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 hyperproliferation development is accelerated in mic

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

5 TEC proliferation is reduced in wild-type mice given ant

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

7 TEC-reactive CD4 T-cell proliferation was significantly

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

9 TEC-specific Irf4 deficiency resulted in a significantly

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

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

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

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

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

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

16 th each dsRNA segment attached directly to a TEC.

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

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

19 ent cells were present in neonatal and adult TECs.

20 main differences between neonatal and adult TECs: 1) neonatal TECs proliferated more actively than a

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

22 l TECs proliferated more actively than adult TECs; 2) whereas cTECs and mTECs had similar turnover ra

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

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 ls (TECs) help orchestrate thymopoiesis, and TEC differentiation relies on bidirectional interactions

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

30 sion impaired TEC proliferation and arrested TEC differentiation at an early progenitor stage.

31 ta stimulates release of stalled or arrested TECs.

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

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

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

35 Because TECs are targets of donor T-cell alloimmunity, we tested

36 eased migration and abnormal angiogenesis by TEC.

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

38 CD8 T-cell and NK cell responses induced by TECs in vitro and questioned how these processes are aff

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

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

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

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

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

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

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

46 gens (TSAs) in human thymic epithelial cell (TEC) cultures.

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

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

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

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

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

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

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

54 our understanding of thymic epithelial cell (TEC) renewal and homeostasis is hindered by the lack of

55 llelic series of the thymic epithelial cell (TEC) specific transcription factor Foxn1, we showed that

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

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

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

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

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

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

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

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

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

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

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

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

68 both on T cells and thymic epithelial cells (TECs) and play a role in defining the thymus microenviro

69 4 was generated by tubular epithelial cells (TECs) and promoted Mo-mediated TEC destruction during AK

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

71 m cells to generate thymic epithelial cells (TECs) capable of supporting T cell development represent

72 Thymic epithelial cells (TECs) help orchestrate thymopoiesis, and TEC differentia

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

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

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

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

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

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

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

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

81 xpression in renal tubular epithelial cells (TECs) was found to be an important component of experime

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

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

84 d proliferation of thyroid epithelial cells (TECs), or thyrocytes, in IFN-gamma(-/-) autoimmune-prone

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

86 nsion of functional thymic epithelial cells (TECs).

87 in purified murine thymic epithelial cells (TECs).

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

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

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

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

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

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

94 hybrid within a ternary elongation complex (TEC).

95 is through a transcriptional enzyme complex (TEC).

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

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

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

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

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 Using ground-based total electron content (TEC) maps and measurements from the THEMIS spacecraft, w

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

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

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

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

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

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

111 for thymus organization, and affect cortical TEC subpopulation phenotype and location.

112 is common between medullary (m) and cortical TEC, further elaborated in mTEC, and completed in mature

113 nd it thereby reduces the number of cortical TEC.

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

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

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

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

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

119 k-like protein containing a CARD domain(-/-) TECs demonstrated a phenotype similar to that of Nlrp3(-

120 unaffected by lipid raft disruption of donor TEC.

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

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

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

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

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

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

127 tasis is hindered by the lack of markers for TEC progenitors.

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

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

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

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

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

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

134 wever, progress toward generating functional TECs has been limited.

135 -derived TEPs further mature into functional TECs that support T cell development upon transplantatio

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

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

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

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

140 Ectopic Tbx1 expression impaired TEC proliferation and arrested TEC differentiation at an

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

142 assessed the effect of selective deletion in TEC of TNF receptor-associated factor 3 (TRAF3), an inhi

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

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

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

146 (CAF) that stimulate oncogenic signaling in TEC.

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

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

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

150 triggers the overexpression of alpha-AChR in TECs and not of other TSAs.

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

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

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

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

155 These data show that Foxn1 function in TECs is required for normal thymus size and to generate

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

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

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

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

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

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

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

163 These data suggest that Foxn1 is required in TECs both to recruit endothelial cells and for endotheli

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

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

166 f several solute and solvent transporters in TECs.

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

168 ely colocalized and complexed with VEGFR2 in TECs.

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

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

171 on of CD40 is required for anti-CD40-induced TEC proliferation, but lymphoid cells do not have to exp

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

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

174 cause they produce IFN-gamma, which inhibits TEC proliferation.

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

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

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

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

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

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

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

182 degranulation of NK cells, NK cell-mediated TEC lysis was efficiently inhibited by prednisolone (P<0

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

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

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

186 transcription factor implicated in medullary TEC function.

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

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

189 specifically expressed in Aire(+) medullary TECs (mTECs) induced efficient deletion via direct prese

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

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

192 A poly(I:C) effect was also observed on MG TECs.

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

194 ome sequencing of carefully identified mouse TEC subpopulations, we discovered a program of PGE that

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

196 igation and thiol-ene radical chemistry (NCL-TEC) on the resulting cysteine thiol has been investigat

197 between neonatal and adult TECs: 1) neonatal TECs proliferated more actively than adult TECs; 2) wher

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

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

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

201 These data further demonstrate a novel TEC-mesenchyme-endothelial interaction required for prop

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

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

204 FGFR1-ETS2 angiocrine cascade that obviates TEC IGFBP7.

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

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

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

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

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

210 nd tumor vessel maturation via modulation of TEC mechanosensitivity.

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

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

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

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

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

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

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

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

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

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

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

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

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

224 role in T cell development and, expressed on TECs, their nonautonomous roles are partially overlappin

225 -B1 and/or ephrin-B2 on either thymocytes or TECs are more severe and specific on thymic epithelium,

226 eractions, explaining why Nun acts on paused TECs.

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

228 that associated with the natively positioned TEC.

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

230 Human primary TEC and peripheral blood mononuclear cells were infected

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

232 ged TEC compartment, rebuilt from progenitor TECs.

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

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

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

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

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

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

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

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

241 In human and mouse primary renal TECs, NLRP3 expression was increased in response to TGF-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 one marrow chimera experiments indicate that TEC expression of CD40 is required for anti-CD40-induced

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

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

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

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

264 The TEC consists of two extensively interacting subunits: an

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

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

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

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

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

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

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

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

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

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

275 ed a Nun-dependent toe print upstream to the TEC.

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

277 magnetopause as measured in situ and through TEC measurements in the ionosphere.

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

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

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

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

282 This inhibition was rescued by treating TEC with TGFbeta.

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

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

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

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

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

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

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

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

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

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

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

294 explored the relationship between Il7(YFP+) TECs and mTECs.

295 Il7(YFP+) TECs are sustained in Rag2(-/-) mice, even following in

296 Still, Il7(YFP+) TECs can generate some CD80(+) mTECs in a stepwise diffe

297 the thymocyte-induced reduction in Il7(YFP+) TECs dissociates from the receptor activator of NF-kappa

298 As the frequency of Il7(YFP+) TECs gradually declines as mTEC development unfolds, we

299 oderately reduces the frequency of Il7(YFP+) TECs, whereas negative selection provokes a striking los

300 ection provokes a striking loss of Il7(YFP+) TECs.

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