ライフサイエンスコーパス: lymphoid

1 an adipose tissue, the omentum also contains lymphoid aggregates, called milky spots (MSs), that cont

2 neuroinvasion without substantial antecedent lymphoid amplification.

3 an hemopoietic progenitor cells that produce lymphoid and granulocytic-monocytic (myeloid) lineages i

4 olling antiviral T cell responses in the non-lymphoid and lymphoid organs during acute and persistent

5 t EBOV primarily infects CD11b(+) DCs in non-lymphoid and lymphoid tissues, but spares the main cross

6 stem cell polarity and a restored balance of lymphoid and myeloid cells in peripheral blood.

7 ells, and at relatively low levels on normal lymphoid and myeloid cells, and in some tissues of nonhe

8 Multiple progenitor populations produce lymphoid and myeloid cells, but they remain incompletely

9 NLRC3 is predominantly expressed in lymphoid and myeloid cells.

10 ury, concomitant with an influx of CCDC88B(+)lymphoid and myeloid cells.

11 concepts on the role of clonal evolution in lymphoid and myeloid leukemia as a driver of tumor initi

12 major revision of the WHO classification of lymphoid and myeloid neoplasms and acute leukemia was re

13 hierarchy of STAT5 dependency for populating lymphoid and nonlymphoid tissues.

14 ency, autoimmunity, genomic instability, and lymphoid and other cancers.

15 rrelated with the levels of the myeloid- and lymphoid-associated transcription factors measured.

16 xpress myeloid (GR1, CD11b, and CD16/32) and lymphoid (B220 and CD19) lineage markers.

17 ferentiation into multipotent and downstream lymphoid-biased progenitors.

18 leukemia (CML)-like disease manifesting in "lymphoid blast crisis." The biological heterogeneity of

19 ate and adaptive immune components in blood, lymphoid (bone marrow, spleen, lymph nodes), and mucosal

20 gulation of Notch1, leading to inhibition of lymphoid, but not myeloid, lineage potential.

21 as early as 4 days after birth), late-onset lymphoid cancer development, and premature death.

22 e treatment of hairy cell leukemia and other lymphoid cancers, it also has activity against myeloid n

23 apeutic intervention in specific myeloid and lymphoid cancers.

24 ate early T cell progenitor (ETP) and innate lymphoid cell (ILC) development remains unclear.

25 Little is known about innate lymphoid cell (ILC) populations in the human gut, and th

26 ed the development of tissue-resident innate lymphoid cell (ILC) subsets.

27 binant HpARI abrogated IL-33, group 2 innate lymphoid cell (ILC2) and eosinophilic responses to Alter

28 y gene expression, and TH and group 2 innate lymphoid cell (ILC2) responses.

29 ing IL-22 production from the group 3 innate lymphoid cell (ILC3) in an aryl hydrocarbon receptor dep

30 ), lymphoid tissue inducer (LTi), and innate lymphoid cell 1 (ILC1) cells, but not ILC2 or ILC3 cells

31 ich previously has only been associated with lymphoid cell biology.

32 whether AHR antagonism could promote innate lymphoid cell differentiation from hESCs.

33 d protein axis specifies innate and adaptive lymphoid cell fate.

34 roteins were detected in both epithelial and lymphoid cell populations expressing CD155 in the tonsil

35 eased STAT1 and STAT3 signaling responses in lymphoid cell subsets after surgery, consistent with enh

36 PRKCQ gene expression was assessed in innate lymphoid cell subsets purified from human PBMCs and mous

37 It also caused a reduction in innate lymphoid cell, ILC2, and IL-9(+) and IL-13(+) ILC2 numbe

38 Adipose type 1 innate lymphoid cells (AT1-ILCs) promote pro-inflammatory macro

39 eletion led to an overall increase in innate lymphoid cells (CD45(+)lin(-)CD25(+) cells) and IL-13(+)

40 Recently, several groups of innate lymphoid cells (ILC), distinct from NK cells in developm

41 ritical negative regulator of group 2 innate lymphoid cells (ILC-2s).

42 , we show that tissue-resident type 1 innate lymphoid cells (ILC1) serve an essential early role in h

43 the features that distinguish type 1 innate lymphoid cells (ILC1s) from natural killer (NK) cells is

44 creased the proportion of ST2-bearing innate lymphoid cells (ILC2) in blood and kidneys, and adoptive

45 Type 2 innate lymphoid cells (ILC2) mediate inflammatory immune respon

46 Type 2 innate lymphoid cells (ILC2) share cytokine and transcription f

47 )-Rorasg/sg mice deficient in group 2 innate lymphoid cells (ILC2), and C57BL/6 wild-type mice treate

48 Group 2 innate lymphoid cells (ILC2s) and type 2 helper T cells (Th2 ce

49 Group 2 innate lymphoid cells (ILC2s) are a potential innate source of

50 Group 2 innate lymphoid cells (ILC2s) are a recently identified group o

51 Group 2 innate lymphoid cells (ILC2s) are key regulators of type 2 infl

52 d interleukin (IL)-9-producing type 2 innate lymphoid cells (ILC2s) as the mediators of a molecular a

53 ablished, the newly identified type 2 innate lymphoid cells (ILC2s) can also contribute to orchestrat

54 Group 2 innate lymphoid cells (ILC2s) expand in the lungs of mice durin

55 Group 2 innate lymphoid cells (ILC2s) have recently been shown to play

56 ced eosinophilia and expanded group 2 innate lymphoid cells (ILC2s) in aspirin-exacerbated respirator

57 models of allogeneic BMT, that type 2 innate lymphoid cells (ILC2s) in the lower GI tract are sensiti

58 servations in prostate cancer.Group 2 innate lymphoid cells (ILC2s) modulate inflammatory and allergi

59 The recently identified type 2 innate lymphoid cells (ILC2s) play significant roles in the pat

60 Group 2 innate lymphoid cells (ILC2s) produce type 2 cytokines, and alt

61 In innate immunity, IL-33 and group 2 innate lymphoid cells (ILC2s) provide an essential axis for rap

62 Type 2 innate lymphoid cells (ILC2s) represent an important type 2 imm

63 Type 2 innate lymphoid cells (ILC2s) resemble TH2 cells and produce th

64 Group 2 innate lymphoid cells (ILC2s) reside in multiple organs in the

65 Group 2 innate lymphoid cells (ILC2s), which promote tissue eosinophili

66 (Treg) cells and the emerging type 2 innate lymphoid cells (ILC2s).

67 activity of islet-associated group 2 innate lymphoid cells (ILC2s).

68 inflammation, eosinophils and group 2 innate lymphoid cells (ILC2s).

69 ne (IL-5, IL-13) production by type 2 innate lymphoid cells (ILC2s).

70 Group 3 innate lymphoid cells (ILC3s) are important regulators of the i

71 Innate lymphoid cells (ILCs) are rapidly-responding cells that

72 Innate lymphoid cells (ILCs) are tissue-resident "first respond

73 Innate lymphoid cells (ILCs) communicate with other haematopoie

74 In particular, the discovery of innate lymphoid cells (ILCs) has opened entirely new avenues fo

75 Innate lymphoid cells (ILCs) have an important role in the immu

76 Innate lymphoid cells (ILCs) have been classified into "functio

77 Innate lymphoid cells (ILCs) patrol environmental interfaces to

78 Innate lymphoid cells (ILCs) play critical roles in immune home

79 Recent findings that innate lymphoid cells (ILCs) regulate adaptive T cell responses

80 GR is selectively deleted in NKp46(+) innate lymphoid cells (ILCs), we demonstrated a major role for

81 Type 2 innate lymphoid cells and basophils were scarce in BAL fluid.

82 tion of chemokine responses in primary human lymphoid cells and cell lines that express CXCR4.

83 colon tissues, which activated type 2 innate lymphoid cells and dendritic cells to promote differenti

84 mbers of eosinophils, IL-13(+) type 2 innate lymphoid cells and IL-13(+)CD4(+) T cells and IL-5 and I

85 cells and antigen-presenting cells to innate lymphoid cells and regulatory T cells.

86 ulted in loss of AHR-dependent type 3 innate lymphoid cells and T helper 17 cells and increased susce

87 lly, we provide evidence that group 2 innate lymphoid cells are a source of IL-13, which promotes lun

88 In adaptive lymphoid cells EZH2 prevented the premature expression o

89 atural killer cells constitute potent innate lymphoid cells that play a major role in both tumor immu

90 (IELs) are a large and diverse population of lymphoid cells that reside between the intestinal epithe

91 pithelial cells, dendritic cells, and innate lymphoid cells translates to T-cell outcomes, with an em

92 ese mice, ozone increased lung IL-13+ innate lymphoid cells type 2 (ILC2) and IL-13+ gammadelta T cel

93 (vagina and cervix), whereas APCs and innate lymphoid cells were mainly located in the upper tract (u

94 inflammation, mast cells, and group 3 innate lymphoid cells were more enriched in adult-onset severe

95 es of alloantigens, the cross talk of innate lymphoid cells with damaged epithelia and with the recip

96 ress, required extrinsic signals from innate lymphoid cells, and limited bacterial dissemination.

97 ely, eosinophils, Th2 T cells, type 2 innate lymphoid cells, and possibly Foxp3+ Tregs protect agains

98 epithelial cells, macrophages, type 2 innate lymphoid cells, and TH2 cells along with increased Il33

99 l developmental intermediates, non-NK innate lymphoid cells, and the capacity for NK cells to adapt a

100 , we detect ERbeta protein in testis, ovary, lymphoid cells, granulosa cell tumours, and a subset of

101 rived cytokines that activate group 2 innate lymphoid cells, induce migration and activation of dendr

102 uced IL-22 expression, which required innate lymphoid cells, prevented microbiota encroachment and pr

103 ssed on natural killer (NK) cells and innate lymphoid cells, recognizes PDGF-DD.

104 ns of specific subsets of T cells and innate lymphoid cells, which are key drivers of inflammatory di

105 ue injury in sepsis, activates type 2 innate lymphoid cells, which promote polarization of M2 macroph

106 of using an immunomodulatory mAb to regulate lymphoid cells, which then recruit and activate myeloid

107 hemokine axis and by IL-13 expressing innate lymphoid cells.

108 eosinophils, mast cells, and group 3 innate lymphoid cells.

109 per development of adaptive, but not innate, lymphoid cells.

110 Murine pericardial lymphoid clusters were visualized in mice subjected to c

111 ipose tissue (AT) contains a high density of lymphoid clusters.

112 nimals exhibit delayed repopulation of the B-lymphoid compartment after the early lymphoid progenitor

113 detect (-) YFV-17D RNA in specific secondary lymphoid compartments and cell subsets not previously re

114 ts identify a distinct pathway that supports lymphoid development in the spleen during acute Plasmodi

115 Innate and adaptive lymphoid development is orchestrated by the activities o

116 involved in hematopoietic organ development, lymphoid development, and immune responses.

117 signaling components involved in myeloid and lymphoid development.

118 piration) failed to self-renew and displayed lymphoid differentiation defects.

119 icient Cxcr4 desensitization is critical for lymphoid differentiation of HSPCs, and its impairment is

120 ity that persistent or occult neurologic and lymphoid disease may occur following clearance of periph

121 uch as T and eomesodermin (EOMES; mesoderm), lymphoid enhancer-binding factor 1 (LEF1) and mesoderm p

122 teracts with some nuclear proteins, i.e. the lymphoid enhancer-binding factor 1 (Lef1), histone H3, a

123 ophy of intestinal villus and colon-resident lymphoid follicle, and degeneration and atrophy of brain

124 cytes and displayed morphologically in large lymphoid follicles along the intestine.

125 is expressed in the alveolar epithelium and lymphoid follicles from patients with IPF, and AKAP13 mR

126 issue-specific antiviral immune responses in lymphoid follicles that limit SIV replication in this pa

127 ntly, another subset of T cells in secondary lymphoid follicles was described, follicular regulatory

128 are a subset of CD4(+) T cells in secondary lymphoid follicles.

129 d in the pathogenesis of several myeloid and lymphoid hematological malignancies.

130 The control of lymphoid homeostasis is the result of a very fine balanc

131 included nevus (492 [61%]), benign reactive lymphoid hyperplasia (BRLH) (38 [5%]), nodular conjuncti

132 histopathology similar to pulmonary reactive lymphoid hyperplasia (PRLH), a condition associated with

133 Comparison of benign reactive lymphoid hyperplasia vs lymphoma revealed lymphoma with

134 Autoimmunity and peripheral lymphoid hyperplasia were found in 43% of 79 patients wi

135 necrosis, alveolar space consolidation, and lymphoid hyperplasia; indicating lagged unfavorable effe

136 athological findings (n=7) revealed atypical lymphoid infiltrates, Kupffer cell hyperplasia with eryt

137 The combination of total lymphoid irradiation and anti-T-cell antibodies safely i

138 use model to test the hypothesis that, after lymphoid irradiation, host CD8(+) DCs play a requisite r

139 ursor-cell ALL was very close to that of all lymphoid leukaemias combined, with similar variation.

140 2005-09, when age-standardised survival for lymphoid leukaemias ranged from 52.4% (95% CI 42.8-61.9)

141 Lymphoid lineage commitment is an important process in h

142 nic activity of MLL-Af4 was interlinked with lymphoid lineage commitment.

143 e potencies and can give rise to myeloid and lymphoid lineage progenitors.

144 n in the haematopoietic system causes skewed lymphoid lineage specification.

145 to the myeloid and to a lesser extent to the lymphoid lineage.

146 olling PLZF expression exclusively in innate lymphoid lineages.

147 poietic stem cells (HSCs) to the myeloid and lymphoid lineages.

148 t common human chromosomal translocations in lymphoid malignancies, yet the mechanism of how breaks o

149 in inhibitors showed preferential benefit in lymphoid malignancies.

150 leukemia (T-PLL) is a rare and aggressive T-lymphoid malignancy usually refractory to current treatm

151 shedding in the gastrointestinal tract) and lymphoid/monocytic cells in tonsils and Peyer's patches

152 mponents of commitment, resolving how innate lymphoid, myeloid, and dendritic, and B-cell fate altern

153 nscript analysis of these cultures indicates lymphoid, myeloid, and erythroid differentiation, indica

154 by the expression of Thy1.2 and the lack of lymphoid, myeloid, and NK lineage markers.

155 ntiation data to foster our understanding of lymphoid/myeloid cell-fate decisions.

156 with a 3% increase in incidence of offspring lymphoid neoplasms (hazard ratio = 1.03, 95% confidence

157 ed the impact of parental age on the risk of lymphoid neoplasms by subtype.

158 World Health Organization classification of lymphoid neoplasms recently acknowledged the complexity

159 ly diagnosed mature lymphomas, 321 precursor lymphoid neoplasms, 314 myeloid disorders, and 200 nonhe

160 ol study, we identified 32,000 patients with lymphoid neoplasms, diagnosed at ages 0-79 years during

161 ar disease detection in selected myeloid and lymphoid neoplasms, with a focus on the current and futu

162 rophils, B lymphocytes and T cell subsets in lymphoid or mucosal sites did not vary with clinical sta

163 emoattractant gradient created from stromal, lymphoid, or antigen presenting cell interactions.

164 ment and hematopoietic progenitor cells, and lymphoid organ hypoplasia.

165 preferentially colonizes Peyer's patches, a lymphoid organ in which microfold cells (M cells) overla

166 The thymus is a primary lymphoid organ required for the induction and maintenanc

167 nfected distinct CD4(+) T cells in secondary lymphoid organs (SLOs) and within the lamina propria of

168 cribed to circulate between blood, secondary lymphoid organs (SLOs), and lymph in the steady state.

169 d to decreased T-cell migration to secondary lymphoid organs (SLOs), reduced in vivo proliferation wi

170 e progression of autoreactivity in secondary lymphoid organs (SLOs), we characterized the localizatio

171 ly regulated the egress of Treg cells out of lymphoid organs and subsequent non-lymphoid tissue distr

172 markedly improve Ag/adjuvant co-delivery to lymphoid organs and sustain Ag presentation on dendritic

173 at circulate in the blood and are present in lymphoid organs are an essential component of long-lived

174 ral T cell responses in the non-lymphoid and lymphoid organs during acute and persistent viral infect

175 of FRCs in shaping the suppressive milieu of lymphoid organs during homeostasis.

176 We show that NK cells in secondary lymphoid organs from chronically SIVagm-infected African

177 1P) mediates egress of immune cells from the lymphoid organs into the lymphatic vessels; we investiga

178 enting cells with T lymphocytes in secondary lymphoid organs is essential for the initiation of alloi

179 but knowledge of their function in secondary lymphoid organs is incomplete.

180 Significantly, FRCs of human lymphoid organs manifest similar COX-2/PGE2 hyperactivit

181 r, neither T cell recruitment into secondary lymphoid organs nor initial T cell activation was affect

182 ase of the intestinal tract, report tertiary lymphoid organs present within the mucosal wall, along w

183 ive T cells that circulate through secondary lymphoid organs ready to be activated upon pathogenic ch

184 nce and function of the immune system and on lymphoid organs that coordinate both the maintenance of

185 b-, and dsPMCAb-derived PrP(Sc) to secondary lymphoid organs was monitored in wild type mice.

186 ess as recent thymic emigrants to peripheral lymphoid organs where they undergo an additional maturat

187 In secondary lymphoid organs, Ag-driven B cell activation induces ter

188 P) guides T cell circulation among secondary lymphoid organs, including spleen, lymph nodes and Peyer

189 ific B cells arrive in Ag-draining secondary lymphoid organs, they may join the ongoing GC response.

190 ention of memory T cell subsets in secondary lymphoid organs, via S1PR2.

191 T cells proved hyporesponsive in peripheral lymphoid organs, whereas they retained effector function

192 hroughout the intestine but rare in systemic lymphoid organs.

193 highly specialized immune cells in secondary lymphoid organs.

194 reg) with a significant decrease of iTreg in lymphoid organs.

195 ed early IL-22 production from the liver and lymphoid organs.

196 tream and the trafficking of T cells through lymphoid organs.

197 tory T cells in atherosclerotic arteries and lymphoid organs.

198 een on a majority of CD8(+) TILs, but not in lymphoid organs.

199 ncreased with tumor growth but was absent in lymphoid organs.

200 ng their recruitment to inflamed tissues and lymphoid organs.

201 ile excessive IL-22 induced atrophy in these lymphoid organs.

202 e maintenance of naive T cells in peripheral lymphoid organs.

203 tration with increased formation of tertiary lymphoid organs.

204 its effects remain unclear, particularly in lymphoid organs.

205 The balance of myeloid populations and lymphoid populations must be well controlled.

206 skewing came at the expense of the number of lymphoid-primed MPP4s, which appeared to be compensated

207 eloid progenitor populations in cord blood - lymphoid-primed multi-potential progenitors (LMPPs), gra

208 rd megakaryocyte-erythrocyte progenitors and lymphoid-primed multipotent progenitors.

209 decreased the numbers of MPP-derived common lymphoid progenitor (CLP), common myeloid progenitor (CM

210 ILC2s develop in the bone marrow from common lymphoid progenitor cells, but little is known about how

211 eage(-)Sca-1(+)c-Kit(-) (LSK(-)) cells are a lymphoid progenitor population that expands in the splee

212 f the B-lymphoid compartment after the early lymphoid progenitor stage.

213 cyte-macrophage progenitors (GMPs) and multi-lymphoid progenitors (MLPs) - were functionally and tran

214 ing during B cell programming of multipotent lymphoid progenitors by restricting chromatin accessibil

215 at all newly made ILCs originate from common lymphoid progenitors in the bone marrow.

216 tic effects were maintained with infusion of lymphoid progenitors that lack myeloid potential and wer

217 leukocyte counts, early depletion of common lymphoid progenitors, and a monocytic bias in comparison

218 Mbd3/NuRD therefore controls the fate of lymphoid progenitors, ensuring appropriate production of

219 way, Mbd3/NuRD protects the multipotency of lymphoid progenitors, preventing B cell-programming tran

220 inhibits B lymphopoiesis by acting on early lymphoid progenitors, S100A9 inhibits B lymphopoiesis by

221 n the number and proportion of bone marrow B-lymphoid progenitors.

222 ng and RNA sequencing, we identify a novel B-lymphoid program for transcriptional repression of gluco

223 ed to DC changes similar to those induced by lymphoid radiation, suggesting that apoptotic body inges

224 This lymphoid replication phase appears to precede neuroinvas

225 nabinoid receptor) as central effectors of B-lymphoid restriction of glucose and energy supply.

226 follicles and support the use of tonsils as lymphoid sites for the study of germinal center reaction

227 es), associated lymph nodes (LNs), and other lymphoid sites from 78 individuals ranging from less tha

228 signals that promote T cell residency in non-lymphoid sites, which could be used to enhance vaccine e

229 entifies numerous opportunities for enhanced lymphoid-specific combination chemotherapies that have t

230 In a murine model of lymphoid-specific EZH2 deficiency we found that EZH2 was

231 d with autoimmunity and caused by defects in lymphoid-specific V(D)J recombination.

232 previously unrecognized pathway involved in lymphoid stroma polarization and as a potential therapeu

233 f lymph node-like structures called tertiary lymphoid structures (TLS) is associated with improved pa

234 gatively affects the development of tertiary lymphoid structures and abrogates their prognostic value

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 and having a unique conjunctival associated lymphoid tissue.

260 , specifically, in locations associated with lymphoid tissue.

261 ) expression in trout nasopharynx-associated lymphoid tissue.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

294 eflecting a redistribution of these cells to lymphoid tissues.

295 followed by rapid dissemination to systemic lymphoid tissues.

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

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

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

299 ation of immunomodulatory genes in secondary lymphoid tissues.

300 B-lymphoid transcription factors, such as PAX5 and IKZF1,