ライフサイエンスコーパス: lymphoid

1 Denoted as foliate lymphoid aggregates (FLAgs), these structures show incom

2 clones within the rejecting kidney suggested lymphoid aggregation.

3 Innate lymphoid and adaptive immune cells are known to regulate

4 nucleosis, chronic active EBV infection, and lymphoid and epithelial cancers.

5 tributor to the development of many types of lymphoid and epithelial cancers.

6 ned by complex interactions between resident lymphoid and myeloid cells and their communications with

7 LILRB1 gene expression in lymphoid and myeloid cells arises from two distinct prom

8 red by serial ultrasound, tumor-infiltrating lymphoid and myeloid cells were characterized, and overa

9 ation, diabetes, premature death, and severe lymphoid and myeloid hypoplasia together with diminished

10 human cells produced a normal repertoire of lymphoid and myeloid progeny in transplanted mice for ma

11 ar exist as two major subpopulations in both lymphoid and nonlymphoid organs that can be distinguishe

12 ly, cDC1 are less abundant than cDC2 in both lymphoid and nonlymphoid organs.

13 fies a simultaneous activity of neuronal and lymphoid CB(2)that protects against spontaneous and evok

14 s to suppress excessive activation of innate lymphoid cell (ILC) 2 during allergic lung inflammation.

15 eported the selective loss of group 3 innate lymphoid cell (ILC) number and function in a Dock8-defic

16 ells are known to convert to a type 1 innate lymphoid cell (ILC1)-like phenotype in response to TGF-b

17 L-33 synergistically promoted group 2 innate lymphoid cell (ILC2) activation to induce innate allergi

18 Alternaria-induced pulmonary group 2 innate lymphoid cell (ILC2) responses and IL-33 release.

19 nstrate that helminth-induced group 2 innate lymphoid cell (ILC2) responses are exaggerated in the ab

20 nt repairing AAMs, as well as group-2 innate lymphoid cell (ILC2)-mediated AAM activation.

21 oes not alter the balance of NK cell/ innate lymphoid cell 1 generation and slightly decreases the nu

22 and straightforward identification of innate lymphoid cell 2 progenitor populations.

23 eport that MAIT cells repress group 2 innate lymphoid cell activation and restrict allergen-induced a

24 ed permeability, IL-33 levels, type 2 innate lymphoid cell activation, and T(h)2 cell differentiation

25 ression but differed in terms of myeloid and lymphoid cell counts.

26 ucial at several stages of T cell and innate lymphoid cell development and differentiation.

27 Here, we review roles for Ikaros factors in lymphoid cell development, differentiation, and function

28 D94(+)NKp80(-)) NKDIs promoted non-NK innate lymphoid cell differentiation at the expense of NK cell

29 proliferation in the P493-6 and RAMOS human lymphoid cell lines.

30 t may interact with immune cells to regulate lymphoid cell organization and type 2 inflammation.

31 tosis and markedly decreasing premalignant B lymphoid cell populations.

32 Finally, the discovery of a prominent innate lymphoid cell-2 cluster links the single-cell RNA sequen

33 During early pregnancy, decidual innate lymphoid cells (dILCs) interact with surrounding materna

34 Although innate lymphoid cells (ILC) and natural killer (NK) cells are f

35 Innate lymphoid cells (ILC) are a heterogeneous family of immun

36 ssed eosinophils, T cells, Tregs, and innate lymphoid cells (ILC) from peripheral blood using flow cy

37 ntly "time stamp" NK cells and type 1 innate lymphoid cells (ILC1s) to characterize the dynamics of t

38 e report that tissue-resident group 2 innate lymphoid cells (ILC2) accumulate in the choroid plexus o

39 Group 2 innate lymphoid cells (ILC2) are stimulated by IL-33 to increas

40 Group 2 innate lymphoid cells (ILC2) are tissue-resident innate effecto

41 ls expressing CRTh2), eosinophils and innate lymphoid cells (ILC2).

42 e expansion of IL-13-producing type 2 innate lymphoid cells (ILC2s) and dependent on IL-25 and IL-33.

43 ocation and release, increased type 2 innate lymphoid cells (ILC2s) and monocyte-derived dendritic ce

44 Type-2 innate lymphoid cells (ILC2s) are a potent source of T-helper 2

45 The recently discovered group 2 innate lymphoid cells (ILC2s) are capable of secreting copious

46 Group 2 innate lymphoid cells (ILC2s) are effector cells of type 2 immu

47 Human type 2 innate lymphoid cells (ILC2s) are identified by coupled detecti

48 Type 2 Innate lymphoid cells (ILC2s) are implicated in helminth infect

49 Group 2 innate lymphoid cells (ILC2s) are implicated in host defense an

50 Group 2 innate lymphoid cells (ILC2s) are rare innate immune cells that

51 Group 2 innate lymphoid cells (ILC2s) are tissue-resident cells promine

52 limited regarding the role of group 2 innate lymphoid cells (ILC2s) in regulating humoral immunity.

53 Group 2 innate lymphoid cells (ILC2s) mediate allergic immunity but hav

54 t activation of lung-resident group 2 innate lymphoid cells (ILC2s) orchestrated suppression of natur

55 Group 2 innate lymphoid cells (ILC2s) regulate immunity, inflammation,

56 Group 2 innate lymphoid cells (ILC2s) represent a subset of newly disco

57 results in the activation of group 2 innate lymphoid cells (ILC2s), which subsequently drive increas

58 phenotype that is dependent on type 2 innate lymphoid cells (ILC2s).

59 ant and persistent decrease in type 3 innate lymphoid cells (ILC3) in the lamina propria.

60 te activation hubs containing group 3 innate lymphoid cells (ILC3) that continuously produce interleu

61 sponses that are controlled by type-3 innate lymphoid cells (ILC3)(1-3).

62 Type 3 innate lymphoid cells (ILC3s) are critical for lung defense aga

63 CCR6- group 3 innate lymphoid cells (ILC3s) are mediators of intestinal immun

64 Group 3 innate lymphoid cells (ILC3s) have emerged as master regulators

65 RORgammat(+) group 3 innate lymphoid cells (ILC3s) maintain intestinal homeostasis t

66 As such, group 3 innate lymphoid cells (ILC3s) that reside in the intestinal muc

67 Group 3 innate lymphoid cells (ILC3s), but not ILC1s or ILC2s, were sim

68 but not T cells, B cells nor group 3 innate lymphoid cells (ILC3s), is critical specifically for the

69 Innate lymphoid cells (ILCs) and CD4(+) T cells produce IL-22,

70 Innate lymphoid cells (ILCs) are generated early during ontogen

71 athways underlying the development of innate lymphoid cells (ILCs) are mostly unknown.

72 Innate lymphoid cells (ILCs) are tissue-resident lymphocytes th

73 s and they control the development of innate lymphoid cells (ILCs) in the bone marrow.

74 ne production by CRTH2(-)IL7Ralpha(-) innate lymphoid cells (ILCs) is unknown.

75 factor alpha [TNF-alpha]) produced by innate lymphoid cells (ILCs) located in the colon secondary to

76 Although innate lymphoid cells (ILCs) play fundamental roles in mucosal

77 wo independent cohorts, we found that innate lymphoid cells (ILCs) were depleted in the blood and gut

78 pid depletion of all three subsets of innate lymphoid cells (ILCs), ILC1s, ILC2s and ILC3s, which is

79 rescued IL-22 production from group 3 innate lymphoid cells (ILCs), whereas IL-6 administration durin

80 Ti) cells are regarded as a subset of innate lymphoid cells (ILCs).

81 , demonstrating an important role for innate lymphoid cells (ILCs).

82 ular bacterial mutant, is produced by innate lymphoid cells (ILCs).

83 ique characteristics of skin-resident innate lymphoid cells (ILCs).

84 in beta1, distinguishes NK cells from innate lymphoid cells 1 and other leukocytes.

85 ically marked as an active enhancer in human lymphoid cells and not monocytes.

86 Natural killer (NK) cells are innate lymphoid cells being explored as they engage tumor cells

87 hether engrafted miR-210-positive myeloid or lymphoid cells contribute to paracrine miR-210 delivery,

88 pacity of MYC-driven normal and neoplastic B lymphoid cells depends on MNT, a MYC-related transcripti

89 At pre-tumorous stages, lymphoid cells from the animals exhibit deregulated phos

90 Characteristic of memory responses, more lymphoid cells infiltrated the prostate in a second infe

91 Maturation of lymphoid cells is controlled by the action of stage and

92 hat chronic SIV-infected gut contains innate lymphoid cells producing inflammatory cytokines.

93 T(reg) cells, which activated group 2 innate lymphoid cells to provide a feed-forward mechanism for a

94 IL-13 from T helper 2 (Th2) cells and innate lymphoid cells type 2 (ILCs), and increased airway smoot

95 The lymphoid cells were positive for CD3, CD4, CD5, CD7 and

96 bsence of other inflammatory stimuli, innate lymphoid cells, and adaptive immunity.

97 ils, mast cells, T(H)2 cells, group 2 innate lymphoid cells, and antigen-presenting cells; and T3 CRS

98 ether with CD14(+) CD16(+) monocytes, innate lymphoid cells, and natural killer cells.

99 n natural killer (NK) cells and other innate lymphoid cells, competent enhancers are primed during li

100 e mutations, Langerhans cells, type 2 innate lymphoid cells, IL-33, TSLP) that have important roles i

101 prisingly, besides CD4(+) T cells and innate lymphoid cells, mast cells are a source of GM-CSF in thi

102 with pathways associated with type 2 innate lymphoid cells, monocytes, neutrophil trafficking, and T

103 el mechanistic roles for macrophages, innate lymphoid cells, natural killer cells, innate gammadelta

104 tudies that predated the discovery of innate lymphoid cells-2 cells.

105 endritic cells, natural killer cells, innate lymphoid cells-2, and CD (cluster of differentiation)-8

106 ing a strong atheroprotective role of innate lymphoid cells-2.

107 meostasis by shaping the fate of myeloid and lymphoid cells.

108 s, IL1B+ monocytes, and fewer group 1 innate lymphoid cells.

109 pon daunorubicin-induced DNA damage of human lymphoid cells.

110 ppressor cells at the cost of tumor-reactive lymphoid cells.

111 rection of functional defects in myeloid and lymphoid cells.

112 d antigens is a cardinal feature of adaptive lymphoid cells.

113 ecretion from mature miR-146a-/- myeloid and lymphoid cells.

114 mechanism of p53-induced cell death in pre-B lymphoid cells.

115 issue homeostasis and repair, such as innate lymphoid cells.

116 sceral adipose tissue rich in fat-associated lymphoid clusters (FALCs) that collects peritoneal conta

117 um, an adipose tissue rich in fat-associated lymphoid clusters in the peritoneal cavity, is associate

118 o the omental milky spots and fat-associated lymphoid clusters, in mice, the serous surface of the me

119 44 proteins and 96 genes (928 RNA probes) in lymphoid, colorectal tumor and autoimmune tissues by usi

120 on by PLX5622 indeed affects the myeloid and lymphoid compartments, causes long-term changes in bone

121 s, which recapitulated the liver myeloid and lymphoid composition, and underwent partial reprogrammin

122 lets, mature/immature red cells, and myeloid/lymphoid/compound white cells) and 49 haemostasis traits

123 Intestinal lymphoid defects caused by ITGB7 deficiency have not pre

124 ocused on the role of these factors in early lymphoid development, as their absence resulted in sever

125 r, CD34(+)PRLR(+) myeloid progenitors lacked lymphoid developmental potential, but when stimulated wi

126 regulated in the bone marrow and involved in lymphoid differentiation and activation.

127 e evidence for the existence of myeloid- and lymphoid-dominant human hematopoietic stem and progenito

128 iation programs, including myeloid-dominant, lymphoid-dominant, and balanced cell subsets.

129 eased expression of the canonical Wnt target lymphoid enhancer binding factor 1.

130 cetylase 1 (HDAC1), as well as T cell factor/lymphoid enhancer-binding factor (TCF/LEF), causing subs

131 We found that NRARP interacts with lymphoid enhancer-binding factor 1 (LEF1) and potentiate

132 of beta-catenin and increased expression of lymphoid enhancer-binding factor 1 (LEF1), a downstream

133 formation, forms a ternary complex with the lymphoid-enriched OCT2 and GC-specific MEF2B transcripti

134 ed a dynamic shift from myeloid expansion to lymphoid expansion and subsequent development of lymphom

135 ues such as cryptopatches (CPs) and isolated lymphoid follicles (ILFs) constitute steady-state activa

136 ne system in submucosal and mucosal isolated lymphoid follicles (SM-ILFs and M-ILFs, respectively) as

137 g high endothelial venules within intragraft lymphoid follicles and the recruitment of B cells, but n

138 dtype hosts mediates B cell recruitment into lymphoid follicles within the allograft, resulting in a

139 o promote dissemination of infected cells to lymphoid follicles.

140 opulations at the expense of erythroid and B lymphoid fractions.

141 sufficient to recapitulate the age-dependent lymphoid hypertrophy and autoinflammation seen in animal

142 ammatory airway disease, deficient in innate lymphoid (Il2rg knockout mice [Il2rg (KO)]), adaptive im

143 DNA damage and limits extrinsic myeloid and lymphoid immunosuppression.

144 ltiple gastric biopsies showed a small-sized lymphoid infiltrate, expanding the lamina propria, with

145 D subjects with noninfectious complications, lymphoid infiltrations, inflamatory conditions, or autoi

146 otal marrow irradiation and total marrow and lymphoid irradiation in multi-centric phase 2-3 trials.

147 total marrow irradiation or total marrow and lymphoid irradiation in new conditioning regimens seems

148 otal marrow irradiation and total marrow and lymphoid irradiation, highlighting both the possible adv

149 ts (12%) (smoldering myeloma, n = 2; chronic lymphoid leukemia, n = 1; and refractory cytopenia with

150 event-free survival of pediatric pre-B acute lymphoid leukemia, suggesting that SHOC2 could be a pote

151 ronic myeloid leukemia and a subset of acute lymphoid leukemias.

152 sults suggested a more complex effect on the lymphoid lineage.

153 ly mutated genes in adult myeloid as well as lymphoid malignancies and in clonal hematopoiesis.

154 irus (EBV) is associated with epithelial and lymphoid malignancies, establishes latent infection in m

155 The MYC oncogene drives T- and B- lymphoid malignancies, including Burkitt's lymphoma (BL)

156 nalysis demonstrates a shared mechanism with lymphoid malignancy in the formation of public rheumatoi

157 The other subtypes differed in nature (lymphoid, myeloid, mesenchymal) and abundance of tumor-i

158 miR-223 restricts the EHT of lymphoid-myeloid lineages by suppressing the mannosyltra

159 beta-receptor (LTbetaR) signalling promotes lymphoid neogenesis and the development of tertiary lymp

160 m cell function or the development of mature lymphoid or myeloid lineages.

161 s also inhibited virion attachment to CD4(-) lymphoid organ fibroblastic reticular cells that mediate

162 f) ligand 21 in lung lymphatics and tertiary lymphoid organ formation, and then decreased as lung inj

163 on, a T-cell subset critically implicated in lymphoid organ formation, in COPD.Methods: Myeloid cell

164 is first observed in the thymus, the primary lymphoid organ that generates and selects T cells.

165 The thymus is a primary lymphoid organ that plays an essential role in T lymphoc

166 long been known that the thymus, the central lymphoid organ, changes markedly during pregnancy(3).

167 The thymus is a primary lymphoid organ, essential for T cell maturation and sele

168 o explore whether it functions as a tertiary lymphoid organ.

169 ar interactions, ILC3s crucially orchestrate lymphoid organogenesis, promote tissue protection or reg

170 Secondary lymphoid organs (SLOs) are important initiators and regu

171 vidence supports a crucial role for tertiary lymphoid organs (TLOs) in chronic obstructive pulmonary

172 nt mature B cell population in the secondary lymphoid organs and blood of both humans and mice.

173 nd lymphatic vessels that resemble secondary lymphoid organs and can be induced at nonlymphoid sites

174 creases the burden of bacteria in intestinal lymphoid organs and intestinal inflammation after induct

175 Tertiary lymphoid organs are aggregates of immune and stromal cel

176 In lymphoid organs associated with the gut, however, germin

177 describe the asymptomatic infection of human lymphoid organs by IAV in children.

178 after a year on ART, with virus in blood and lymphoid organs confirmed to be replication competent.

179 s constitutively expressed at high levels in lymphoid organs during homeostasis, where it controls im

180 Intestinal lymphoid organs from mice with deletion of LACC1 had an

181 e form on their surface and can easily reach lymphoid organs in intact form for optimal activation of

182 arious antigens, usually form transiently in lymphoid organs in response to infection or immunization

183 egress and T cell lymphopenia in peripheral lymphoid organs in vivo.

184 unction of lymphatic vessels within tertiary lymphoid organs remains poorly understood.

185 lerance, Foxp3+ cells accumulate in tertiary lymphoid organs that are induced within the pulmonary gr

186 functional T cells, have low CCL22 levels in lymphoid organs, and this can be restored by adoptive tr

187 l scenarios of antigen access into secondary lymphoid organs, antigen valency and cellular environmen

188 This differs from lymphoid organs, in which immune cells adopt spatially b

189 etween CD8+ memory T cells in peripheral vs. lymphoid organs, revealing a novel tissue-specific parad

190 a and altered T-cell cytokines in intestinal lymphoid organs, similar to Lacc1(-/-) mice.

191 This contrasts with lymphoid organs, such as the spleen and mesenteric lymph

192 ty to direct immunomodulators to tumours and lymphoid organs, to alter the way biologics engage with

193 howed uptake in the tumor, spleen, and other lymphoid organs, whereas the human-specific control BiTE

194 n increased burden of bacteria in intestinal lymphoid organs, which expressed lower levels of T helpe

195 nd expanded B cell compartments in secondary lymphoid organs.

196 e into nodules that may mature into tertiary lymphoid organs.

197 re associated with the induction of tertiary lymphoid organs.

198 affecting naive T cell entry into secondary lymphoid organs.

199 od circulation and shear forces unlike other lymphoid organs.

200 mantle cell lymphoma (MCL) cells survival in lymphoid organs.

201 of antigen presentation in uninflamed distal lymphoid organs.

202 constituted up to 10% of TCRdelta+ cells in lymphoid organs.

203 le-negative (DN) T cells, in mouse secondary lymphoid organs.

204 vestigators to further fine-tune delivery to lymphoid organs.

205 T cells, which damage peripheral tissues and lymphoid organs.

206 s fail to home to lymph nodes as well as non-lymphoid organs.

207 and IgD isotypes respond to Ag in secondary lymphoid organs.

208 ll function, thymic involution and decreased lymphoid output with a skewing toward myeloid developmen

209 bling that of tumor infiltrating myeloid and lymphoid populations, but with higher expression of lymp

210 d changes in specific subsets of myeloid and lymphoid populations.

211 The lymphoid-primed IRF8(hi) pathway, marked by CD123 and BT

212 which defines the common helper-like innate lymphoid progenitor (ChILP), but not cytokine signaling.

213 of Orp3 results in an aberrant expansion of lymphoid progenitor cells and a high penetrance formatio

214 Impaired lymphoid progenitor development led to deficiencies of B

215 ST2) in ILC2p and common helper-like innate lymphoid progenitors (CHILP), at least partially through

216 atelet lineage bias, increased generation of lymphoid progenitors and rebalanced HSC lineage output i

217 ction of hematopoietic stem cells and common lymphoid progenitors causing a severely depleted acquire

218 yte development, deletion of Arid1a in early lymphoid progenitors in mice resulted in a pronounced de

219 us and were a major contributor to blood and lymphoid reservoir size.

220 We found that myeloid and lymphoid resident immune cells concentrate around peripo

221 Lymphoid-restricted membrane protein (LRMP, Jaw1) and in

222 ls supporting kidney vascularization in host lymphoid sites and omenta.

223 ne levels by the chromatin remodeling factor lymphoid-specific helicase (LSH), an epigenetic driver o

224 Mutation of HELLS (Helicase, Lymphoid-Specific)/Lsh in human DNA causes a severe immu

225 Immune aggregates organized as tertiary lymphoid structures (TLS) are observed within the kidney

226 tions may have driven the formation of these lymphoid structures by a process of convergent evolution

227 in which T cells in tumours without tertiary lymphoid structures had a dysfunctional molecular phenot

228 e of O-MALT and other secondary and tertiary lymphoid structures in mammals.

229 mphoid tissues and the neogenesis of ectopic lymphoid structures in nonlymphoid organs, particularly

230 Finally, our temporal studies suggest that lymphoid structures in the lung restrict the spread of m

231 o the potential role of B cells and tertiary lymphoid structures in the response to ICB treatment, wi

232 with CD20 reveals the formation of tertiary lymphoid structures in these CD8(+)CD20(+) tumours.

233 as characterized by the presence of tertiary lymphoid structures that contain T cells and follicular

234 ravels the potential of B-cell-rich tertiary lymphoid structures to guide clinical decision-making an

235 option that combines prevention of tertiary lymphoid structures(1) and inhibition of apoptosis with

236 d neogenesis and the development of tertiary lymphoid structures(1,2), which are associated with seve

237 fic body sites to form primary and secondary lymphoid structures.

238 al macrophage activation, whereas the innate lymphoid system contributes to MCM, mucin production, an

239 pioids had higher reservoirs in CNS than the lymphoid system.

240 alysis of the subnetworks regulated by the B-lymphoid TF Ebf1 and T-lymphoid TF Gata3 revealed a surp

241 ks regulated by the B-lymphoid TF Ebf1 and T-lymphoid TF Gata3 revealed a surprising role in common a

242 cent work has shown that bronchus-associated lymphoid tissue (BALT), characterized by the development

243 iscovered that inducible bronchus-associated lymphoid tissue (iBALT) forms in response to infection w

244 d cells in the inducible bronchus-associated lymphoid tissue (iBALT) likely contributed to dysregulat

245 In the nasal-associated lymphoid tissue (NALT), a muted inflammatory response to

246 ion trajectory of regulatory T cells between lymphoid tissue and colon.

247 humanized rodent models developed with human lymphoid tissue and hematopoietic stem cell transplants.

248 in vivo characteristics, with high uptake in lymphoid tissue and hPBMC xenografts.

249 hed in intestinal macrophages, and a generic lymphoid tissue cDC cluster associated with Ccr7.

250 ession at the injection site and in draining lymphoid tissue compared to a nonamphiphilic control and

251 etion of NLK does not affect mouse health or lymphoid tissue development.

252 cluding TRM cells, in nasopharynx-associated lymphoid tissue from children and adults.

253 er investigation of ASFVsRNA2 detected it in lymphoid tissue from pigs with ASF.

254 Lymphoid tissue inducer (LTi) cells are regarded as a su

255 t T cell-intrinsic role of mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1)

256 follicles had features of mucosa-associated lymphoid tissue lymphoma.

257 reactive CD8(+) T cells isolated from murine lymphoid tissue retained developmentally plastic phenoty

258 cluding TRM cells, in nasopharynx-associated lymphoid tissue, demonstrating its strong capacity to ex

259 moking-related inducible bronchus-associated lymphoid tissue, induced regeneration of lung tissue, an

260 populations tend to have a greater amount of lymphoid tissue, smaller airways, and smaller lower faci

261 of human memory B cells of mucosa-associated lymphoid tissue.

262 t virus in blood, CSF, intestinal tissue, or lymphoid tissue.

263 esponses in the periphery and gut-associated lymphoid tissue.

264 a method for isolating human gut-associated lymphoid tissues (GALTs) that allows unprecedented profi

265 cient Trm cells progressively decayed in non-lymphoid tissues and expressed dysregulated Trm-specific

266 ontrols the normal organization of secondary lymphoid tissues and the neogenesis of ectopic lymphoid

267 of activated Tregs that readily migrate into lymphoid tissues and the pancreas while inhibiting autoa

268 increase their activation and migration into lymphoid tissues and the pancreas.

269 n together, these results suggest that human lymphoid tissues can be sites of silent IAV infections w

270 We sought to investigate whether these lymphoid tissues could be sites of viral replication and

271 (89)Zr-muS110 uptake in the spleen and other lymphoid tissues decreased and was comparable to uptake

272 8 RNA levels in various organs revealed that lymphoid tissues have the highest levels of expression o

273 evaluation of humoral immunity and secondary lymphoid tissues in an established KS (Kmt2d(+/betaGeo))

274 ll T lymphocytes in the peripheral blood and lymphoid tissues in mice and humans.

275 cation scheme to segregate B cells from four lymphoid tissues into twelve unique subsets, including a

276 The cellular homeostasis of lymphoid tissues is determined by the continuous interac

277 The data indicate that lymphoid tissues not only harbor expression of IAV prote

278 rstood, the host responses within organs and lymphoid tissues remain poorly characterized.

279 sue injury in the liver, adrenal glands, and lymphoid tissues remains limited.

280 w immune cells in the gut and gut-associated lymphoid tissues respond to IL-2C is not well characteri

281 Analysis of lymphoid tissues showed early upregulation of genes that

282 Solitary intestinal lymphoid tissues such as cryptopatches (CPs) and isolate

283 odeficiency virus 1 infection are located in lymphoid tissues that are difficult to access.

284 ransport of solutes across it and associated lymphoid tissues that play a sentinel role.

285 ing fetal ILC1-like NKPs travel to secondary lymphoid tissues to initiate the formation of diversifie

286 ownregulation of humoral immune responses in lymphoid tissues were confirmed with flow cytometry.

287 ubs for HIV dissemination but that blood and lymphoid tissues were the main source; (c) that viral ex

288 In contrast to the lymph nodes and mucosal lymphoid tissues with well-defined entry and exit routes

289 full-thickness fetal skin, autologous fetal lymphoid tissues, and autologous fetal liver-derived hem

290 n full-thickness skin, along with autologous lymphoid tissues, and autologous immune cells.

291 In lymphoid tissues, CSF1R-FRed highlighted diverse MPS pop

292 ating HIV reservoirs in peripheral blood and lymphoid tissues, residual sources of virus may remain i

293 Tem biology, including enhanced presence in lymphoid tissues, robust IL-2 production, and recall pot

294 In the intestine, DC are found in organized lymphoid tissues, such as the mesenteric lymph nodes and

295 immunity despite persistence of infection in lymphoid tissues.

296 ction through continuous surveillance of non-lymphoid tissues.

297 mic immune response in primary and secondary lymphoid tissues.

298 ng blood flow and immune cell recruitment in lymphoid tissues.

299 t V(D)J recombination and the development of lymphoid tumors.

300 lveolar macrophages, dendritic cells, innate lymphoid type 2 cells, and subpopulations of lung struct