanced spleen tyrosine kinase (SYK) activity and uptake of Stap

254 Spleen tyrosine kinase (Syk) is an intracellular nonrece

255 Here we show that spleen tyrosine kinase (SYK) is upregulated during brown

256 Spleen tyrosine kinase (Syk) promotes leukocyte recruitm

257 1, a C-type lectin receptor that signals via spleen tyrosine kinase (Syk) to induce ROS.

258 cellular signaling proteins FcepsilonRgamma, spleen tyrosine kinase (SYK), and EWS/FLI1-Activated Tra

259 conjunction with Src family kinases (SFKs), spleen tyrosine kinase (Syk), and phospholipase gamma2 (

260 sphotyrosinylation and specifically recruits spleen tyrosine kinase (Syk), initiating cellular activa

261 tment of early signaling proteins, including spleen tyrosine kinase (Syk), linker for activation of T

262 ell antigen receptor (BCR)-proximal effector spleen tyrosine kinase (SYK), which we identified as an

263 mediator release, as well as Lyn kinase and spleen tyrosine kinase activation and signaling through

264 ing reactive oxygen species, thus preventing spleen tyrosine kinase dephosphorylation and perpetuatin

265 Spleen tyrosine kinase expression was found in human and

266 Spleen tyrosine kinase inhibition directly attenuates ai

267 ivation via the SFK (Src family kinase)-Syk (spleen tyrosine kinase)-PLCgamma2 (phospholipase Cgamma2

268 ession of several BCR kinases including LYN, spleen tyrosine kinase, Bruton tyrosine kinase and AKT.

269 Several spleen tyrosine kinase-coupled C-type lectin receptors (

270 an intense abnormal splenic uptake, whereas spleen uptake was inconclusive with BMS.

271 rtion of patients with a >/=35% reduction in spleen volume as determined by blinded CT and MRI at a c

272 point was a reduction by at least 35% in the spleen volume at 24 weeks compared with baseline.

273 f 52 in the BAT group had a reduction in the spleen volume by at least 35% compared with baseline (pr

274 primary endpoint of 35% or more reduction in spleen volume from baseline assessed by MRI or CT.

275 om a baseline and at least one post-baseline spleen volume measurement was available) and the safety

276 ymphoproliferation with lymph node sizes and spleen volumes reduced by 39% (mean; range, 26%-57%) and

277 f prions upon FDC in Peyer's patches and the spleen was impaired, and disease susceptibility signific

278 Her spleen was not palpable, and a quantitative polymerase c

279 Binding in the PD-L1(+) spleen was reduced by coadministration of BMS-986192.

280 The spleen was the single tissue showing regulation of only

281 , using time-lapse intravital imaging of the spleen, we identify a tropism for Streptococcus pneumoni

282 simism' was associated with smaller relative spleen weight, which is a documented consequence of chro

283 that express LMP2A, Cks1 deficiency reduces spleen weights, restores B-cell follicle formation, impe

284 bed doses in the bladder, liver, kidney, and spleen were 58.5, 6.6, 6.3, and 4.3 mGy, respectively.

285 ns with high TSPO densities such as lung and spleen were greater in HABs than in LABs.

286 renal IVC, lungs, heart, liver, kidneys, and spleen were harvested at necropsy.

287 phocyte populations from the bone marrow and spleen were harvested from heterozygous Notch2HCS mice a

288 Deltasse DeltasagA mutants in the liver and spleen were likely due to their reduction in the systemi

289 e, the germinal center (GC) responses in the spleen were more enhanced in our mouse model.

290 82% of immunogen-responding cells in the pup spleen were produced through maternal educational immuni

291 kidney cortex and medulla, liver, lungs, and spleen were used from previous studies in which mice wer

292 cell development is a formative stage in the spleen where autoreactive specificities are censored as

293 they eventually mature and accumulate in the spleen where TCR and IL-15/STAT5 signaling promotes thei

294 ry (2 degrees ) lymphatic tissues (e.g., the spleen) where, in the absence of autoantigen, they estab

295 800)-TOC was primarily through the liver and spleen whereas (64)Cu-DA(IR800)-TOC was cleared through

296 Mild uptake was seen in the kidneys and spleen, which also decreased with time.

297 cifically increased Lactobacillus RNA in the spleen, which localized in spleen monocytes.

298 regulatory T cells both in aortic sinus and spleen with higher mRNA expression of CTLA4 (3 fold), Fo

299 The highest uptake was found in the spleen, with doses ranging from 1.54 to 3.60 mGy/MBq.

300 man primate showed binding in the PD-L1-rich spleen, with rapid blood clearance through the kidneys a