ライフサイエンスコーパス: TEC

1 TEC exposed to media conditioned by drug-treated CAFs ex

2 TEC H/P develops much earlier in CD28(-/-) mice and near

3 TEC populations are capable of expressing up to 19,293 p

4 TEC was classified into 2 groups: systemic TEC, defined

5 TEC-reactive CD4 T-cell proliferation was significantly

6 TEC-specific deficiency of mTORC1 (mTORC1KO) impaired TE

7 TEC-specific Irf4 deficiency resulted in a significantly

8 TECs are critical for T cell development.

9 ated with Kollicoat SR, plasticized with 10% TEC.

10 dies were included, comparing 286 PTSDs, 203 TECs and 155 NTCs.

11 Manipulation of the ILC-IL-22-TEC axis may be useful for augmenting immune reconstitut

12 perturbations with amplitudes of up to 0.25 TEC units and traveling ionospheric perturbations (TIDs)

13 d resulted in a reduction of TEC risk by 2.5 TEC per 100 patient-years.

14 There were 97 TEC in 81 patients (29%); 32 were systemic, yielding an

15 th each dsRNA segment attached directly to a TEC.

16 ogical activation of TRPV4 restored aberrant TEC mechanosensitivity, migration and normalized abnorma

17 ed and tumor necrosis factor-alpha-activated TECs, the NK degranulation response was significantly re

18 nwhile, inducible expression of Myc in adult TEC similarly promotes thymic growth.

19 ent cells were present in neonatal and adult TECs.

20 We conclude that LRCs in adult TECs are not senescent postmitotic cells and may represe

21 Anticoagulation was protective against TEC and resulted in a reduction of TEC risk by 2.5 TEC p

22 Conversely, forced notch signaling in all TECs resulted in widespread expression of mTEC progenito

23 To test this hypothesis, we analyzed TEC subset frequency and phenotype, early thymic progeni

24 95% confidence interval: 1.61 to 4.64), and TEC were associated with higher risk of death and hospit

25 e investigated the interplay between BKV and TEC in more detail.

26 we evaluated the cross-talk between CAF and TEC isolated from tumors generated in a mouse model of K

27 tic signatures in TGFbeta-stimulated NEC and TEC cultures.

28 d by TECs for the development of T cells and TECs without manipulating the intracellular Wnt signalin

29 ta stimulates release of stalled or arrested TECs.

30 s, INPs made sub-10 s actuations possible at TEC temperatures as warm as -13 degrees C.

31 ed their own collagen matrix in fibrin-based TECs and better recapitulated the gene expression, colla

32 I-6 blocks granzyme B-mediated death because TEC from SPI-6 null kidneys have increased susceptibilit

33 Only chimeras that lacked GILT in both TECs and hematopoietic cells had a high conventional T/T

34 eased migration and abnormal angiogenesis by TEC.

35 rs and enhanced PI-9 or SPI-6 expressions by TEC may provide protection from diverse forms of inflamm

36 analyzed the role of Wnt ligands provided by TECs for the development of T cells and TECs without man

37 C exhibited an increased capacity to capture TEC-derived MHC, which correlated with direct expression

38 of up to 73% in mean total ecosystem carbon (TEC) by the end of the 590-year simulation.

39 n led to expansion of Foxn1(+)Ly51(-)CD80(+) TECs.

40 promoted expansion of Foxn1(+)Ly51(+)CD80(-) TECs, castration led to expansion of Foxn1(+)Ly51(-)CD80

41 cells choose between terminal effector cell (TEC) or memory precursor cell (MPC) fates.

42 tumor vasculature or tumor endothelial cell (TEC) function is not known.

43 s and to what extent thymic epithelial cell (TEC) development is dependent on Wnt signaling.

44 the key regulator of thymic epithelial cell (TEC) development, yet how Foxn1 functions remains largel

45 factor essential for thymic epithelial cell (TEC) differentiation.

46 suggesting that the tubular epithelial cell (TEC) expression of this protein may have a protective ro

47 nd steroids, impairs thymic epithelial cell (TEC) functions and induces the programmed cell death of

48 Postnatal thymic epithelial cell (TEC) homeostatic defect- or natural aging-induced thymic

49 characterized by thyrocyte epithelial cell (TEC) hyperplasia and proliferation (H/P).

50 and proliferation of thymic epithelial cell (TEC) progenitors.

51 ondary to changes in thymic epithelial cell (TEC) stimuli that drive thymocyte selection.

52 ed expression of the thymic epithelial cell (TEC)-specific transcription factor Forkhead box N1 (FOXN

53 lations of tumor-specific endothelial cells (TEC) from a spontaneous mammary tumor model undergo dist

54 nteractions between thymic epithelial cells (TEC) and developing thymocytes are essential for T cell

55 oblasts that contact tumor epithelial cells (TEC) can become irreversibly activated as cancer-associa

56 s required to prime thymic epithelial cells (TEC) for effective Treg induction.

57 expression (PGE) by thymic epithelial cells (TEC) is essential for generating a diverse T cell antige

58 dies revealed that tubular epithelial cells (TEC) show a limited response towards BKV infection.

59 ricted Ags (TRA) by thymic epithelial cells (TEC).

60 and human proximal tubule epithelial cells (TEC; HK2) were exposed to inflammatory mix (IM), a combi

61 nt heterogeneity of tumor endothelial cells (TECs) on tumorigenesis is unclear.

62 Tumor-associated endothelial cells (TECs) regulate tumor cell aggressiveness.

63 We discovered that tumor endothelial cells (TECs), but not normal ECs, express doppel; tumors from p

64 iated protection of thymic epithelial cells (TECs) and impairing recovery of thymopoiesis.

65 4 was generated by tubular epithelial cells (TECs) and promoted Mo-mediated TEC destruction during AK

66 on the function of thymic epithelial cells (TECs) and thymopoiesis and postulated that these effects

67 Although thymic epithelial cells (TECs) are crucial for thymopoiesis and T cell generation

68 d chemokines from tracheal epithelial cells (TECs) in vitro and tracheal tissue ex vivo in response t

69 The importance of thymic epithelial cells (TECs) is evidenced by clear links between their dysfunct

70 icum with chicken tracheal epithelial cells (TECs) mediated the upregulation of chemokine and inflamm

71 city against renal tubular epithelial cells (TECs) plays a crucial role during rejection, the degree

72 Thymic epithelial cells (TECs) provide crucial microenvironments for T-cell devel

73 vented by medullary thymic epithelial cells (TECs) through their expression and presentation of tissu

74 young, engraftable thymic epithelial cells (TECs) to a middle-aged or defective thymus leads to thym

75 e that human renal tubular epithelial cells (TECs) trigger selective proliferation of recipient T-cel

76 cholesterol efflux, thymic epithelial cells (TECs) use LXRalphabeta for self-renewal and thymocytes f

77 n, is expressed by tubular epithelial cells (TECs), and binds to the cFMS receptor on macrophages and

78 GILT expression in thymic epithelial cells (TECs), but not hematopoietic cells, was sufficient for c

79 bustly expressed in thymic epithelial cells (TECs), in this study, we show that deleting SPL in CD11c

80 gulatory effects on thymic epithelial cells (TECs), inducing a decreased protein expression of the ab

81 in purified murine thymic epithelial cells (TECs).

82 ransition (EMT) of tubular epithelial cells (TECs).

83 stroma, especially thymic epithelial cells (TECs).

84 e report a class of T6SS effector chaperone (TEC) proteins that are required for effector delivery th

85 s, such as chemokine-expressing and ciliated TEC, which warrant further characterisation.

86 ate that TseC secretion requires its cognate TEC protein and an associated VgrG protein.

87 fects the size of the medullary compartment, TEC-specific HIPK2 deletion only mildly affects AIRE-dir

88 d with the transcription elongation complex (TEC) as it escapes the pause and transcribes the late ge

89 y onto the transcription elongation complex (TEC) in trans.

90 cript in a transcription elongation complex (TEC) promotes tethering but not direct contact of TthCsm

91 upting the transcription elongation complex (TEC), detail the rate of and requirements for Eta-mediat

92 hybrid within a ternary elongation complex (TEC).

93 is through a transcriptional enzyme complex (TEC).

94 vity of Nun on ternary elongation complexes (TECs) assembled with templates lacking the lambda nut se

95 chia coli RNAP ternary elongation complexes (TECs) with and without Nun by single-particle cryo-elect

96 lymerase transcription elongation complexes (TECs).

97 risk of thrombotic and embolic complication (TEC) in adults with atrial arrhythmia after Fontan opera

98 Using the VARION algorithm we compute TEC variations at 56 GPS receivers in Hawaii as induced

99 Consequently, TEC-derived LXRalphabeta protects against homeostatic pr

100 Consequently, TECs are an attractive target for cell therapies to rest

101 Using the conserved TEC domain sequence, we identified a large family of TEC

102 c analyses, our approach using the conserved TEC domain will facilitate the discovery and functional

103 r fibrin-based tissue engineered constructs (TECs).

104 il using ionospheric total electron content (TEC) measurements collected by continuously operating gr

105 thways and molecular regulators that control TEC development are becoming clearer, as are their influ

106 ce to decipher new determinants that control TEC homeostasis in vivo.

107 ellular and molecular mechanisms controlling TEC development, function, dysfunction, and regeneration

108 ll-footprint Peltier thermoelectric coolers (TECs), and the times required for channel freezing (valv

109 a defect that spreads to the adult cortical TEC compartment.

110 nd it thereby reduces the number of cortical TEC.

111 mokines, decreased medullary TEC to cortical TEC ratios, and altered thymic architecture, leading to

112 ear cells were cocultured with donor-derived TECs for 7 days.

113 Donor-derived TECs were co-cultured with recipient peripheral blood mo

114 al respiration, decreased OCR, and disrupted TEC metabolic fitness.

115 equires upstream DNA sequences, and disrupts TECs to release the nascent RNA to solution.

116 long RNA associated with the promoter-distal TEC restores NusA's stimulatory effect.

117 unaffected by lipid raft disruption of donor TEC.

118 .0 x 1.0 cm thermoelectric cooling elements (TECs) to generate dynamic temperature changes along the

119 mediated regeneration stems from an enlarged TEC compartment, rebuilt from progenitor TECs.

120 Coculture of macrophages with Rlow-exposed TECs also resulted in prolonged expression of chemokine

121 ther a non-trauma (NTC) or a trauma-exposed (TEC) comparison control group.

122 Here we find that, during renal fibrosis, TECs acquire a partial EMT program during which they rem

123 Thus, mTORC1 is central for TEC development/function and establishment of thymic env

124 iopulmonary connection was a risk factor for TEC (hazard ratio: 2.31; 95% confidence interval: 1.61 t

125 sent the elusive progenitors responsible for TEC maintenance in the adult thymus.

126 Here, we show that forced, TEC-specific upregulation of FOXN1 in the fully involute

127 th large fractions of Foxn1(low) or Foxn1(-) TECs accumulating with age.

128 pecific; thymic DC readily acquired MHC from TEC plus thymic or splenic DC, whereas thymic or splenic

129 ene signatures of purified mTEC subsets from TEC-specific Hipk2 knockout mice with control mice and i

130 Conditioned medium from TECs exposed to the virulent Rlow strain induced macroph

131 for thymopoiesis and T cell generation, how TEC development and function are controlled is poorly un

132 BKV infection of primary human TEC did not induce an antiviral response, whereas infect

133 ulation of AIRE expression in cultured human TECs, human thymic tissue grafted to immunodeficient mic

134 e from Foxn1-expressing progenitors/immature TECs and it is widely assumed that TECs as a whole are d

135 fic deficiency of mTORC1 (mTORC1KO) impaired TEC maturation and function such as decreased expression

136 Notch1 is expressed by and active in TEC progenitors.

137 ciated with enhanced ribosomal biogenesis in TEC.

138 C progenitor markers and profound defects in TEC differentiation.

139 Enforced Myc expression in TEC induces the prolonged maintenance of a fetal-specifi

140 BKV specifically evades innate immunity in TEC and is not susceptible to an intrinsic interferon re

141 We evaluated Foxn1 expression patterns in TEC subsets and its dynamics during normal thymus develo

142 ies age-specific transcriptional programs in TEC, and establishes that Myc controls thymus size.

143 thymic epithelium owing to Clec16a's role in TEC autophagy.

144 (CAF) that stimulate oncogenic signaling in TEC.

145 n and the role of anticoagulation therapy in TEC prevention.

146 sunami Research and we observe variations in TEC that correlate in time and space with the tsunami wa

147 Moreover, expression of IL-34 in TECs correlates with disease activity.

148 ery when miR-205 is conditionally ablated in TECs.

149 the cell membrane, prevented VEGF binding in TECs, and suppressed tumor growth.

150 umor site and that genetic loss of doppel in TECs decreases LHbisD4 binding and targeting both in vit

151 bited expression of alpha-AChR and HLA-DR in TECs, suggesting that estrogens may alter the tolerizati

152 CSF-1 expression in TECs did not compensate for IL-34 deficiency.

153 icle, we demonstrate that Prdm1 functions in TECs to prevent autoimmunity in mice.

154 ype TECs, indicating that Prdm1 functions in TECs to regulate autoantibody production.

155 report here that mTOR complex 1 (mTORC1) in TECs plays critical roles in thymopoiesis and thymus fun

156 Deletion of Notch1 in TECs resulted in depletion of mTEC progenitors and drama

157 r mTEC differentiation, deficiency of p53 in TECs altered multiple functional modules of the mTEC tra

158 GF1 activates the FGF4-FGFR1-ETS2 pathway in TECs and converts naive tumor cells to chemoresistant TS

159 Thus, inhibition of the EMT program in TECs during chronic renal injury represents a potential

160 tive targets of miR-205 were up-regulated in TECs lacking miR-205, consistent with an important role

161 locking doppel can control VEGF signaling in TECs and selectively inhibit tumor angiogenesis.

162 iminating TGF-beta signaling specifically in TECs or by pharmacological means increased the size of t

163 get transcripts, instead of unwound ssDNA in TECs, for immunity against double-stranded DNA (dsDNA) p

164 f several solute and solvent transporters in TECs.

165 ce with conditional inactivation of Trp53 in TECs (p53cKO).

166 ely colocalized and complexed with VEGFR2 in TECs.

167 I/R expressed IL-34, c-FMS, and PTP-zeta in TECs during AKI that increased with advancing injury.

168 re 16-fold higher, on average, in individual TEC than in the mTEC population.

169 unosuppressive drugs significantly inhibited TEC-induced CD8+ T-cell proliferation.

170 regs, and transfer of CD28(+) Tregs inhibits TEC H/P.

171 dings demonstrate TME-dependent intertumoral TEC heterogeneity in CRC.

172 for the first time that resistance of kidney TEC to cytotoxic T-cell granzyme B-induced death in vitr

173 hibitory conformation adopted by full-length TEC kinases, creating opportunities to target the regula

174 n a mouse kidney proximal tubular cell line (TEC) and a human retinal pigment epithelial cell line (A

175 Anticoagulation was associated with lower TEC rate and lower risk of death and hospitalization, wi

176 and positive selection, while medullary (m) TECs impose central tolerance on the T cell repertoire.

177 analyzed the transcriptome of the three main TEC subsets in wild-type and Aire knockout mice.

178 All mature TECs arise from Foxn1-expressing progenitors/immature TE

179 l-induced CD8 degranulation and CD8-mediated TEC lysis were preferentially inhibited by tacrolimus an

180 o explore CD8+-mediated and NK cell-mediated TEC lysis.

181 is accumulation leads to macrophage-mediated TEC apoptosis.

182 helial cells (TECs) and promoted Mo-mediated TEC destruction during AKI that worsened subsequent CKD

183 thymotropic chemokines, decreased medullary TEC to cortical TEC ratios, and altered thymic architect

184 transcription factor implicated in medullary TEC function.

185 In mature medullary TEC, AIRE-driven pGE upregulates non-TRA coding genes th

186 rimarily disrupts the integrity of medullary TEC (mTEC) niche, a defect that spreads to the adult cor

187 enes and delayed maturation of the medullary TEC compartment in nu/+ mice.

188 e, we found that both cortical and medullary TECs (cTECs and mTECs) proliferated more actively in fem

189 r presenting a neo-self-antigen by medullary TECs, displaying decreased negative selection-related ma

190 Moreover, TEC were stimulated with genomic double-stranded (ds)DNA

191 Prdm1 is expressed by a subset of mouse TECs, and conditional deletion of Prdm1 in either Kerati

192 C, yielding an event rate of 4.4 nonsystemic TEC per 100 patient-years.

193 r systemic arterial embolus; and nonsystemic TEC, defined as Fontan conduit/right atrial thrombus or

194 r 100 patient-years, and 65 were nonsystemic TEC, yielding an event rate of 4.4 nonsystemic TEC per 1

195 uclear Abs when transplanted with Prdm1 null TECs, but not wild-type TECs, indicating that Prdm1 func

196 We observe TEC perturbations with amplitudes of up to 0.25 TEC unit

197 FGFR1-ETS2 angiocrine cascade that obviates TEC IGFBP7.

198 rs, T cells that developed in the absence of TEC-secreted Wnt ligands were functionally competent, an

199 Accelerated development of TEC H/P in IFN-gamma(-/-)CD28(-/-) mice is a result of r

200 in sequence, we identified a large family of TEC genes coupled to putative T6SS effectors in Gram-neg

201 hich serves a nonredundant role, and lack of TEC-provided Wnt ligands led to thymic hypotrophy, as we

202 on of the EMT program and the maintenance of TEC integrity, while also restoring cell proliferation,

203 nd tumor vessel maturation via modulation of TEC mechanosensitivity.

204 s of RNAP by restricting lateral movement of TEC along the DNA register.

205 Prevalence of TEC was 18% and 55% at 5 and 10 years, respectively.

206 dentify distinct transcriptional programs of TEC that account for their age-specific properties, incl

207 Our data show substantial proliferation of TEC-reactive CD4CD28 memory T cells, which are resistant

208 e against TEC and resulted in a reduction of TEC risk by 2.5 TEC per 100 patient-years.

209 tween NOTCH and FOXN1, a master regulator of TEC differentiation.

210 translocation states through restriction of TEC lateral mobility, Nun represents a novel class of tr

211 This study sought to determine the risk of TEC in this population and the role of anticoagulation t

212 ify the tumor-suppressive checkpoint role of TEC-expressed insulin growth factor (IGF) binding protei

213 In contrast, stabilization of TEC by Nun in a posttranslocated register allowed NTP bi

214 (q-CPV) and the in situ atomic structures of TEC within CPV in both quiescent and transcribing (t-CPV

215 ote prolonged TGF-beta1-induced G2 arrest of TECs, limiting the cells' potential for repair and regen

216 engraftment and proliferative capacities of TECs diminish early in life, whereas the receptivity of

217 sic changes in the proliferative capacity of TECs, and further show that young TECs can engraft and d

218 ctor diminished rATG-induced cytotoxicity of TECs and restored their IL-7 and IL-15 secretion.

219 ding domain essential for the development of TECs but not keratinocytes.

220 The extreme stability required of TECs to processively transcribe large genomic regions ne

221 ell development is not directly dependent on TEC-provided Wnt ligands.

222 cell development, but molecular insights on TEC and thymus homeostasis are still lacking.

223 Cytotoxic effects on TECs link the rATG-induced thymic damage to the delayed

224 olled by (upstream first) four, two, and one TECs.

225 nst BTK and excellent selectivity over other TEC, EGFR and Src family kinases, (ii) desirable ADME, e

226 eractions, explaining why Nun acts on paused TECs.

227 Here, by performing TEC-specific deletion of the thymus medulla regulator ly

228 The PH-TEC homology (PHTH) domain within the TEC family of tyro

229 that associated with the natively positioned TEC.

230 atrophied thymus by utilizing both postnatal TEC-defective (resulting from FoxN1-floxed conditional k

231 A primary TEC culture was established and the binding and cytotoxi

232 Human primary TEC and peripheral blood mononuclear cells were infected

233 Prestimulation of primary TEC with IFNalpha or dsDNA did not hamper replication of

234 equires active NOTCH signaling in progenitor TEC and that, once specified, further mTEC development i

235 ged TEC compartment, rebuilt from progenitor TECs.

236 he differentiation of immediately protective TECs and was correspondingly required for the clearance

237 is/IM is an adaptive mechanism that protects TEC, organs, and the host by preserving mitochondrial fu

238 onal deletion of Twist1 or Snai1 in proximal TECs resulted in inhibition of the EMT program and the m

239 Here, we isolated pure TECs from human colorectal carcinomas (CRCs) that exhibi

240 Rather, TEC-secreted Wnt ligands are essential for normal thymus

241 on of serum thyroxine levels does not reduce TEC H/P.

242 thymic Treg homeostasis because it regulates TEC-specific expression of several chemokines and costim

243 he hypothesis that Tbx1 negatively regulates TEC growth and differentiation, and that extinction of T

244 ed and NK cell-mediated lysis of human renal TECs.

245 Renal/TEC metabolic fitness was assessed by monitoring the exp

246 Foxn1 expression changed and the responding TEC subsets depended on the type of treatment.

247 CD28(-/-)IFN-gamma(-/-) mice develop severe TEC H/P, and 2-3 wk of NaI is sufficient for optimal dev

248 )IFN-gamma(-/-)CD28(-/-) mice develop severe TEC H/P.

249 ice and nearly 100% (both sexes) have severe TEC H/P at 4 mo of age.

250 t is not required for, development of severe TEC H/P, as CD40(-/-)IFN-gamma(-/-)CD28(-/-) mice develo

251 sufficient for optimal development of severe TEC H/P.

252 Mice with severe TEC H/P are hypothyroid, and normalization of serum thyr

253 Ionosphere Observation), and estimate slant TEC (sTEC) variations in a real-time scenario.

254 n of vessels in breast tumors contain SMA(+) TECs, suggesting that not all endothelial cells (EC) res

255 Compared with NECs, SMA(+) TECs were 40% less motile in wound-healing assays and fo

256 Although some TECs strikingly upregulate alpha smooth muscle actin (SM

257 retained, indicating a region that specifies TEC functions.

258 When Nun stabilized TEC in a pretranslocated register, immediately after NMP

259 s can disrupt the otherwise extremely stable TEC and we demonstrate that one of the last universally

260 emic, yielding an event rate of 2.1 systemic TEC per 100 patient-years, and 65 were nonsystemic TEC,

261 TEC was classified into 2 groups: systemic TEC, defined as intracardiac thrombus, ischemic stroke,

262 gmented dsRNAs in CPV are organized with ten TECs in a specific, non-symmetric manner, with each dsRN

263 CD11c(+) dendritic cells (DCs), rather than TECs or other stromal cells, disrupts the S1P gradient,

264 We demonstrate that TEC express SPI-6 protein, the murine homolog of PI-9, b

265 They further indicate that TEC heterogeneity is regulated by SPARCL1, which promote

266 /immature TECs and it is widely assumed that TECs as a whole are defined by Foxn1 expression.

267 We found that TECs are the main source of Wnt ligands in the thymus, w

268 We found that TECs exhibit reduced TRPV4 expression and function, whic

269 The TEC consists of two extensively interacting subunits: an

270 The TEC proteins share a highly conserved domain (DUF4123) a

271 ation of endogenous RNA transcription by the TEC inside the virus.

272 rchaea, eukarya, and bacteria to disrupt the TEC may be conserved, and that Eta stimulates release of

273 analyze localized variations of power in the TEC time series and we find perturbation periods consist

274 Nun fits tightly into the TEC by taking advantage of gaps between the RNAP and the

275 Analysis of the TEC compartment showed reduced expression of FOXN1 targe

276 and is highly selective for a subset of the TEC kinase family.

277 Notch activated a major portion of the TEC-specific gene-expression program and suppressed the

278 Nun binding to and action on the TEC requires a 9-bp RNA-DNA hybrid.

279 ruton's tyrosine kinase (BTK) belongs to the TEC family of nonreceptor tyrosine kinases and plays a c

280 demonstrate that binding of sigma(70) to the TEC in trans can have a particularly large impact on the

281 The PH-TEC homology (PHTH) domain within the TEC family of tyrosine kinases is also a crucial compone

282 Gene expression comparisons in the TECs with/without miR-205 revealed a significant differe

283 CL1 was most strongly upregulated in Th1-TME TECs.

284 fe, whereas the receptivity of the thymus to TEC engraftment remains relatively constant with age.

285 howed a comparable dose-dependent binding to TECs and exerted a similar complement-independent, dose-

286 onstrate that sigma(70) can bind in trans to TECs that emanate from either a sigma(70)-dependent prom

287 ed CD4(+) T cells are sufficient to transfer TEC H/P to SCID recipients.

288 This inhibition was rescued by treating TEC with TGFbeta.

289 However, chemotherapy triggers TECs to suppress IGFBP7, and this stimulates IGF1R(+) TS

290 nted with Prdm1 null TECs, but not wild-type TECs, indicating that Prdm1 functions in TECs to regulat

291 anulation after an encounter of unstimulated TECs, represented by a high cell surface expression of C

292 CD4 T-cell proliferation upon TEC encounter was mainly executed by memory T cells.

293 ctivity in the right lingual gyrus (PTSD vs. TEC).

294 However, the core mechanism by which TECs confer stem cell-like activity to indolent tumors i

295 tional knockout mice (FoxN1-Gpr177) in which TECs are unable to secrete Wnt ligands.

296 dial prefrontal cortex (mPFC); compared with TEC, PTSD showed hyperactivity in the ventral mPFC.

297 Thyroids of mice with TEC H/P have infiltrating T cells and expanded numbers o

298 oculture of chicken macrophages (HD-11) with TECs exposed to live mycoplasma revealed the upregulatio

299 re of this unusual expression program within TEC populations and single cells are unknown.

300 apacity of TECs, and further show that young TECs can engraft and directly drive the growth of involu