ライフサイエンスコーパス: Peyer's patch

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 re deposited in the spleen, lymph nodes, and Peyer's patches.

35 ix structures within the dome regions of the Peyer's patches.

36 rotection against entry of reovirus T1L into Peyer's patches.

37 DC recruitment to the dome regions of mouse Peyer's patches.

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

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

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

41 follicular dendritic cells within intestinal Peyer's patches.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 from bovine gut-associated lymphoid tissues (Peyer's patch and mesenteric lymph node cells) as a sour

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

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

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

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

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

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

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

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

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

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

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

73 acteria induced germinal center reactions in Peyer's patches and led to the production of intestinal

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

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

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

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

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

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

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

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

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

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

84 e CR including arteritis and fibrosis in the Peyer's patches and mesenteric lymph nodes was found in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 g in the spleen, mesenteric lymph nodes, and Peyer's patches and the ability to provide effector Gag-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 ition, the hypermutated JH2 to JH4 region in Peyer's patch B cells showed no effects as a result of M

126 6-deficient mice had a reduced proportion of Peyer's patch B lymphocytes and an associated re-duction

127 In Peyer's patches, B cell entry is dependent on CXCR5 in a

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

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

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

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

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

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

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

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

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

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

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

139 ant have greatly reduced inflammation in the Peyer's patches compared to those infected with wild-typ

140 ion with elevated IL-12 p40 mRNA expression, Peyer's patch DC instead preferentially displayed increa

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

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

143 s and effector activity in T cells, but only Peyer's patch dendritic cells induced high levels of alp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 on of anti-sigma1 IgA and IgG MAbs prevented Peyer's patch infection in adult mice, but other MAbs di

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

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

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

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

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

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

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

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

183 e control Ab (IsoAb) for 5 days, followed by Peyer's patches, lamina propria, and intraepithelial lym

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

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

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

187 In rodents and rabbits, Peyer's patch M cells selectively bind and endocytose se

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

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

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

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

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

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

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

195 Lymphocytes, sensitized to antigens in Peyer's patches, migrate via mesenteric lymph nodes and

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

197 into the subepithelial dome (SED) region of Peyer's patch mucosa, an area rich in dendritic cells (D

198 activity of M cells to enter and infect the Peyer's patch mucosa.

199 pe 1 Lang (T1L) adhered to rabbit M cells in Peyer's patch mucosal explants and to tissue sections in

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

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

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

203 APCs from the Peyer's patch of OVA-fed knockout animals could induce a

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

205 number in the subepithelial dome regions of Peyer's patches of both wild type and CCR6 -/- mice.

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

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

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

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

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

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

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

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

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

215 d in decreased colonization of the cecum and Peyer's patches of the terminal ileum and colonization t

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

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

218 ult mice, but the same did not hold true for Peyer's patches or spleen.

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

220 8-expressing T cells by dendritic cells from Peyer's patches, peripheral lymph nodes and spleen induc

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

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

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

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

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

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

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

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

229 tivated CD4+ T cells recruited to intestinal Peyer's patches (PP) and lamina propria (LP) up-regulate

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

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

232 role for CXCL13 (BLC) in the development of Peyer's patches (PP) and some peripheral lymph nodes (LN

233 Peyer's patches (PP) are believed to be the principal si

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

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

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

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

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

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

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

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

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

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

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

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

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

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

248 Peyer's patches (PPs) and/or mesenteric lymph nodes (MLN

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

296 elial layers in a manner similar to those in Peyer's patches, which permit enteric pathogens to invad

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

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

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

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