ライフサイエンスコーパス: Peyer

1 Peyer patches are the major entrance of Salmonella infec

2 Peyer's patches (PPs) are unique compared to other secon

3 Peyer's patches (PPs) of the small intestine are antigen

4 Peyer's patches (PPs) play a central role in supporting

5 or, E-cadherin, whereas translocation across Peyer's patches through M-cells is InlA-independent.

6 LSR-II flow cytometer analyzed Peyer patches and lamina propria isolated lymphocytes fo

7 igated small bowel loops without M cells and Peyer's patches.

8 , Flt3L significantly contributes to ILC and Peyer's patches development by targeting lymphoid progen

9 d from the LT-dependent formation of ILF and Peyer's patches by not requiring the presence of an inta

10 t tissues, in particular small intestine and Peyer's patches.

11 and yopH mutants colonize the intestines and Peyer's patches in single-strain infections but fail to

12 omorphometric analyses of ileum, jejunum and Peyer's patches were carried out, to determine the infla

13 naive T cells (T(N)) to lymph nodes (LN) and Peyer patches (PP), putative sites of GVHD initiation.

14 cordingly, CD4(+) T cells within the LNs and Peyer's patches failed to express the T(FH) key transcri

15 ficient mice, lymphocyte egress from LNs and Peyer's patches is blocked.

16 required for lymphocyte egress from LNs and Peyer's patches, and suggest a role for S1P in lymphatic

17 cture of the germinal centers in the LNs and Peyer's patches.

18 were found in the mesenteric lymph node and Peyer patches.

19 (LTi) cells are required for lymph node and Peyer's patch (PP) organogenesis, but where these specia

20 tivation of the mesenchyma in lymph node and Peyer's patch anlagen.

21 i cell-mediated activation of lymph node and Peyer's patch mesenchyma forms the necessary platform fo

22 both the mucosal (mesenteric lymph node and Peyer's patch) and systemic (spleen) tissues of TLR4-mut

23 from the spleen, mesenteric lymph node, and Peyer's patch.

24 ation was rescued in spleen, lymph node, and Peyer's patches.

25 ssues such as the mesenteric lymph nodes and Peyer patches.

26 idence time of TDLs in major lymph nodes and Peyer's patches (10 hours).

27 members of this pathway lack lymph nodes and Peyer's patches and have abnormal spleen architecture.

28 were measured in mesenteric lymph nodes and Peyer's patches cells.

29 ow that mice lacking spleen, lymph nodes and Peyer's patches generate unexpectedly robust primary B-

30 spleen into blood, and from lymph nodes and Peyer's patches into lymph.

31 r T-cells in both mesenteric lymph nodes and Peyer's patches without obviously affecting expression o

32 ly mice, which are devoid of lymph nodes and Peyer's patches, acutely rejected fully allogeneic skin

33 sues, such as the mesenteric lymph nodes and Peyer's patches, as well as in the lamina propria.

34 lpha-deficient mice lack all lymph nodes and Peyer's patches, mice deficient in LT beta retain mesent

35 id organs, including spleen, lymph nodes and Peyer's patches, where T cells search for antigens.

36 ry lymphoid tissues, such as lymph nodes and Peyer's patches.

37 they induce the formation of lymph nodes and Peyer's patches.

38 ells initiate development of lymph nodes and Peyer's patches.

39 ed with early development of lymph nodes and Peyer's patches.

40 in mice that lacked spleen, lymph nodes, and Peyer's patches (SLP mice).

41 from the spleen, mesenteric lymph nodes, and Peyer's patches of orally tolerized mice showed increase

42 ges and in the bone marrow, lymph nodes, and Peyer's patches.

43 ral lymph nodes, mesenteric lymph nodes, and Peyer's patches.

44 c immune functions in the lamina propria and Peyer's patches.

45 had increased levels of IgA in both sera and Peyer's patches.

46 higher expression of Gal-1 in the spleen and Peyer's patches of mice infected orogastrically with Y.

47 e show normal architecture of the spleen and Peyer's patches, suggesting that TNF is not essential fo

48 of the normal architecture of the spleen and Peyer's patches; and abnormal trafficking of immunoglobu

49 , in the mesenteric lymph nodes, spleen, and Peyer's patches at 14 weeks, and in the tongue 20 weeks

50 cum, heart, kidney, liver, lung, spleen, and Peyer's patches) and were elevated most significantly in

51 ganogenesis but normal splenic structure and Peyer's patches.

52 asopharyngeal associated lymphoid tissue and Peyer's patch epithelium, they showed an abnormal morpho

53 anized MALT (O-MALT) such as the tonsils and Peyer patches.

54 and lymphoid/monocytic cells in tonsils and Peyer's patches (explaining viremia), extending previous

55 and lymphoid/monocytic cells in tonsils and Peyer's patches (explaining viremia), thereby supplement

56 ciated lymphoid tissues, such as tonsils and Peyer's patches, which is hard-wired to secrete interleu

57 production, TCRgamma gene transcription, and Peyer's patch development.

58 s, spleens, and livers of both wild-type and Peyer's patch-deficient mice.

59 opically in intestinal lamina propria around Peyer's patches.

60 vade the intestinal lymphoid tissue known as Peyer's patches (PPs) and disrupt the integrity of the i

61 roA(-)) to such secondary lymphoid organs as Peyer's patches in the small intestine, elicited marked

62 n organized mucosal lymphoid tissues such as Peyer's patches of the small intestine.

63 -associated lymphoid tissues (GALT), such as Peyer's patches, and mature GP2(+) M cells.

64 but more environmentally regulated, such as Peyer's patches, nasal-associated lymphoid tissue, bronc

65 ry mucosal lymphoid tissues (O-MALT) such as Peyer's patches, tonsils, and adenoids.

66 -associated lymphoid tissues (GALT), such as Peyer's patches, which contain high numbers of mature M

67 mice lacking TLR11, apparent hemorrhages at Peyer patches are induced by highly invasive Salmonella,

68 with the intestinal mucosa by crossing both Peyer's patches and non-Peyer's patch areas but does not

69 equal abilities to cross the mucosa in both Peyer's patch and non-Peyer's patch segments of normal m

70 d follicles, which shares properties of both Peyer's patches and tertiary lymphoid tissues.

71 transcription factor RORgammat-dependent but Peyer's patch-independent somatic mutations drive the di

72 ves the induction of alpha4beta7 and CCR9 by Peyer's patch and mesenteric lymph node (MLN) dendritic

73 host, S Typhimurium preferentially colonizes Peyer's patches, a lymphoid organ in which microfold cel

74 ranging from the developmentally determined Peyer's patches to the inflammatory derived tertiary lym

75 tic cells, inducing the formation of ectopic Peyer's patch-like structures.

76 articles utilize epithelial M cells to enter Peyer's patches, small areas of the intestine concentrat

77 s into mucosal sites (mainly gut, especially Peyer patches), and CD8 T(M)s into lymph nodes and splee

78 C17orf99(-/-) mice have smaller and fewer Peyer's patches and lower numbers of IgA-secreting cells

79 Finally, Peyer's patch GC B cells generate a reservoir of V exons

80 rate that RET signalling is also crucial for Peyer's patch formation.

81 nt and normal lymph-node genesis, except for Peyer's patches.

82 IgA(+)CD138(+) plasma cells from Peyer's patches and lamina propria were analyzed by flow

83 Rotavirus-specific CD8 T cells from Peyer's patches of orally infected mice expressed high l

84 ells as well as germinal center B cells from Peyer's patches showed marked increases in apoptosis and

85 ronic region in germinal center B cells from Peyer's patches.

86 ronic region in germinal center B cells from Peyer's patches.

87 tropism is mediated by dendritic cells from Peyer's patches.

88 prevents egress of IgA-secreting cells from Peyer's patches.

89 ating a role for IFN-gamma-producing DC from Peyer's patches in the development of Ag-specific IEL po

90 Also, treatment of wild-type DC from Peyer's patches with Ab to IFN-gamma abrogates their abi

91 with rotavirus, the donor cells derived from Peyer's patches of orally infected mice were more effici

92 low cytometry studies with DCs isolated from Peyer's patches after TCI suggested that activated DCs c

93 liferative plasmablasts that originated from Peyer's patches and produced IgAs reactive to commensal

94 PN reduces respiratory tract (RT) and GALT Peyer patch and lamina propria lymphocytes, lowers gut a

95 nd a reduction in the number of hyperplastic Peyer's patches.

96 The continuous ileal Peyer's patches (IPP) of sheep are regarded as a type of

97 half of all Cgamma transcripts in the ileal Peyer's patches (IPPs) and mesenteric lymph nodes but on

98 owing oral inoculation, prions bind to ileal Peyer patch and cecal patch microfold cells (M cells) in

99 the density of microfold (M) cells in ileum Peyer's patch (PP) follicle-associated epithelia (FAE) t

100 es (ILFs), but not embryonically 'imprinted' Peyer's patches.

101 In Peyer's patches (PPs), transforming growth factor-beta (

102 In Peyer's patches, such TH17 cells acquired a follicular h

103 In Peyer's patches, we found that compared with wild-type,

104 KT cells produce the majority of the IL-4 in Peyer's patches and provide indirect help for B-cell cla

105 GCs were also absent in Peyer's patches of naive Irf4(-/-) mice.

106 inoculation blocked PrP(Sc) accumulation in Peyer's patches and mesenteric lymph nodes and prevented

107 on frequency at Ig loci in the spleen and in Peyer's patches, whereas knock-in mice with a mutagenic

108 ocyte recruitment, and cellular apoptosis in Peyer's patches (PPs), mesenteric lymph node (MLN), and

109 we found that entry of commensal bacteria in Peyer's patches (PP) via the M cell pathway was mediated

110 ced frequencies of apoptotic CD4+ T cells in Peyer patches as compared with healthy controls.

111 on can increase CD4+ central memory cells in Peyer patches.

112 Though the host M cells in Peyer's patch and the bacterial invasion protein interna

113 m treatment reduced the number of B cells in Peyer's patches and downmodulated adaptive immune respon

114 rmation of robust germinal center B cells in Peyer's patches and had restored B-1-cell and ILC2 funct

115 e of IgA(+)CD38(+)CD138(-) memory B cells in Peyer's patches and LP was decreased only in IL-21R(-/-)

116 l as IgA(+)CD38(+)CD138(-) memory B cells in Peyer's patches and LP.

117 n of naive flagellin-specific CD4 T cells in Peyer's patches and mesenteric lymph nodes, which was ac

118 xpressed on virus-specific CD8(+) T cells in Peyer's patches or lymph nodes and spleens were examined

119 ulted in reduced numbers of B and T cells in Peyer's patches, reduced numbers of intraepithelial CD8a

120 mma interferon(-) CD107a/b(+) CD8 T cells in Peyer's patches.

121 ted uptake from microfold cells (M-cells) in Peyer's patches of small intestine.

122 Profound histomorphologic changes in Peyer's patches were associated with depletion of organ

123 Cell contraction in Peyer's Patches is associated with the apoptosis of mult

124 L-specific precursor CTL and effector CTL in Peyer's patches (PP) of reovirus 1/L-inoculated mice.

125 all intestine, both viruses were detected in Peyer's patches, but only the wild-type virus reached th

126 the early accumulation of prions upon FDC in Peyer's patches and the spleen was impaired, and disease

127 d a marked increase in mutation frequency in Peyer's patches, revealing a pattern that was similar to

128 pression of several classes of host genes in Peyer's patches, the liver, and the spleen following ora

129 eletion of either iE(kappa) or 3'E(kappa) in Peyer's patch germinal center B cells.

130 ileum but did not inhibit basal NF-kappaB in Peyer's patches.

131 LT stimulates LTbetaR in Peyer's patches (PP) to activate NF-kappaB via the nonca

132 rn of polarization that was also observed in Peyer's patches.

133 gh IL-21 producing Tfh cells present only in Peyer's Patches.

134 neous LNs) or the gut (mesenteric LNs) or in Peyer's patches.

135 nt revealed pronounced mutant persistence in Peyer's patches.

136 sion occurred within hours of starting PN in Peyer's patches, but not mesenteric lymph nodes or the i

137 , and a previously undescribed population in Peyer's patches (PP).

138 lios+CD4+ T cell population predominantly in Peyer patches.

139 that 19(+)45R(lo) cells are also present in Peyer's patches and in the spleen throughout the life sp

140 nfluence the early accumulation of prions in Peyer's patches can directly influence disease pathogene

141 at the defective germinal centre reaction in Peyer's patches of aged mice can be rescued by faecal tr

142 nto the IgA repertoire upon recirculation in Peyer's patches.

143 requencies of SHM in Igh variable regions in Peyer's patch cells, and of double-strand breaks in the

144 utrophil-dominated innate immune response in Peyer's patches, limited dendritic cell migration to mes

145 izing and inducing inflammatory responses in Peyer's patches (PPs) and mesenteric lymph nodes (MLNs).

146 d upregulation of innate immune responses in Peyer's patches and pancreatic lymph nodes.

147 olecule-1 (MAdCAM-1) and T cell responses in Peyer's patches following stimulation of the immune syst

148 demonstrate that a specialized DC subset in Peyer's patches (PPs) mediates the rapid activation of p

149 central memory CD4(+) T cells and increased Peyer's patch effector memory CD4(+) T cells in septic C

150 kely by the shedding of prions from infected Peyer patches.

151 is a double-stranded RNA virus that infects Peyer's patches (PPs) after peroral inoculation of mice.

152 Intestinal Peyer's patches are essential lymphoid organs for the ge

153 st GCs are transient(3), those in intestinal Peyer's patches (PPs)-which depend on the gut microbiota

154 gA) induction primarily occurs in intestinal Peyer's patches (PPs).

155 ts, wild-type H18N11 was found in intestinal Peyer's patches and was shed to high concentrations in r

156 iated lymphatic tissue, including intestinal Peyer's patches, followed by extensive infection of lymp

157 rly discernible in mice devoid of intestinal Peyer's patches and mesenteric lymph nodes.

158 M cells overlying intestinal Peyer's patches (PPs), isolated lymphoid follicles, and

159 itic cells (FDC) within the small intestinal Peyer's patches is essential to establish host infection

160 Here, we report that intestinal Peyer's patches (PPs) contain a specialized conduit syst

161 follicular dendritic cells within intestinal Peyer's patches.

162 xhibited the highest expression in intestine Peyer's patch, whereas NK2C was expressed almost exclusi

163 In the healthy intestine, Peyer's patches and isolated lymphoid follicles generate

164 propria lymphocytes of the small intestine, Peyer's patches, and mesenteric lymph nodes.

165 on into blood but stimulated absorption into Peyer patches.

166 ut epithelium in a transwell system and into Peyer's patch myeloid DCs.

167 ropagation of prions from the gut lumen into Peyer's patches.

168 tight control of pathogens penetrating into Peyer patches.

169 enterocolitica is able to efficiently invade Peyer's patches with the aid of invasin, an outer member

170 used cells were most abundant in the kidney, Peyer's patches, and cardiac tissue.

171 lpha-deficient (LTalpha(-/-)) mice that lack Peyer's patches and mesenteric lymph nodes were orally i

172 B-cell knockout (KO) mice, which lack Peyer's patches, were used to demonstrate that M. avium

173 in these organs in mouse mutants that lacked Peyer's patches.

174 Lymphotoxin alpha knockout mice lacking Peyer's patches (PPs) and pretreated orally with CpG DNA

175 on Th17 responses within intestinal lymphoid Peyer's patches (PP).

176 ry function is a unique feature of mammalian Peyer patches but not the O-MALT of birds or ectotherms.

177 oduction of Yersinia enterocolitica in mouse Peyer's patches.

178 nsport of microparticles by the FAE of mouse Peyer's patches in vivo.

179 specifically secreted from the FAE of mouse Peyer's patches, CCL9 (MIP-1gamma, CCF18, MRP-2).

180 ed donor-derived HSPCs in intestinal mucosa, Peyer's patches, mesenteric lymph nodes, and liver.

181 smacytoid dendritic cells (pDCs) from murine Peyer's patches (PPs).

182 Salmonella from penetrating into the murine Peyer patches and spreading systemically.

183 inguinal nodes were absent and there were no Peyer's patches.

184 mphoid organs (SLOs), including lymph nodes, Peyer's patches, and the spleen, have evolved to bring c

185 ondary lymphoid tissues such as lymph nodes, Peyer's patches, or the spleen.

186 d in T-cell zones of mesenteric lymph nodes, Peyer's patches, spleen, and thymus.

187 Strikingly, the mice lacked lymph nodes, Peyer's patches, splenic marginal zones, and follicular

188 osa by crossing both Peyer's patches and non-Peyer's patch areas but does not translocate or dissemin

189 oss the mucosa in both Peyer's patch and non-Peyer's patch segments of normal mice.

190 lymphocytes in the interfollicular areas of Peyer's patches.

191 polyclonal and related to GFP(-)Tfh cells of Peyer's Patches in TCR repertoire composition and overal

192 ta cause an acute decrease in cellularity of Peyer's Patches while cell numbers in the lamina propria

193 and myeloid cells, although colonization of Peyer patches and the peritoneal cavity is significantly

194 ed to differences in vaccine colonization of Peyer's patch (PP) and spleen or in their respective tis

195 articular, were deficient in colonization of Peyer's patches and liver.

196 and grossly expanded red pulp, a deficit of Peyer patches, and small lymph nodes with marked reducti

197 at Nfil3 is essential for the development of Peyer's patches and ILC2 and ILC3 subsets.

198 estine, resulting in impaired development of Peyer's patches.

199 Thus, the FAE of Peyer's patches responds to TLR2 ligands in a manner tha

200 the follicle-associated epithelium (FAE) of Peyer's patches.

201 n agent-based simulation of the formation of Peyer's patches (PP), gut-associated lymphoid organs tha

202 in has an important role in the formation of Peyer's patches.

203 (+) cells resulted in a reduced frequency of Peyer's Patches IgG1 and germinal center B cells in addi

204 at Gfra3-deficiency results in impairment of Peyer's patch development, suggesting that the signallin

205 To define the importance of Peyer's patch (PP) M cells during MNV pathogenesis, we u

206 Invasion of Peyer's patches by M. avium subsp. paratuberculosis occu

207 e gastrointestinal tract, the involvement of Peyer's patches was not observed in either infection.

208 iver inflammation, splenomegaly, and loss of Peyer's patches.

209 Geo) mice have decreased size and numbers of Peyer patches, a finding confirmed in human samples.

210 colitis, significantly increased numbers of Peyer's patch (PP) phenotype M cells were induced at the

211 Organogenesis of Peyer's patches (PP), follicle-associated epithelium, an

212 ction of acute GVHD requires the presence of Peyer patches (PPs).

213 ity before aggregation into the primordia of Peyer's patches, a major component of the gut-associated

214 6-deficient mice had a reduced proportion of Peyer's patch B lymphocytes and an associated re-duction

215 ecretory IgA is sufficient for protection of Peyer's patches against oral reovirus challenge and, if

216 llicle-associated epithelium (FAE) region of Peyer's patches.

217 We explored the role of Peyer's patch (PP) dendritic cell (DC) populations in th

218 ociated re-duction in the number and size of Peyer's patch follicular domes.

219 x2.3 regulates the vascular specification of Peyer patches in mice through determining endothelial ad

220 ndary lymphoid organs, not in bone marrow or Peyer's patches, in contrast to the case for many mammal

221 e specialized epithelial cells situated over Peyer's patches (PP) and other organized mucosal lymphoi

222 nding of these bacteria to M cells overlying Peyer's patches and subsequent entry into lymphoid tissu

223 ells that reside in the epithelium overlying Peyer's patch and nasopharyngeal associated lymphoid tis

224 STAT6-deficient macrophages and parasitized Peyer's patches from mice orally challenged with strain

225 backpack tumors, however, the IgA prevented Peyer's patch infection, but the IgG did not.

226 topoiesis and, with the exception of reduced Peyer's patches, normal architecture and cellularity of

227 Loss of Nfil3 selectively reduced Peyer's patch formation and was accompanied by impaired

228 an additional lymphoid structure resembling Peyer's patches (PP) in composition and architecture has

229 ost completely suppressed it, even restoring Peyer's patches.

230 appearance of PrP(RES) in the brain, spleen, Peyer's patches, lymph nodes, pancreatic islets of Lange

231 d organs (SLOs) include lymph nodes, spleen, Peyer's patches, and mucosal tissues such as the nasal-a

232 ptosis compared to wild-type thymus, spleen, Peyer's patches, and the white matter of the brain.

233 secretes histamine, significantly suppressed Peyer patch IL-2, IL-4, IL-5, IL-12, TNF-alpha, and GM-C

234 immune arthritis model, we demonstrated that Peyer's patch (PP) Tfh cells were essential for gut comm

235 These findings establish that Peyer's patch dendritic cells imprint gut-homing specifi

236 The Peyer's patches (PP) and mesenteric lymph nodes (MLN) ar

237 The Peyer's patches and mesenteric lymph nodes were markedly

238 explore the requirement for M cells and the Peyer's patch (PP) in induction of oral tolerance and ad

239 nts of proinflammatory molecules in both the Peyer's patches and pancreatic lymph nodes.

240 ceptors for CCL9, CCR1, was expressed by the Peyer's patch CD11b(+) DCs and in a chemotaxis assay, CD

241 IgA antibodies (IgA MAbs) produced from the Peyer's patches and mesenteric lymph nodes of BALB/c mic

242 ic disease and inflammatory responses if the Peyer's patches are bypassed.

243 CD4+ T cells did not accumulate early in the Peyer patches and failed to induce acute injury to the s

244 od-activated CD44+Helios+CD4+ T cells in the Peyer patches are controlled by the immune checkpoint mo

245 ific regulatory T cells were assessed in the Peyer patches, mesenteric lymph nodes, and spleens by us

246 and germinal centers (p < 0.01) with in the Peyer's patch were significantly decreased in comparison

247 d enteric bacteria that were detected in the Peyer's patches (4/5), mesenteric lymph nodes (4/5), spl

248 stricted: Salmonella transcribed fliC in the Peyer's Patches (PP) but not in the mesenteric lymph nod

249 detected mucosal-resident commensals in the Peyer's patches (PPs), triggered IL-6 and IL-23p19 expre

250 of CD11c(+) CD11b(+) dendritic cells in the Peyer's patches after oral immunization.

251 with accumulation of TFH-cells mainly in the Peyer's patches and FRT.

252 hips revealed a complex host response in the Peyer's patches and mesenteric lymph nodes after oral in

253 elper 2 cytokine IL-10 was suppressed in the Peyer's patches and mesenteric lymph nodes and IL-4 mRNA

254 ulted in their preferential expansion in the Peyer's patches and mesenteric lymph nodes and subsequen

255 (+) CD25(+) IL-10(+) cell populations in the Peyer's patches and mesenteric lymph nodes, while 6'-sia

256 . pylori-infected wild-type (WT) mice in the Peyer's patches and mesenteric lymph nodes.

257 CD8+ T cells and activated the cells in the Peyer's patches and pancreatic lymph nodes, together wit

258 s was dependent on the bacterial load in the Peyer's patches for mice infected with WT, dam mutant, o

259 ived follicular dendritic cells (FDC) in the Peyer's patches in the small intestine is essential for

260 rus-specific CD8 T cells was observed in the Peyer's patches of orally infected mice and in the lungs

261 ratuberculosis interacts with M cells in the Peyer's patches of the small intestine.

262 ology and greater numbers of bacteria in the Peyer's patches than NL --> NL chimeras.

263 t AIEC is causing a primary infection in the Peyer's patches that is necessary for the initiation or

264 Moreover, a bacterial load threshold in the Peyer's patches was necessary to stimulate the host gene

265 IL-5-secreting T cells were decreased in the Peyer's patches, mesenteric lymph nodes, and intestinal

266 and for persistence of the bacterium in the Peyer's patches, mesenteric lymph nodes, and spleen, sug

267 rce of de novo TGF-beta transcription in the Peyer's patches, mesenteric lymph nodes, and spleen.

268 the number of activated B lymphocytes in the Peyer's patches.

269 ly events of the infection that occur in the Peyer's patches.

270 atory and helper cell differentiation in the Peyer's patches.

271 rne pathogen that preferentially infects the Peyer's patches and mesenteric lymph nodes, causing an a

272 filtration of alloactivated T cells into the Peyer's patches and small bowels, coupled with increased

273 tion of mice induces rapid disruption of the Peyer's patches but not of other secondary lymphoid orga

274 ne resulted in defective colonization of the Peyer's patches of the terminal ileum but normal coloniz

275 ted in the subepithelial dome regions of the Peyer's patches, and mice deficient in the receptor for

276 the colonization of the cecum but not of the Peyer's patches, mesenteric lymph nodes, and spleen.

277 accumulation in the GALT, in particular the Peyer's patches, is obligatory for the efficient transmi

278 he small intestinal lumen and reinfected the Peyer's patches.

279 y IFN-alpha blocks B-cell trafficking to the Peyer's patches by downregulating expression of the homi

280 lling Y. enterocolitica infection within the Peyer's patches and mesenteric lymph nodes of mice.

281 ng into the gut-associated lymphoid tissues, Peyer's patches, and thus reduced the systemic autoantib

282 ) cells exhibited increased firm adhesion to Peyer patch venules but reduced homing to the gut.

283 y activated alpha4beta7 enhanced adhesion to Peyer's patch venules, but suppressed lymphocyte homing

284 Homing of B cells to Peyer's patches was partially rescued by expression of h

285 l adhesion molecule-1 and enhanced homing to Peyer's patches (PP).

286 icient B cells revealed diminished homing to Peyer's patches and splenic white pulp cords.

287 verexpression abolishes lymphocyte homing to Peyer's patches, much like beta7 deficiency does.

288 y inhibited CXCR5-dependent B cell homing to Peyer's patches.

289 Immunostaining confirmed delivery of F.IX to Peyer's patches in the ileum.

290 contrast, S1P1-/- T cells homed normally to Peyer patches (PPs), whereas S1P1-/- B cells had a marke

291 ls migrate to the periphery, particularly to Peyer's patches and small intestine lamina propria, wher

292 ns presumably invade the small intestine via Peyer's patches to initiate dissemination.

293 nd were able to translocate, most likely via Peyer's patches and mesenteric lymph nodes, to the inter

294 Whereas Peyer's patch germinal center B cells developed at norma

295 s well as Microfold cells and T-cells within Peyer's patches.

296 orally administered prions toward FDC within Peyer's patches in order to establish host infection.IMP

297 yed orally acquired prions toward FDC within Peyer's patches was not known.

298 t how high endothelial venules (HEVs) within Peyer's patches (PPs) are patterned to display dominantl

299 ntly, a pDC population was identified within Peyer patches (PPs) of the gut that is distinguished by

300 tion the early accumulation of prions within Peyer's patches was reduced and survival times significa