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1 ated hemorrhagic shock and tissue trauma (HS/T).

2 ially administered D who crossed over to D + T).

3 y and distribution of transposable elements (TEs).

4 ge into adulthood, a phenomenon not found in TD.

5 178.8 nA/mug mL(-1), A = 92.9 nA/mug mL(-1), T = 1.4 nA/mug mL(-1), and C = 15.1 9 nA/mug mL(-1)), lo

6 displayed a rapid dose-dependent clearance (t(1/2) 10-60 h) in contrast to 1F11, which presented a d

7 scovered that PDK4 is a short lived protein (t(1/2) approximately 1 h) and is specifically degraded b

8 the dominant dissipation pathways occurs at T 110 K with relatively larger contributions from phon

9 tober 13, 2016, 18 patients who received D + T 150/2 remained in the study (13 [24%] of 54 enrolled a

10 icantly associated with childhood adversity (T = 2.3; P = .03).

11 MR assignments, and JM mutants (ST(296)AA or T(304)A) investigated, confirm that the backbone amide o

12 change bias field (HEX) started to appear at T 40 K and its value increased by decreasing the tempera

13 he absence of a surface, FXII-R353A and FXII-T activate prekallikrein and cleave the tripeptide S-230

14 genes and pathways, and stage or subtype of T-ALL.

15 The protective T allele at rs7178051 was also associated with reduced A

16 scription assays demonstrated that the minor T allele variation at rs604723 increased the activity of

17 elevated in carriers of the GABRA6 rs3219151 T allele with several independent markers and predictors

18 (possibly including tissue macrophages) and T and B lymphocytes in the presence of detectable inflam

19 r relapse, showed significant suppression of TEs and interferon pathways.

20 Trichosporon asahii (T. asahii) has emerged as a dangerous pathogen that caus

21 Results Relaxivities in serum (0.94 T at room temperature) of Fe-tCDTA (r1 = 2.2 mmol(-1) .

22 o found that rmIFN induces the activation of T, B, and NK cells and exhibits antiviral, antiprolifera

23 pathways to generate mutations at G-C and A-T base pairs, respectively.

24 induction of Th17-type CD4 T cells, reduced T-bet expression by natural killer cells, and expansion

25 itor of mTORC1, we were able to identify six T-bet phosphorylation sites.

26 Additionally, T-bet-deficient Treg cells lacked expression of the Th1-

27 Conversion of pyruvate to CO2 in the T. brucei bloodstream form provides new support for the

28 ce-associated PKs provides new insights into T. brucei-host interaction and reveals novel potential p

29 levels of VSG expression in bloodstream form T. brucei.

30 w limit of detection (G, A = 0.5 mug mL(-1); T, C = 1.0 mug mL(-1)), and high selectivity in the pres

31 TE classes, and showed that 95.6% of tested TEs can function as either transcriptional activators or

32 T (TFR) cells are a newly defined regulatory T cell (Treg) subset that suppresses follicular helper T

33 s with biased capacity for CD4(+) and CD8(+) T cell activation are asymmetrically distributed in lymp

34 The cell surface receptor CD6 regulates T cell activation in both activating and inhibitory mann

35 not affect HIV-1 gene expression induced by T cell activation in these rCD4s.

36 vent of pAg sensing that ultimately leads to T cell activation.

37 ling, costimulatory pathways are involved in T cell activation.

38 The interaction between the T cell antigen receptor (TCR) expressed by natural kille

39 Unlike B cell depletion, pan-T cell aplasia is prohibitively toxic.

40 nt mechanism that involves caspase-dependent T cell apoptosis and upregulation of inhibitory immune c

41 sion of MYC signaling and an increase in the T cell chemoattractant CCL5.

42 n elevated mutation load in combination with T cell clonal dominance among intratumoral lymphocytes p

43 In our in vitro T cell culture system, MART1-specific CD8 T cells were e

44 has a crucial role in positive selection and T cell development.

45 ted T cells were determined by a novel CD154 T cell epitope mapping assay.

46 After identification of T cell epitope-containing parts on each of the 3 parenta

47 Thus, sequence homology between T cell epitopes of 2 self-proteins and a related order o

48 This phenotype, known as T cell exhaustion, occurs during chronic infections caus

49 CD70 expression in T cells, and CD70 limits T cell expansion via a regulatory T cell-independent mec

50 ciated with Wnt-responsive enhancers through T cell factors (TCF) and kept silent by Groucho/TLE co-r

51 )alpha4beta7(high) subsets enhanced Th1/Th17 T cell generation and accumulation in the intestine, and

52 Blockade of ICOSL rescues T cell ICOS surface expression and rescues, at least in

53 current helminth infection potently inhibits T cell immunity; however, whether helminthes prevent T c

54 n-2 inducible T cell kinase (Itk) results in T cell immunodeficiency in mice and humans.

55 des a proof of principle that suboptimal CD8 T cell in old organisms can be optimized by manipulating

56 he Tec family kinase Interleukin-2 inducible T cell kinase (Itk) results in T cell immunodeficiency i

57 whereas B cell-deficient mice showed CD4(+) T cell loss but recovered from infection without lethali

58 Pdcd1 (PD-1) disruption augmented CAR T cell mediated killing of tumor cells in vitro and enha

59 ntDeltadriven vectorial migration, while CD8 T cell migration across LEC was not.

60 Effector T cell migration through tissues can enable control of i

61 CARs are designed with elements that augment T cell persistence and activity.

62 mmunity; however, whether helminthes prevent T cell priming or skew clonal recruitment and effector d

63 ly shown to be involved in the regulation of T cell proliferation and function.

64 ophages is one pathway that suppresses local T cell proliferation.

65 functional studies define landscapes of the T cell proteome and phosphoproteome and reveal signaling

66 a hepatitis B virus-specific (HBV-specific) T cell receptor (TCR) may supplement HBV-specific immune

67 Defects in T cell receptor (TCR) repertoire are proposed to predisp

68 se (ROCK)2 downregulates the proinflammatory T cell response while increasing the regulatory arm of t

69 The immune system can mount T cell responses against tumors; however, the antigen sp

70 key transcriptional determinant controlling T cell responses during transplantation.

71 were successful in the induction of NAbs and T cell responses in guinea pigs.

72 Fibroblasts possess the capacity to suppress T cell responses, although the molecular mechanisms of t

73 esponses in preclinical models, particularly T cell responses, remain sparse.

74 itizing cytokines and promotion of antitumor T cell responses.

75 n and the subsequent development of effector T cell responses.

76 CD8(+) T cell specificity depends on the recognition of MHC cla

77 Collectively, these findings identify CD4(+) T cell subsets with properties critical for improving ca

78 At T0, the frequencies of CD4 T cell subsets, including peripheral T follicular helper

79 s and steps controlling postinfection CD8(+) T cell terminal effector versus memory differentiation a

80 ibitory receptor blockade partially reversed T cell unresponsiveness.

81 etection method, phenotype/genotype (B cell, T cell, Philadelphia chromosome), and EFS and OS.

82 ility of using rapamycin in conjunction with T cell-activating agents in HIV-1 cure strategies.

83 D70 limits T cell expansion via a regulatory T cell-independent mechanism that involves caspase-depen

84 eg) subset that suppresses follicular helper T cell-mediated B cell responses in the germinal center

85 sms whereby HIV infection impedes successful T cell-mediated control of M. tuberculosis have not been

86 Central to CD8(+) T cell-mediated immunity is the recognition of peptide-m

87 T cell-specific deletion of talin in Tln1(fl/fl)Cd4(Cre)

88 THEMIS, a T cell-specific protein with high expression in CD4(+)CD

89 timulates the CD27 pathway, which results in T-cell activation and antitumor activity in tumor models

90 We undertook translatome analysis of CD8 T-cell activation, combining polysome profiling and micr

91 igands and receptors play important roles in T-cell co-stimulation and co-inhibition.

92 1-cell-associated molecules IL-10, inducible T-Cell costimulator (ICOS), lymphocyte activation gene 3

93 py (ART) correlated with HIV viremia, CD4(+) T-cell counts, and immune activation markers, suggesting

94 -controllers from those who experience CD4(+)T-cell decline.

95 Antibody-mediated CD4(+) T-cell depletion in HF mice (starting 4 weeks after liga

96 (SCID) is characterized by severely impaired T-cell development and is fatal without treatment.

97 Furthermore, T-cell diapedesis became equivalent between control and

98 disease, chronic immune activation leads to T-cell exhaustion.

99 is is an autoimmune disease characterized by T-cell infiltration in the skin that leads to fibrosis,

100 1 (HTLV-1) is the etiological agent of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/t

101 Human T-cell leukemia virus type 1 (HTLV-1) is the etiological

102 de of Aspergillus fumigatus and ensuing CD4+ T-cell polarization are poorly characterized.

103 Sequence analysis of T-cell receptors of CD8(+) T cells revealed the presence

104 activity has been correlated with activated T-cell recognition of neoantigens, which are tumour-spec

105 This study aimed to determine the T-cell response to Phl p 12 in profilin-sensitized patie

106 the cultured ELISPOT assay detected a higher T-cell response to pp65 than to IE-1 or IE-2, whereas in

107 escribe the appearance of transgene-specific T-cell responses in two subjects that were part of the p

108 kade (ICB) therapies can unleash anti-tumour T-cell responses.

109 roduced less interferon-gamma in response to T-cell stimulation.

110 here, integrates the activities of distinct T-cell subsets and by definition is dynamic and responsi

111 Efforts to improve the efficacy of adoptive T-cell therapies and immune checkpoint therapies in myel

112 ed from PD-1(+) TILs can be used in adoptive T-cell therapy (ACT).

113 tate safer application of effective CD19 CAR T-cell therapy.

114 tively promoted reactivation of resting CD4+ T-cell, as indicated by an increased viral transcription

115 gammadelta-T-cell-deficient mice developed profound RPE and retinal

116 When regulatory T cells (2 x 106/mouse) were intravenously administered

117 whereas adoptive transfer of splenic CD4(+) T cells (and, to a lesser extent, cardiac CD3(+) T cells

118 n receptor (TCR) expressed by natural killer T cells (NKT cells) and the antigen-presenting molecule

119 to proliferation, is common in newly arising T cells (so-called "recent thymic emigrants") in adults,

120 (OXPHOS) for energy production, and effector T cells (Teffs) rely on glycolysis for proliferation, th

121 he distinct metabolic features of regulatory T cells (Tregs) are less well established.

122 these cells into CD4+CD25+FoxP3+ regulatory T cells (Tregs).

123 Here, we report that T cells activated in such a context are mainly IFN-gamma

124 ent CD4(+) T cells, as well as murine CD4(+) T cells activated in the presence of rapamycin, a pharma

125 cytes prior to treatment or among peripheral T cells after treatment would be associated with effecti

126 evealed the presence of H-2L(d)/AH1-specific T cells and an expansion of sequence diversity in treate

127 d that a discrete proportion of infiltrating T cells and B cells underwent proliferation within the p

128 imulatory molecules such as ICOS, regulatory T cells and by compounds such as nicotine.

129 Additionally, both CD8(+) T cells and CD8(+) dendritic cells were identified in th

130 including CD8(+) T cells for age and CD4(+) T cells and monocytes for sex, we detected a direct effe

131 ated" DCs stimulated the activation of naive T cells and polarized a subset of these cells into CD4+C

132 tion) reduced cardiac infiltration of CD4(+) T cells and prevented progressive left ventricular dilat

133 phosphorylated in both Rheb-deficient CD4(+) T cells and T cells treated with rapamycin, suggesting m

134 ights into the nature of neoantigen-specific T cells and the effects of checkpoint blockade immunothe

135 f interferon-gamma (IFN-gamma) expression in T cells and to generate pathogenic TH17 cells in vivo.

136 Absolute counts and % of CD4+ T cells and Treg cells (CD4 + CD25 + FOXP3 + CD127dim/-)

137 nd -independent activation of Vgamma9Vdelta2 T cells and, importantly, strongly reduced the productio

138 anisms leading to IL-10 expression by CD4(+) T cells are being elucidated, with several cytokines imp

139 tumor cells, and mice with NFATc1-deficient T cells are defective in controlling Listeria infection.

140 elements of the cytokine genes in the memory T cells are marked by activating histone modifications e

141 s constitutively acetylated and naive CD4(+) T cells are potentiated in Th17/Treg cell differentiatio

142 e E-selectin binding among CD4(+) and CD8(+) T cells but no binding by B cells.

143 Determination of HCMV-specific T cells by cultured ELISPOT, in pregnant women with prim

144 in thymic negative selection of autoreactive T cells by promoting the ectopic expression of tissue-sp

145 IFN-gamma-primed MCs guide activation of T cells by Staphylococcus aureus superantigen and, when

146 the inhibitory microenvironment and how CAR T cells can be further engineered to maintain efficacy.

147 CD4 T cells can differentiate into multiple effector subsets

148 In resting T cells cholesterol keeps TCRs in the resting conformati

149 ed that soluble CD137 produced by regulatory T cells contributed to their autoimmune-suppressive func

150 ansferred polyclonal cancer antigen-reactive T cells deficient in the regulator diacylglycerol kinase

151 nclear how RICD sensitivity is calibrated in T cells derived from different individuals or subsets.

152 fter ischemia, little is known about whether T cells directly impact cardiac fibroblasts (CFBs) to pr

153 lets and suggest that therapeutic regulatory T cells directly or indirectly regulate their influx by

154 Adoptive transfer of T cells engineered to express a hepatitis B virus-specif

155 and sex on gene expression, including CD8(+) T cells for age and CD4(+) T cells and monocytes for sex

156 and positive selection of conventional human T cells from all sources of HSPCs.

157 D57 was significantly up-regulated in CD8(+) T cells from patients with hepatitis delta.

158 tative restriction factors in primary CD4(+) T cells from rhesus macaques under various conditions, f

159 d CCR10, are upregulated on HSV-specific CD8 T cells in blood.

160 udy is to explore the role of natural killer T cells in impaired liver regeneration.

161 Pathogenic T cells in individuals with rheumatoid arthritis (RA) in

162 Despite emerging data indicating a role for T cells in profibrotic cardiac repair and healing after

163 ShRNA knockdown of La in HEK 293 T cells increased Sendai virus infection efficiency, dec

164 The differentiation of naive CD8 T cells into effector cytotoxic T lymphocytes upon antig

165 capable of transforming primary human CD4(+) T cells into immortalized cell lines indistinguishable f

166 ghlight the need for further analysis of the T cells involved in insulitis to elucidate their role in

167 T cells isolated from TAC-treated hearts show enhanced p

168 ed of extracellular release by infected CD4+ T cells on protein quality control and autophagy in card

169 Indeed, absence of CD8(+) T cells prevented recovery from MRV infection and led to

170 pe mice, and adoptive transfer of gammadelta T cells prevented sensitization.

171 In addition, CD4 T cells produced less interferon-gamma in response to T-

172 The TCR repertoire of Gag293-specific CD4(+) T cells proved highly biased, with a predominant usage o

173 ur findings demonstrate that lung gammadelta T cells provide an early source of innate IL-17, which p

174 CD8(+) T cells require sustained Ca(2+) signaling for inflammat

175 We find that EZH2 deficiency in FOXP3(+) T cells results in lethal multiorgan autoimmunity.

176 uence analysis of T-cell receptors of CD8(+) T cells revealed the presence of H-2L(d)/AH1-specific T

177 l rates result in near-optimal production of T cells that are capable of surviving selection and reco

178 activin-A instructs the generation of CD4(+) T cells that express the Tr1-cell-associated molecules I

179 In dysfunctional T cells that have a decreased cytotoxic capacity, 4-1BB

180 and chemotaxis of previously activated human T cells to CXCL11, but not CXCL10 or CXCL12.

181 egs and M2-like macrophages and reduces CD8+ T cells to promote lung tumor growth.

182 cursor effector subset of virus-specific CD8 T cells transferred into antigen-free mice revealed that

183 ed in both Rheb-deficient CD4(+) T cells and T cells treated with rapamycin, suggesting mTORC1 signal

184 equivalent between control and EVL/VASP dKO T cells upon alpha4 integrin blockade.

185 While quiescent T cells use oxidative phosphorylation (OXPHOS) for energ

186 n resting naive, central and effector memory T cells using ChIP-Seq and found that unlike the naive c

187 ncy of Pf-specific polyfunctional CD4 memory T cells was associated with protection.

188 patients, the frequency of CD1b-autoreactive T cells was increased compared with that in healthy cont

189 ive capacity of M. tuberculosis-specific CD4 T cells was markedly impaired in HIV-infected individual

190 Mitochondrial flux from ASMCs to T cells was partially FGF2b and FGFR1 dependent.

191 5) Finally, SERCA2a 971-990-sensitized T cells were able to transfer disease to naive recipient

192 eads in the inner chamber produced ET-1 when T cells were activated with antigen or anti-CD3 antibody

193 te infection pp65-, IE-1-, and IE-2-specific T cells were detected at comparable levels.

194 The Ag specificities of these activated T cells were determined by a novel CD154 T cell epitope

195 ro T cell culture system, MART1-specific CD8 T cells were expanded from healthy donors using artifici

196 a recently discovered, innate-like subset of T cells with cytotoxic function, the role of which in lu

197 lls (and, to a lesser extent, cardiac CD3(+) T cells) from donor mice with HF induced long-term left

198 also demonstrate that a norovirus can infect T cells, a previously unrecognized target, in vitro.

199 few PD-1+ (programmed cell death 1-positive) T cells, an immunophenotypic pattern also observed in ot

200 al that IFN-gamma induces CD70 expression in T cells, and CD70 limits T cell expansion via a regulato

201 d murine wild-type and Rheb-deficient CD4(+) T cells, as well as murine CD4(+) T cells activated in t

202 ng human pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK cells, with 49 recombinant chem

203 oint therapies target tumor antigen-specific T cells, but less is known about their effects on natura

204 purified immune subsets including human pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK

205 subsets including human pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK cells, with 49

206 exosomes, derived from IL-2 stimulated CD4+ T cells, effectively promoted reactivation of resting CD

207 nity by regulating natural killer and CD8(+) T cells, epigenetic downregulation of HLA-E by high-risk

208 differentiation pathways in autoreactive CD4 T cells, highlighting its potential as a therapeutic tar

209 Activated and memory CD4 T cells, macrophages, and dendritic cell (DC) showed che

210 FN-gamma-, IL-5-, and IL-13-producing CD4(+) T cells, reduced expression of Th1 and Th2 associated tr

211 trauma, including induction of Th17-type CD4 T cells, reduced T-bet expression by natural killer cell

212 lying dermis, predominantly composed of CD3+ T cells, scattered CD20+ B cells, and relatively few PD-

213 d the frequency of IFN-gamma secreting total T cells, T-helper and CTLs against both H1N2 and H1N1 Sw

214 ression of the transcription factor Foxp3 in T cells, trans-presentation of IL-6 by DC-bound IL-6Ralp

215 l cells to recruit and activate alloreactive T cells.

216 n suppress activation of diabetogenic CD8(+) T cells.

217 t), with antibody-mediated depletion of CD4+ T cells.

218 nd reduced production of IFN-gamma by CD8(+) T cells.

219 bited a faster development and maturation of T cells.

220 type 1 diabetes-relevant autoreactive CD8(+) T cells.

221 nique subset of innate-like CD1d-independent T cells.

222 nt epitopes for gluten-specific CD4-positive T cells.

223 tic cells and macrophages as well as resting T-cells, SAMHD1 blocks HIV-1 infection through this dNTP

224 Selective inhibition of T-channels and global deletion of CaV 3.1 channels compl

225 ASD and 65 age-matched typically developing (TD) children were compared by using lectin microarrays a

226 r in young ASD cases compared to age-matched TD controls (<18 years old) and (b) decreases in the amy

227 Among several pathways implicated in E-T coupling, activation of voltage-gated L-type Ca(2+) ch

228 ant element to support the implementation of T cruzi screening programmes at primary health centres i

229 RNA expression profiling data from hearts of T. cruzi infected mice.

230 Mouse models of T. cruzi infection have been used to study heart damage

231 Wild-type T. denticola and the purified PF triggered activation of

232 stimulate, and the complemented PF-positive T. denticola strain restored the activation.

233 le in the flagellar assembly and motility of T. denticola.

234 We postulate that resistance to T-DM1 occurs through multiple mechanisms, one of which i

235 The MEF8 T-DNA insertion (mef8) line exhibited reduced editing at

236 Although polyoma virus middle T-driven tumors showed altered primary and metastatic pr

237 , most strikingly in the least abundant CD8+ T effector population.

238 of CD4 T cell subsets, including peripheral T follicular helper (pTfh) cells, which provide help to

239 ce expression and rescues, at least in part, T follicular helper numbers and the abnormal Ab producti

240 (59%), representing 235 Leeds and 191 Oxford TS+/FT+ cases.

241 eases with increasing water content, and its T g decreases correspondingly.

242 on-phonon and electrostatic interactions for T > 110 K and larger contributions from clamping losses

243 es induced by naive and in vivo-primed human T helper 2 cells.

244 the ability to suppress lymphadenopathy and T helper cell type 2 activation.

245 erein, we exhibit that CD26 identifies three T helper subsets with distinct immunological properties

246 Immunization with low doses of gp96 primes T helper type 1 (Th1) immune responses, whereas high-dos

247 Interleukin (IL)-13 is a pleiotropic T helper type 2 cytokine frequently associated with asth

248 Levels of interleukin 23 (IL23) and T-helper (Th) 17 cell pathway molecules are increased in

249 quency of IFN-gamma secreting total T cells, T-helper and CTLs against both H1N2 and H1N1 SwIV.

250 varies over time after cessation of nucleos(t)ide analog (NA) treatment in patients with chronic hep

251 Thus, the dichotomy between T-like and B-like cells and the presence of dedicated ly

252 he lectin domain, thus modulating the GalNAc-Ts' long-range preferences.

253 a peripheral element of the RNA that forms a T-loop module and a subset of nucleotides in the cobalam

254 arger contributions from clamping losses for T < 110 K.

255 istetraprolin-deficient mice after cytotoxic T lymphocyte depletion, but also in WSX-1/tristetraproli

256 e autophagic machinery in DCs in a cytotoxic T-lymphocyte-associated protein 4-dependent (CTLA4-depen

257 ted by antigen-specific interactions between T lymphocytes and dendritic cells (DCs).

258 of naive CD8 T cells into effector cytotoxic T lymphocytes upon antigen stimulation is necessary for

259 it an immune response from CD4(+) and CD8(+) T lymphocytes.

260 l reduction in the number of tumor cytotoxic T lymphocytes.

261 presenting immunogenic peptides to cytotoxic T lymphocytes.

262 IS is essential for the development of B and T lymphocytes.

263 f antigens by dendritic cells (DCs) to naive T lymphocytes.

264 Mucosal-associated invariant T (MAIT) cells are a recently discovered, innate-like su

265 lculations using the B3LYP, CASPT2, and CCSD(T) methods all predict linear geometries for both the an

266 lonisation increased aphid phloem feeding on T. monococcum MDR037 and MDR045, colonisation also incre

267 In-bore 3-T MR-guided prostate biopsy was performed in 134 targets

268 ield-induced metamagnetic phase transitions (T N = 58 K) and high spontaneous polarization ( 63.3 mu

269 ugh a sT domain that also inhibits MCV large T oncoprotein turnover.

270 se anaerobic digestion (AD), thermal drying (TD), or lime stabilization (LS) treatment processes.

271 m a heterozygous mutant PEX6 allele (c.2578C>T [p.Arg860Trp]) was overrepresented due to allelic expr

272 An induced switch of the T reg cell TCR repertoire to a random repertoire also pr

273 Recent studies suggest that T reg cells can participate in tissue repair in a manner

274 f food allergies in offspring by instructing T reg formation via neonatal Fc receptor (FcRn)-mediated

275 search, we also assessed the extent to which T's effects on aggressive behavior would depend on varia

276 Merkel cell polyomavirus (MCV) small T (sT) oncoprotein induces centrosome overduplication, a

277 The agreement for T stage was good/substantial (k=0.790) and for N stage w

278 educed PDW was significantly correlated with T stage, N stage, TNM stage, and histological type of th

279 The unpaired t test and chi(2) analysis were used to determine signif

280 Statistical analysis included a 2-sample t test to compare continuous variables, chi-square testi

281 performed with the chi(2) test, the Student t test, and logistic regression.

282 cohorts were measured using the independent t test, Wald chi(2), and binomial regression analysis.

283 nalyzed using an unpaired two-sample Welch's t-test assuming unequal variance and Z test of compariso

284 ke was correlated with the lesion site using t-test statistics.

285 erences were evaluated using paired 2-tailed t tests.

286 -carotenoid triplet-triplet energy transfer (T-TET) is slow, in the tens of nanoseconds range, wherea

287 Abnormal development of follicular helper T (TFH) cells can induce the GC response to self-antigen

288 Follicular regulatory T (TFR) cells are a newly defined regulatory T cell (Tre

289 primes responses characterized by regulatory T (Treg) cells and immunosuppression.

290 ivation of host immunosuppressive regulatory T (Treg) cells.

291 were detected in the blubber of 4 adult male T. truncatus.

292 Our novel findings, including T-tubule dilatation and disorganization, associated with

293 itude and frequency of Ca(2+) influx through T-type and L-type Ca(2+) channels.

294 that critically links cellular properties of T-type Ca(2+) channels to their physiological roles.

295 at Ca(2+) entry exerts a feedback control on T-type channel activity, by modulating the channel avail

296 The transcribed ultraconserved regions (T-UCRs) encode long non-coding RNAs implicated in human

297 In contrast, DHS-diminished TEs under darkness were enriched in Copia, LINE, and MuD

298 and alternating phenylene (P) and thiophene (T) units as PTP and TPT.

299 ge reduction (QS in V1-V3) and inferolateral T-wave inversion.

300 ation during hypoglycemia as demonstrated by T-wave symmetry and principal component analysis ratio c