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1 from the spleen, mesenteric lymph node, and Peyer's patch.
2 nt revealed pronounced mutant persistence in Peyer's patches.
3 oduction of Yersinia enterocolitica in mouse Peyer's patches.
4 es (ILFs), but not embryonically 'imprinted' Peyer's patches.
5 nt and normal lymph-node genesis, except for Peyer's patches.
6 cture of the germinal centers in the LNs and Peyer's patches.
7 mma interferon(-) CD107a/b(+) CD8 T cells in Peyer's patches.
8 ganogenesis but normal splenic structure and Peyer's patches.
9 ronic region in germinal center B cells from Peyer's patches.
10 in has an important role in the formation of Peyer's patches.
11 t tissues, in particular small intestine and Peyer's patches.
12 ileum but did not inhibit basal NF-kappaB in Peyer's patches.
13 rn of polarization that was also observed in Peyer's patches.
14 had increased levels of IgA in both sera and Peyer's patches.
15 in these organs in mouse mutants that lacked Peyer's patches.
16 inguinal nodes were absent and there were no Peyer's patches.
17 c immune functions in the lamina propria and Peyer's patches.
18 igated small bowel loops without M cells and Peyer's patches.
19 llicle-associated epithelium (FAE) region of Peyer's patches.
20 estine, resulting in impaired development of Peyer's patches.
21 opically in intestinal lamina propria around Peyer's patches.
22 the number of activated B lymphocytes in the Peyer's patches.
23 ells initiate development of lymph nodes and Peyer's patches.
24 ral lymph nodes, mesenteric lymph nodes, and Peyer's patches.
25 y inhibited CXCR5-dependent B cell homing to Peyer's patches.
26 tropism is mediated by dendritic cells from Peyer's patches.
27 ly events of the infection that occur in the Peyer's patches.
28 ed with early development of lymph nodes and Peyer's patches.
29 re deposited in the spleen, lymph nodes, and Peyer's patches.
30 ix structures within the dome regions of the Peyer's patches.
31 rotection against entry of reovirus T1L into Peyer's patches.
32 DC recruitment to the dome regions of mouse Peyer's patches.
33 gh IL-21 producing Tfh cells present only in Peyer's Patches.
34 hes, but also in germinal centers within the Peyer's patches.
35 diator of the development of lymph nodes and Peyer's patches.
36 irements for B cell entry to lymph nodes and Peyer's patches.
37 n exclusively within epithelial cells in the Peyer's patches.
38 ropagation of prions from the gut lumen into Peyer's patches.
39 prevents egress of IgA-secreting cells from Peyer's patches.
40 atory and helper cell differentiation in the Peyer's patches.
41 ost completely suppressed it, even restoring Peyer's patches.
42 neous LNs) or the gut (mesenteric LNs) or in Peyer's patches.
43 iver inflammation, splenomegaly, and loss of Peyer's patches.
44 ry lymphoid tissues, such as lymph nodes and Peyer's patches.
45 the follicle-associated epithelium (FAE) of Peyer's patches.
46 ation was rescued in spleen, lymph node, and Peyer's patches.
47 s well as Microfold cells and T-cells within Peyer's patches.
48 nto the IgA repertoire upon recirculation in Peyer's patches.
49 lymphocytes in the interfollicular areas of Peyer's patches.
50 they induce the formation of lymph nodes and Peyer's patches.
51 follicular dendritic cells within intestinal Peyer's patches.
52 he small intestinal lumen and reinfected the Peyer's patches.
53 ges and in the bone marrow, lymph nodes, and Peyer's patches.
54 ronic region in germinal center B cells from Peyer's patches.
56 d enteric bacteria that were detected in the Peyer's patches (4/5), mesenteric lymph nodes (4/5), spl
57 host, S Typhimurium preferentially colonizes Peyer's patches, a lymphoid organ in which microfold cel
58 ity before aggregation into the primordia of Peyer's patches, a major component of the gut-associated
59 ly mice, which are devoid of lymph nodes and Peyer's patches, acutely rejected fully allogeneic skin
61 low cytometry studies with DCs isolated from Peyer's patches after TCI suggested that activated DCs c
62 ecretory IgA is sufficient for protection of Peyer's patches against oral reovirus challenge and, if
63 ves the induction of alpha4beta7 and CCR9 by Peyer's patch and mesenteric lymph node (MLN) dendritic
64 from bovine gut-associated lymphoid tissues (Peyer's patch and mesenteric lymph node cells) as a sour
65 ells that reside in the epithelium overlying Peyer's patch and nasopharyngeal associated lymphoid tis
66 equal abilities to cross the mucosa in both Peyer's patch and non-Peyer's patch segments of normal m
67 ative suppression at 2 days postburn in both Peyer's patch and splenic cells and a significant suppre
68 uction were suppressed substantially in both Peyer's patch and splenic T cells 3 days after either th
70 m treatment reduced the number of B cells in Peyer's patches and downmodulated adaptive immune respon
72 rmation of robust germinal center B cells in Peyer's patches and had restored B-1-cell and ILC2 funct
73 members of this pathway lack lymph nodes and Peyer's patches and have abnormal spleen architecture.
75 that 19(+)45R(lo) cells are also present in Peyer's patches and in the spleen throughout the life sp
77 acteria induced germinal center reactions in Peyer's patches and led to the production of intestinal
79 C17orf99(-/-) mice have smaller and fewer Peyer's patches and lower numbers of IgA-secreting cells
80 hips revealed a complex host response in the Peyer's patches and mesenteric lymph nodes after oral in
81 elper 2 cytokine IL-10 was suppressed in the Peyer's patches and mesenteric lymph nodes and IL-4 mRNA
82 inoculation blocked PrP(Sc) accumulation in Peyer's patches and mesenteric lymph nodes and prevented
83 ulted in their preferential expansion in the Peyer's patches and mesenteric lymph nodes and subsequen
84 IgA antibodies (IgA MAbs) produced from the Peyer's patches and mesenteric lymph nodes of BALB/c mic
86 activated B, but not T, lymphocytes in both Peyer's patches and mesenteric lymph nodes of rotavirus-
87 e CR including arteritis and fibrosis in the Peyer's patches and mesenteric lymph nodes was found in
89 lpha-deficient (LTalpha(-/-)) mice that lack Peyer's patches and mesenteric lymph nodes were orally i
90 rne pathogen that preferentially infects the Peyer's patches and mesenteric lymph nodes, causing an a
91 nd were able to translocate, most likely via Peyer's patches and mesenteric lymph nodes, to the inter
92 n of naive flagellin-specific CD4 T cells in Peyer's patches and mesenteric lymph nodes, which was ac
93 (+) CD25(+) IL-10(+) cell populations in the Peyer's patches and mesenteric lymph nodes, while 6'-sia
95 with the intestinal mucosa by crossing both Peyer's patches and non-Peyer's patch areas but does not
98 liferative plasmablasts that originated from Peyer's patches and produced IgAs reactive to commensal
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
102 nding of these bacteria to M cells overlying Peyer's patches and subsequent entry into lymphoid tissu
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
107 es showed that cya and crp mutants colonized Peyer's patches and, to a lesser extent, mesenteric lymp
108 both the mucosal (mesenteric lymph node and Peyer's patch) and systemic (spleen) tissues of TLR4-mut
109 cum, heart, kidney, liver, lung, spleen, and Peyer's patches) and were elevated most significantly in
110 nd, the mice that are born lack lymph nodes, Peyer's patches, and an organized splenic microarchitect
115 ted in the subepithelial dome regions of the Peyer's patches, and mice deficient in the receptor for
116 d organs (SLOs) include lymph nodes, spleen, Peyer's patches, and mucosal tissues such as the nasal-a
118 levels, B cell diversification in the ileal Peyer's patches, and specific activity (ELISA activity p
119 required for lymphocyte egress from LNs and Peyer's patches, and suggest a role for S1P in lymphatic
120 mphoid organs (SLOs), including lymph nodes, Peyer's patches, and the spleen, have evolved to bring c
121 ptosis compared to wild-type thymus, spleen, Peyer's patches, and the white matter of the brain.
122 ng into the gut-associated lymphoid tissues, Peyer's patches, and thus reduced the systemic autoantib
123 of the normal architecture of the spleen and Peyer's patches; and abnormal trafficking of immunoglobu
128 osa by crossing both Peyer's patches and non-Peyer's patch areas but does not translocate or dissemin
129 , in the mesenteric lymph nodes, spleen, and Peyer's patches at 14 weeks, and in the tongue 20 weeks
130 ition, the hypermutated JH2 to JH4 region in Peyer's patch B cells showed no effects as a result of M
131 6-deficient mice had a reduced proportion of Peyer's patch B lymphocytes and an associated re-duction
133 ion alone suppressed T-cell proliferation in Peyer's patch but not in splenic T cells at 2 days postb
135 tion of mice induces rapid disruption of the Peyer's patches but not of other secondary lymphoid orga
136 epithelium (FAE) and microfold (M) cells of Peyer's patches, but also in germinal centers within the
137 sion occurred within hours of starting PN in Peyer's patches, but not mesenteric lymph nodes or the i
138 all intestine, both viruses were detected in Peyer's patches, but only the wild-type virus reached th
139 y IFN-alpha blocks B-cell trafficking to the Peyer's patches by downregulating expression of the homi
141 d from the LT-dependent formation of ILF and Peyer's patches by not requiring the presence of an inta
143 ceptors for CCL9, CCR1, was expressed by the Peyer's patch CD11b(+) DCs and in a chemotaxis assay, CD
144 An earlier onset of T-cell suppression in Peyer's patch cells than in the spleen with burn could b
145 requencies of SHM in Igh variable regions in Peyer's patch cells, and of double-strand breaks in the
146 ant have greatly reduced inflammation in the Peyer's patches compared to those infected with wild-typ
147 ion with elevated IL-12 p40 mRNA expression, Peyer's patch DC instead preferentially displayed increa
149 s and effector activity in T cells, but only Peyer's patch dendritic cells induced high levels of alp
150 at Gfra3-deficiency results in impairment of Peyer's patch development, suggesting that the signallin
152 , Flt3L significantly contributes to ILC and Peyer's patches development by targeting lymphoid progen
153 asopharyngeal associated lymphoid tissue and Peyer's patch epithelium, they showed an abnormal morpho
154 and lymphoid/monocytic cells in tonsils and Peyer's patches (explaining viremia), extending previous
155 and lymphoid/monocytic cells in tonsils and Peyer's patches (explaining viremia), thereby supplement
156 cordingly, CD4(+) T cells within the LNs and Peyer's patches failed to express the T(FH) key transcri
158 iated lymphatic tissue, including intestinal Peyer's patches, followed by extensive infection of lymp
159 olecule-1 (MAdCAM-1) and T cell responses in Peyer's patches following stimulation of the immune syst
160 s was dependent on the bacterial load in the Peyer's patches for mice infected with WT, dam mutant, o
163 STAT6-deficient macrophages and parasitized Peyer's patches from mice orally challenged with strain
165 ow that mice lacking spleen, lymph nodes and Peyer's patches generate unexpectedly robust primary B-
168 (+) cells resulted in a reduced frequency of Peyer's Patches IgG1 and germinal center B cells in addi
169 orally administered prions toward FDC within Peyer's patches in order to establish host infection.IMP
170 and yopH mutants colonize the intestines and Peyer's patches in single-strain infections but fail to
171 polyclonal and related to GFP(-)Tfh cells of Peyer's Patches in TCR repertoire composition and overal
172 ating a role for IFN-gamma-producing DC from Peyer's patches in the development of Ag-specific IEL po
174 ived follicular dendritic cells (FDC) in the Peyer's patches in the small intestine is essential for
175 roA(-)) to such secondary lymphoid organs as Peyer's patches in the small intestine, elicited marked
177 ndary lymphoid organs, not in bone marrow or Peyer's patches, in contrast to the case for many mammal
178 transcription factor RORgammat-dependent but Peyer's patch-independent somatic mutations drive the di
179 on of anti-sigma1 IgA and IgG MAbs prevented Peyer's patch infection in adult mice, but other MAbs di
183 half of all Cgamma transcripts in the ileal Peyer's patches (IPPs) and mesenteric lymph nodes but on
185 accumulation in the GALT, in particular the Peyer's patches, is obligatory for the efficient transmi
186 e control Ab (IsoAb) for 5 days, followed by Peyer's patches, lamina propria, and intraepithelial lym
188 utrophil-dominated innate immune response in Peyer's patches, limited dendritic cell migration to mes
189 appearance of PrP(RES) in the brain, spleen, Peyer's patches, lymph nodes, pancreatic islets of Lange
192 i cell-mediated activation of lymph node and Peyer's patch mesenchyma forms the necessary platform fo
193 IL-5-secreting T cells were decreased in the Peyer's patches, mesenteric lymph nodes, and intestinal
194 and for persistence of the bacterium in the Peyer's patches, mesenteric lymph nodes, and spleen, sug
195 rce of de novo TGF-beta transcription in the Peyer's patches, mesenteric lymph nodes, and spleen.
196 the colonization of the cecum but not of the Peyer's patches, mesenteric lymph nodes, and spleen.
197 lpha-deficient mice lack all lymph nodes and Peyer's patches, mice deficient in LT beta retain mesent
199 , including the M cells, and on cells within Peyer's patches, most likely within germinal centers.
201 into the subepithelial dome (SED) region of Peyer's patch mucosa, an area rich in dendritic cells (D
203 pe 1 Lang (T1L) adhered to rabbit M cells in Peyer's patch mucosal explants and to tissue sections in
205 but more environmentally regulated, such as Peyer's patches, nasal-associated lymphoid tissue, bronc
206 topoiesis and, with the exception of reduced Peyer's patches, normal architecture and cellularity of
208 number in the subepithelial dome regions of Peyer's patches of both wild type and CCR6 -/- mice.
209 higher expression of Gal-1 in the spleen and Peyer's patches of mice infected orogastrically with Y.
211 rus-specific CD8 T cells was observed in the Peyer's patches of orally infected mice and in the lungs
213 with rotavirus, the donor cells derived from Peyer's patches of orally infected mice were more effici
214 from the spleen, mesenteric lymph nodes, and Peyer's patches of orally tolerized mice showed increase
219 d in decreased colonization of the cecum and Peyer's patches of the terminal ileum and colonization t
220 ne resulted in defective colonization of the Peyer's patches of the terminal ileum but normal coloniz
221 culation; E. coli infection had no effect on Peyer's patch or splenic T cells at 1 day postinjury.
222 xpressed on virus-specific CD8(+) T cells in Peyer's patches or lymph nodes and spleens were examined
225 8-expressing T cells by dendritic cells from Peyer's patches, peripheral lymph nodes and spleen induc
226 ed to differences in vaccine colonization of Peyer's patch (PP) and spleen or in their respective tis
228 explore the requirement for M cells and the Peyer's patch (PP) in induction of oral tolerance and ad
230 (LTi) cells are required for lymph node and Peyer's patch (PP) organogenesis, but where these specia
231 colitis, significantly increased numbers of Peyer's patch (PP) phenotype M cells were induced at the
232 immune arthritis model, we demonstrated that Peyer's patch (PP) Tfh cells were essential for gut comm
233 alpha(4)beta(7), helps target lymphocytes to Peyer's patches (PP) and intestinal lamina propria (ILP)
234 tivated CD4+ T cells recruited to intestinal Peyer's patches (PP) and lamina propria (LP) up-regulate
236 une responses to enteric Ag are initiated in Peyer's patches (PP) and mesenteric lymph nodes (MLN) fo
237 e specialized epithelial cells situated over Peyer's patches (PP) and other organized mucosal lymphoi
238 role for CXCL13 (BLC) in the development of Peyer's patches (PP) and some peripheral lymph nodes (LN
240 stricted: Salmonella transcribed fliC in the Peyer's Patches (PP) but not in the mesenteric lymph nod
241 an additional lymphoid structure resembling Peyer's patches (PP) in composition and architecture has
242 L-specific precursor CTL and effector CTL in Peyer's patches (PP) of reovirus 1/L-inoculated mice.
244 we found that entry of commensal bacteria in Peyer's patches (PP) via the M cell pathway was mediated
246 n agent-based simulation of the formation of Peyer's patches (PP), gut-associated lymphoid organs tha
249 is a double-stranded RNA virus that infects Peyer's patches (PPs) after peroral inoculation of mice.
250 vade the intestinal lymphoid tissue known as Peyer's patches (PPs) and disrupt the integrity of the i
251 izing and inducing inflammatory responses in Peyer's patches (PPs) and mesenteric lymph nodes (MLNs).
252 Lymphotoxin alpha knockout mice lacking Peyer's patches (PPs) and pretreated orally with CpG DNA
254 t how high endothelial venules (HEVs) within Peyer's patches (PPs) are patterned to display dominantl
256 demonstrate that a specialized DC subset in Peyer's patches (PPs) mediates the rapid activation of p
260 ocyte recruitment, and cellular apoptosis in Peyer's patches (PPs), mesenteric lymph node (MLN), and
263 ulted in reduced numbers of B and T cells in Peyer's patches, reduced numbers of intraepithelial CD8a
265 d a marked increase in mutation frequency in Peyer's patches, revealing a pattern that was similar to
267 ells as well as germinal center B cells from Peyer's patches showed marked increases in apoptosis and
269 articles utilize epithelial M cells to enter Peyer's patches, small areas of the intestine concentrat
271 Strikingly, the mice lacked lymph nodes, Peyer's patches, splenic marginal zones, and follicular
273 e show normal architecture of the spleen and Peyer's patches, suggesting that TNF is not essential fo
275 t AIEC is causing a primary infection in the Peyer's patches that is necessary for the initiation or
276 pression of several classes of host genes in Peyer's patches, the liver, and the spleen following ora
277 or, E-cadherin, whereas translocation across Peyer's patches through M-cells is InlA-independent.
278 ranging from the developmentally determined Peyer's patches to the inflammatory derived tertiary lym
280 id tissues, cervical lymph nodes, lungs, and Peyer's patches using an enzyme-linked immunospot assay.
281 y activated alpha4beta7 enhanced adhesion to Peyer's patch venules, but suppressed lymphocyte homing
282 Moreover, a bacterial load threshold in the Peyer's patches was necessary to stimulate the host gene
284 e gastrointestinal tract, the involvement of Peyer's patches was not observed in either infection.
286 Surprisingly, we found that NALT, unlike Peyer's patch, was formed independently of lymphotoxin (
288 and germinal centers (p < 0.01) with in the Peyer's patch were significantly decreased in comparison
290 omorphometric analyses of ileum, jejunum and Peyer's patches were carried out, to determine the infla
292 id organs, including spleen, lymph nodes and Peyer's patches, where T cells search for antigens.
293 xhibited the highest expression in intestine Peyer's patch, whereas NK2C was expressed almost exclusi
294 on frequency at Ig loci in the spleen and in Peyer's patches, whereas knock-in mice with a mutagenic
295 -associated lymphoid tissues (GALT), such as Peyer's patches, which contain high numbers of mature M
296 ciated lymphoid tissues, such as tonsils and Peyer's patches, which is hard-wired to secrete interleu
297 elial layers in a manner similar to those in Peyer's patches, which permit enteric pathogens to invad
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
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