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 (PP) are believed to be the principal si

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 germinal center regions of mouse spleens and Peyer's patches and to the thymus medulla.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

71 uction were suppressed substantially in both Peyer's patch and splenic T cells 3 days after either th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 8-expressing T cells by dendritic cells from Peyer's patches, peripheral lymph nodes and spleen induc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 follicular dendritic cells within intestinal Peyer's patches.

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

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

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

159 on into blood but stimulated absorption into Peyer patches.

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

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

162 tight control of pathogens penetrating into Peyer patches.

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

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

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

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

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

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

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

170 Lymphocyte Peyer patch adhesion molecule (LPAM) or alpha(4)beta(7)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 epithelium (FAE) and microfold (M) cells of Peyer's patches, but also in germinal centers within the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 6-deficient mice had a reduced proportion of Peyer's patch B lymphocytes and an associated re-duction

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 Rat Peyer's patch and splenic T lymphocytes were isolated by

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 hes, but also in germinal centers within the Peyer's patches.

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

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

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

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

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

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

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

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

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

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

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

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

294 Surprisingly, we found that NALT, unlike Peyer's patch, was formed independently of lymphotoxin (

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

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

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

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

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

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

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