ライフサイエンスコーパス: lymphoid tissue

1 SAMHD1 antibodies were prevalent in tertiary lymphoid tissue.

2 marginal zone lymphoma of mucosa-associated lymphoid tissue.

3 o identify Ag-specific GC Tfh cells in human lymphoid tissue.

4 xis of inflammatory monocytes into blood and lymphoid tissue.

5 AIM also detected non-Tfh cells in lymphoid tissue.

6 rofold cells present in the nasal-associated lymphoid tissue.

7 nvolves stroma-dependent B-CLL growth within lymphoid tissue.

8 oid dendritic cells (pDCs) in both blood and lymphoid tissue.

9 s, B cells and T cells in the gut-associated lymphoid tissue.

10 and having a unique conjunctival associated lymphoid tissue.

11 , specifically, in locations associated with lymphoid tissue.

12 ) expression in trout nasopharynx-associated lymphoid tissue.

13 e peripherally, as well as reside within the lymphoid tissue.

14 om donor DCs that migrated from the graft to lymphoid tissues.

15 metastasized ovarian cancer cells within the lymphoid tissues.

16 tion by B cells, derived from gut-associated lymphoid tissues.

17 s that were present in both lymphoid and non-lymphoid tissues.

18 ation of immunomodulatory genes in secondary lymphoid tissues.

19 the blood, systemic lymph nodes, and mucosal lymphoid tissues.

20 e identified a third major NK cell subset in lymphoid tissues.

21 sponsible for the global surveillance of non-lymphoid tissues.

22 t be adequately maintained in the peripheral lymphoid tissues.

23 eflecting a redistribution of these cells to lymphoid tissues.

24 ent homing receptor switch in gut-associated lymphoid tissues.

25 by abortive HIV infection of CD4 T cells in lymphoid tissues.

26 ns of CD4(+) T cells in peripheral blood and lymphoid tissues.

27 epithelia and lung as well as gut-associated lymphoid tissues.

28 lassification of tumors of hematopoietic and lymphoid tissues.

29 he immune system and disruption of secondary lymphoid tissues.

30 followed by rapid dissemination to systemic lymphoid tissues.

31 peripheral sites to local draining secondary lymphoid tissues.

32 ron-gamma and interleukin 4 in the secondary lymphoid tissues.

33 tifies pDC as a potential viral reservoir in lymphoid tissues.

34 lood and bone marrow but not in the blood or lymphoid tissues.

35 cline in pDCs from circulation and secondary lymphoid tissues.

36 as for organogenesis of thymic and secondary lymphoid tissues.

37 for proinsulin, in the thymus and peripheral lymphoid tissues.

38 recapitulating interactions occurring within lymphoid tissues.

39 B lymphocytes in the bone marrow, blood, and lymphoid tissues.

40 trate stroma-rich solid tumors compared with lymphoid tissues.

41 of FcgammaRIIb-bearing cells with T cells in lymphoid tissues.

42 cell numbers and functions in the liver and lymphoid tissues.

43 WD) replication had expanded to all systemic lymphoid tissues.

44 lusively within B cells of mucosa-associated lymphoid tissues.

45 on IL-7 amounts in the primary and secondary lymphoid tissues.

46 n of B cells in the hematopoietic system and lymphoid tissues.

47 phocytes, including CD4(+) T cells, into gut lymphoid tissues.

48 s exposure to monitor the immune response in lymphoid tissues.

49 distribution of multiple cell populations in lymphoid tissues.

50 roduction within pathologically inflamed non-lymphoid tissues.

51 Herein, we found that mucosa-associated lymphoid tissue 1 (MALT1) is involved in EGFR-induced NF

52 ZIKV infection caused a significant lymphoid tissue activation but limited induction of ZIKV

53 he generation of antibody responses in local lymphoid tissues along the respiratory system in vaccina

54 Lymphoid tissues also express the immunoproteasome subun

55 which deliver antigen to mucosal-associated lymphoid tissue and aim to elicit protective CTL-mediate

56 rast, in the absence of recipient peripheral lymphoid tissue and CD4 T cells, CD8-mediated in vivo al

57 ncluding vaccine-induced bronchus-associated lymphoid tissue and CD8(+) effector memory T cells.

58 , induction of inducible bronchus-associated lymphoid tissue and correlates of bacterial killing, red

59 The frequencies of Th1 cells in regional lymphoid tissue and graft-infiltrating immune cells were

60 tional avidity maturation is orchestrated in lymphoid tissue and how low-affinity cells contribute to

61 cells from peripheral blood, gut-associated lymphoid tissue and lymph node tissue specimens from 8 s

62 A small population of B cells exists in lymphoid tissues and body cavities of mice that is disti

63 cART reduced the size of HIV-1 reservoirs in lymphoid tissues and delayed HIV-1 rebound after cART ce

64 itic cells (DCs), which migrate to recipient lymphoid tissues and directly activate alloreactive T ce

65 effector T cells seeds the lymphoid and non-lymphoid tissues and gives rise to tissue-resident memor

66 oimmunity with reduced Foxp3(+) cells in non-lymphoid tissues and impaired resolution of experimental

67 otic-treated mice, LRCs colonized intestinal lymphoid tissues and induced multiple members of the IL-

68 that only a small number of donor DCs reach lymphoid tissues and investigated how this limited popul

69 the gastrointestinal and respiratory tract, lymphoid tissues and reproductive organs of viremic monk

70 s CD8(+) T-cell population was found only in lymphoid tissues and resided predominantly in the T-cell

71 ls (including Th follicular functionality in lymphoid tissues and Th2 responses in bronchoalveolar la

72 ssification of tumours of haematopoietic and lymphoid tissues and the International Classification of

73 IL-1beta and its actions during EAE, in both lymphoid tissues and within the CNS.

74 raft, E-selectin mediates APC trafficking to lymphoid tissue, and blockade of E-selectin has a modest

75 irculating autoantibodies, lung perivascular lymphoid tissue, and elevated cytokines have been relate

76 ology in the spleen, liver, nasal-associated lymphoid tissue, and olfactory mucosa (OM).

77 tly outnumber recirculating cells within non-lymphoid tissues, and memory subset homing to inflammati

78 romote cell-mediated transport of antigen to lymphoid tissues, and promote antigen retention in LNs.

79 es that bind to CD8(+) T cells in the blood, lymphoid tissues, and tumors of mice.

80 The structured lymphoid tissues are considered the only inductive sites

81 nflammation, structures that mimic secondary lymphoid tissues are observed, suggesting that chronic i

82 esiding in B-cell follicles within secondary lymphoid tissues, are readily infected by AIDS viruses a

83 CWD pathogenesis have implicated pharyngeal lymphoid tissue as the earliest sites of prion accumulat

84 cells were defined and identified in macaque lymphoid tissues as non-T, non-B (lineage-negative), c-K

85 rostate, breast, colon, kidney, thyroid, and lymphoid tissues as well as NETs as reference.

86 ated lymphoid clusters (FALCs) are a type of lymphoid tissue associated with visceral fat.

87 ly promotes the presence of anti-FMDV ASC in lymphoid tissues associated with the respiratory system.

88 follicular immunoreactivity in oropharyngeal lymphoid tissues at 1 and 2 months postexposure (MPE).

89 ut mice, SVNI replicated more efficiently in lymphoid tissues at early times postinfection and induce

90 ut mice, SVNI replicated more efficiently in lymphoid tissues at early times postinfection and induce

91 n lesions that resembled bronchus-associated lymphoid tissue (BALT).

92 emonstrate reduced accumulation in secondary lymphoid tissue because of low levels of proliferation 4

93 om the donor's oral wash and the recipient's lymphoid tissue biopsy had identical latent membrane pro

94 lation in the peripheral blood and secondary lymphoid tissues, bone marrow plasma cells remain a prim

95 hanistic link between acute HIV-1 infection, lymphoid tissue breakdown, and persistent immune dysfunc

96 in healthy lung and lung lesions and in the lymphoid tissues bronchial lymph node, retropharyngeal l

97 ersistence occurs in the germinal centers of lymphoid tissue but that the duration of persistence is

98 dendritic cell (DC) homeostasis in secondary lymphoid tissues but necessary to regulate cellular meta

99 cells are known to reside in peripheral non-lymphoid tissue, but how their presence within solid org

100 ily infects CD11b(+) DCs in non-lymphoid and lymphoid tissues, but spares the main cross-presenting C

101 ucosa itself, despite the lack of structured lymphoid tissues, can act as an inductive site during pr

102 nd resting CD4 T cells and in gut-associated lymphoid tissue, CD4 T-cell-associated HIV RNA, replicat

103 of our assumption that the migration rate of lymphoid tissue cells into the gut remains constant thro

104 Thus, HIV replication in lymphoid tissue, clonal expansion of infected cells, and

105 Starting with cell encapsulation in digested lymphoid tissues, clusters of proliferating B cells with

106 ture antigen-presenting cells trafficking to lymphoid tissue compared with control (6.96 +/- 0.9 vs 1

107 D20(+) B lymphocytes in peripheral blood and lymphoid tissues confirming that SGN-CD19B is pharmacody

108 idence suggest that homing of tumor cells to lymphoid tissue contributes to disease progression in ch

109 ynamics with pathological immune activation, lymphoid tissue damage progressing to significant immuno

110 sing a loss of CD4(+) T cell homeostasis and lymphoid tissue damage that lead to AIDS in HIV-1 and SI

111 ls developed pathological immune activation; lymphoid tissue damage, including fibrosis; and clinical

112 al fluorescence microscopy of thin-sectioned lymphoid tissues demonstrated strong preferential locali

113 these mice nor was the formation of enteric lymphoid tissue, demonstrating that the onset of RA sign

114 Migratory non-lymphoid tissue dendritic cells (NLT-DCs) transport anti

115 Rorc(fm+)) ILCs show a clear ILC3 phenotype, lymphoid tissue-derived Rorc(fm+) ILCs acquire an natura

116 the interface between circulating blood and lymphoid tissue, detect and respond to blood-borne antig

117 ls out of lymphoid organs and subsequent non-lymphoid tissue distribution but also their phenotypic d

118 Ls), including DLBCLs with mucosa-associated lymphoid tissue (DLBCL[MALT]) and without ("pure" DLBCL)

119 while FMDV-specific ASC were detected in all lymphoid tissues draining the respiratory tract, mostly

120 ponses is regulated by environmental cues in lymphoid tissues draining the site of infection.

121 (+) T cells in B cell follicles of secondary lymphoid tissues during asymptomatic disease.

122 imately foster the establishment of tertiary lymphoid tissues during chronic neuroinflammatory condit

123 Despite their absence in secondary lymphoid tissues during homeostasis, gammadeltaT17 cells

124 V infection both in the peripheral blood and lymphoid tissues, especially in the setting of persistin

125 contributes little to HIV infection of human lymphoid tissue ex vivo.

126 ry gp120, decreases viral infection of human lymphoid tissue ex vivo.

127 secondary lymphoid organs, Treg cells in non-lymphoid tissues exhibit an activated Treg (aTreg) cell

128 d the increased APC recruitment to secondary lymphoid tissues expand the scope of known adjuvant effe

129 s present evidence that stromal cells within lymphoid tissue express the Notch ligands Delta-like 1/4

130 on amplification occurs in the oropharyngeal lymphoid tissues followed by rapid dissemination to syst

131 antigen-specific T cell response within key lymphoid tissues following influenza virus infection in

132 ds that partially mimic the B-cell zone of a lymphoid tissue, for efficient and rapid generation of B

133 RANK) ligand (RANKL) plays a pivotal role in lymphoid tissue formation and bone homeostasis.

134 ed, suggesting that chronic inflammation and lymphoid tissue formation share common activation progra

135 phocyte accumulation and bronchus-associated lymphoid tissue formation.

136 protein (PrP(Sc)) was detected in brain and lymphoid tissues from intracranially and orally inoculat

137 a new perspective on DCs as facilitators of lymphoid tissue function.

138 indication of short-lived ASCs in the local lymphoid tissue, further evidence of a TI-2 response to

139 examined lymph node (LN) and gut-associated lymphoid tissue (GALT) biopsies from fully suppressed su

140 show that p38alpha regulates gut-associated lymphoid tissue (GALT) formation in a noncell-autonomous

141 of some prion diseases in the gut-associated lymphoid tissues (GALT) is important for efficient sprea

142 dendritic cells (FDC) within gut-associated lymphoid tissues (GALT) is important for the efficient s

143 (Rag-gammac(-/-)), which lack gut-associated lymphoid tissues (GALT), such as Peyer's patches, and ma

144 e we show that the absence of gut-associated lymphoid tissues (GALT), such as Peyer's patches, which

145 ith immune cell activation in gut-associated lymphoid tissues (GALTs) and significant changes in the

146 ation in intestine and in the gut-associated lymphoid tissues (GALTs).

147 and a site of viral replication, similar to lymphoid tissue, gut-associated lymphoid tissue or semen

148 The studies also revealed that the local lymphoid tissue had detectable FMDV-specific ASCs in the

149 By 4 MPE, the PrP(CWD) burden in all lymphoid tissues had increased and approached levels obs

150 reas, the diabetogenic insulitis lesion, and lymphoid tissues have revealed a broad repertoire of tar

151 In mice, DCs expressing CD8alpha(+) in lymphoid tissues have the capacity to cross-present extr

152 aging in mice to show that, within secondary lymphoid tissues, highly suppressive Treg cells expressi

153 pulation of PB-CLL cells that are primed for lymphoid tissue homing and interaction with T cells.

154 ha) and caused inducible bronchus-associated lymphoid tissue (iBALT) formation in the lung.

155 ount for delayed gastrointestinal-associated lymphoid tissue immune recovery.

156 responses to the formation of gut-associated lymphoid tissue in the neonatal period of life.

157 , we analyzed ILC3 from mucosal and systemic lymphoid tissues in chronically SIV-infected macaques an

158 longitudinally assess early HIV-1 spread in lymphoid tissues in humanized mice.

159 hocyte migration and compartmentalization of lymphoid tissues in mammals, diversified in salmonids le

160 translocation may result in loss of ILC3 in lymphoid tissues in SIV-infected macaques, further contr

161 s are specialized epithelial cells overlying lymphoid tissues in the small intestine.

162 (PPs) are unique compared to other secondary lymphoid tissues in their continual exposure to an enorm

163 lustrated by impaired development of enteric lymphoid tissues in vitamin A-deficient mice.

164 ssification of Tumours of Haematopoietic and Lymphoid Tissues includes new criteria for the diagnosis

165 consisting of cellular infiltration into non-lymphoid tissues, increased TNF-alpha production, and el

166 oxyvitamin D concentration in the peripheral lymphoid tissues, induced Treg cells.

167 al for the development of RORgammat(+) fetal lymphoid tissue inducer (LTi) cells and lymphoid organog

168 Fetal lymphoid tissue inducer (LTi) cells are required for lym

169 xpansion and activation of intestinal CD4(+) lymphoid tissue inducer (LTi) cells was completely abrog

170 nown to be expressed by natural killer (NK), lymphoid tissue inducer (LTi), and innate lymphoid cell

171 es form through intimate interaction between lymphoid tissue inducer and lymphoid tissue organizer (L

172 he pool of alpha4beta7(-) and alpha4beta7(+) lymphoid tissue inducer cell progenitors in the fetal li

173 nally, the percentage of cells thought to be lymphoid tissue inducer cells among donor ILCs was far h

174 ed the number of fetal liver progenitors and lymphoid tissue inducer cells in the neonatal intestine,

175 plantation and support the notion that human lymphoid tissue inducer cells may form in the fetus and

176 The dependence of lymphoid tissue inducer cells on vitamin A was furthermo

177 However, lymphoid tissue inducer cells were not affected in these

178 lated orphan receptor gammat is expressed on lymphoid tissue inducer cells.

179 n the NCR(-) ILC3 subset, which contains the lymphoid tissue inducer cells.

180 s with conventional natural killer cells and lymphoid tissue inducer cells.

181 utively high IL-22 expression was limited to lymphoid-tissue inducer (LTi) cells residing in lymph no

182 hip between innate lymphoid cells (ILCs) and lymphoid tissue-inducer (LTi) cells is poorly understood

183 t, it negatively regulated genes specific to lymphoid tissue-inducer (LTi) or LTi-like ILC3 cells.

184 nnate sources of IL-22 and IL-17 and include lymphoid tissue-inducer (LTi)-like and NKp46(+) subsets.

185 ant development of ILCs, including ILC2s and lymphoid-tissue-inducer-like cells.

186 uding the conventional natural killer cells, lymphoid tissue inducers, type 1, 2, and 3 with signific

187 mobilization of neoplastic B cells from the lymphoid tissues into the blood, which makes them potent

188 Lymphoid tissue is a key reservoir established by HIV-1

189 However, lymphoid tissue is rarely available from immunized human

190 to test whether diversity of virulent FIV in lymphoid tissues is altered in the presence of PLV.

191 arly but not late postinfection in secondary lymphoid tissues is more efficacious in controlling the

192 SPAG6 is expressed in primary and secondary lymphoid tissues, is associated with the centrosome in l

193 tion results in impairment of gut-associated lymphoid tissue leading to systemic immune activation.

194 Altered microenvironmental conditions in lymphoid tissues leading to altered Tfh cell differentia

195 Dissemination of HIV-1 throughout lymphoid tissues leads to systemic virus spread followin

196 in tissues of infected nonhuman primates and lymphoid tissue (LT) biopsies from infected humans.

197 unodeficiency virus (HIV) replication causes lymphoid tissue (LT) fibrosis, which causes CD4(+) T-cel

198 Although secondary lymphoid tissues (LTs) are principal sites of human immu

199 Lymphoid tissues (LTs) are the principal sites where hum

200 analysis, but they represent <2% of cells in lymphoid tissues (LTs).

201 LL/lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma translocation gene 1 (MALT1) to

202 LL/lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1)

203 large B-cell lymphoma and mucosa-associated lymphoid tissue lymphoma, being associated with poor pro

204 mong cases of conjunctival mucosa-associated lymphoid tissue lymphoma, human herpes virus (HHV)-6, HH

205 ll lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (MALT1).

206 rated superior efficacy in mucosa-associated lymphoid tissue lymphoma; however, improvements in EFS a

207 ere the most frequent, and mucosa-associated lymphoid tissue lymphomas (5.8%).

208 products that are secreted and accumulate in lymphoid tissues, mainly within lymph node germinal cent

209 Z) B-cell lymphomas of the mucosa-associated lymphoid tissue (MALT) arise from lymphoid populations t

210 ciated epithelial defects, mucosa-associated lymphoid tissue (MALT) hyperplasia, and dysplasia.

211 ile primary ocular adnexal mucosa-associated lymphoid tissue (MALT) lymphoma (POAML) is the most comm

212 sly received rituximab for mucosa-associated lymphoid tissue (MALT) lymphoma and steroids for prolong

213 mmunohistochemistry showed mucosa-associated lymphoid tissue (MALT) lymphoma with immunoglobulin kapp

214 frequent translocation in mucosa-associated lymphoid tissue (MALT) lymphoma.

215 e best OS in patients with mucosa-associated lymphoid tissue (MALT) lymphomas (HR = 0.26, 95%CI: 0.11

216 igens to interact with the mucosa-associated lymphoid tissue (MALT) to induce both mucosal and system

217 marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT).

218 dritic cells (DCs) in the mucosal-associated lymphoid tissue (MALT).

219 marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT).

220 lymphocytes also establish residency in non-lymphoid tissues, most prominently at barrier sites, inc

221 s a robust Th17 response in nasal-associated lymphoid tissue (NALT).

222 nasal passage to the nasal mucosa-associated lymphoid tissue (NALT).

223 nvestigated the role of the nasal-associated lymphoid tissues (NALTs), which are mucosal-associated l

224 c stem cell transplantation, CD69(+)CXCR6(+) lymphoid tissue NK cells do not exhibit the hyperexpansi

225 CD69(+)CXCR6(+) lymphoid tissue NK cells have an intermediate expression

226 tibodies predominantly occurring in systemic lymphoid tissues, not PPs.

227 erms has evolved organized secondary mucosal lymphoid tissues (O-MALT) such as Peyer's patches, tonsi

228 uence immune responses in the gut-associated lymphoid tissue of a neonate.

229 gD CSR also was detected in nasal-associated lymphoid tissue of WT mice.

230 ed by PrP(CWD) accumulation in the brain and lymphoid tissues of affected animals.

231 mensal bacteria can reside within intestinal lymphoid tissues of healthy mammals.

232 +)CCR7(-) "follicular" T regulatory cells in lymphoid tissues of healthy rhesus macaques, and we stud

233 The amount of PrP(Sc) in the brains and lymphoid tissues of positive pigs was small, especially

234 The lymphoid tissues of the gut are specialized for the indu

235 5 dpi and viral genomes for up to 400 dpi in lymphoid tissues of the head and neck, focused mainly in

236 , similar to lymphoid tissue, gut-associated lymphoid tissue or semen.

237 eraction between lymphoid tissue inducer and lymphoid tissue organizer (LTo) cells.

238 oach now identifies a subset of murine fetal lymphoid tissue organizer cells that gives rise exclusiv

239 ion of epithelial-derived signals that drive lymphoid tissue overgrowth and malignancy.

240 espite such limited CD4 and CCR5 expression, lymphoid tissue pDC were infected to a degree similar to

241 tes such as the lung into the gut-associated lymphoid tissues, Peyer's patches, and thus reduced the

242 The nose, paranasal sinuses, and associated lymphoid tissues play important roles in homeostasis and

243 hat form the reticular networks in organized lymphoid tissues, potentially linking two areas of fibro

244 unts of soluble gp120 are found in plasma or lymphoid tissue, predominantly in the form of gp120-anti

245 on: a robust prion amplification in systemic lymphoid tissues prior to neuroinvasion and establishmen

246 VHD, whereas PD-L1 interactions with CD80 in lymphoid tissue promoted CD8+ T cell survival and expans

247 identification of this NK cell population in lymphoid tissues provides tools to further evaluate the

248 c leukemia (CLL) tumor B cells occurs within lymphoid tissue pseudofollicles, and investigating these

249 assay by using recto-anal mucosa-associated lymphoid tissue (RAMALT) biopsy specimens and nasal brus

250 -QuIC) assay of recto-anal mucosa-associated lymphoid tissue (RAMALT) biopsy specimens and nasal brus

251 on replication in the draining oropharyngeal lymphoid tissues, rapidly followed by dissemination to s

252 Increased size of the pharyngeal lymphoid tissue, rather than enlargement of the upper ai

253 CD4(+) T cells/microL, and CD4(+) T cells in lymphoid tissues remain severely depleted, due in part t

254 ion spread are generally observed: (i) early lymphoid tissue replication or (ii) direct neuroinvasion

255 atment fully suppresses viral replication in lymphoid tissue reservoirs.

256 ir functional properties, we found that only lymphoid-tissue resident Rorc(fm+) ILCs can suppress tum

257 o cross-present Ags to CD8(+) T cells, mouse lymphoid tissue-resident CD8(+) dendritic cells (DCs) an

258 Here, we demonstrate that lymphoid-tissue-resident commensal bacteria (LRC) coloni

259 Secondary lymphoid tissues share the important function of bringin

260 ctures in the gut called solitary intestinal lymphoid tissues (SILT).

261 ith rheumatoid arthritis (RA) infiltrate non-lymphoid tissue sites, maneuver through extracellular ma

262 k hematopoietic APCs requires host secondary lymphoid tissue (SLT).

263 d a progenitor population in human secondary lymphoid tissues (SLTs) that expressed the transcription

264 ng the expression of CD8alpha (traditionally lymphoid tissue specific), CD11b, and CD103 markers.

265 Secondary lymphoid tissues (spleen, ipsilateral axillary LN, and c

266 Within secondary lymphoid tissues, stromal reticular cells support lympho

267 the HIV-induced impairment of gut-associated lymphoid tissue structure and function, especially in mu

268 T follicular helper cell differentiation in lymphoid tissue, suggesting that it might drive autoimmu

269 The lymphoid tissue that drains the upper respiratory tract

270 The thymus is a primary lymphoid tissue that supports the generation of alphabet

271 ystem is the progressive organization of the lymphoid tissues that leads to increased efficiency of i

272 In lymphoid tissues, the interactions of PD-L1 with CD80 au

273 litates their rapid sequester into secondary lymphoid tissues, thereby regulating the accumulation of

274 ce regarded as merely structural features of lymphoid tissues, these cells are now appreciated as ess

275 Because they occur in the immunocyte-rich lymphoid tissues, they are easily accessible to antibodi

276 In contrast to peripheral lymphoid tissue, thymocyte number and subsets were not a

277 During chronic inflammation, tertiary lymphoid tissue (TLT) can form within an inflamed organ,

278 Tertiary lymphoid tissues (TLTs) have been observed in the mening

279 Therefore, modulating gut-associated lymphoid tissue to boost Tr1 cells may be important in t

280 F]-FDG-PET/CT imaging of immune processes in lymphoid tissues to identify patterns of inflammation in

281 corneal stroma quickly mature and migrate to lymphoid tissues to sensitize host T cells.

282 esting and thus nonpermissive CD4 T cells in lymphoid tissues triggers a lethal innate immune respons

283 cells were selected in peripheral blood and lymphoid tissues upon HIV-1 infection.

284 erences in DC subsets localized in blood and lymphoid tissues versus skin, and a striking absence of

285 ification of tumors of the hematopoietic and lymphoid tissues was last updated in 2008.

286 ferential crosstalk among genes expressed in lymphoid tissues was predicted to be orchestrated by spe

287 terestingly, CXCR5(+)PD-1(HIGH) Tfh cells in lymphoid tissues were eventually depleted in macaques wi

288 romal cell networks, a hallmark of organized lymphoid tissue, were also present.

289 Strikingly, NALTs, unlike other lymphoid tissues, were not routinely surveyed during the

290 t decreased proliferation or accumulation in lymphoid tissues when transferred to quiescent mixed chi

291 s the formation of germinal centers (GCs) in lymphoid tissues where self-reactive B cells expand and

292 uding persistent inflammation, especially in lymphoid tissues, where T follicular helper (Tfh) cells

293 o immature B cells that migrate to secondary lymphoid tissues, where they mature.

294 number of Tregs in the thymus and peripheral lymphoid tissues, whereas the number of Foxp3- effector

295 CAD and identified B cells forming tertiary lymphoid tissue with germinal centers.

296 in germinal center (GC) formation throughout lymphoid tissues with GC B cells binding insulin.

297 fector Th1 CD4 T cells in ocular lesions and lymphoid tissues, with Treg becoming predominant over th

298 associated with the development of tertiary lymphoid tissue within the human renal allograft.

299 id cells and, consequently, postnatal formed lymphoid tissues within the small intestines.

300 apidly followed by dissemination to systemic lymphoid tissues without evidence of neuroinvasion.