ライフサイエンスコーパス: TIL

1 TIL correlated moderately ( approximately 0.50) with PD1

2 TIL densities increased when frameshift mutations were p

3 TILs were present in 75% of all osteosarcoma specimens.

4 P = .001) and CD8+ (32.8 vs 13.5; P < .001) TILs compared with microsatellite-stable tumors.

5 , suggesting that cells derived from PD-1(+) TILs can be used in adoptive T-cell therapy (ACT).

6 or CD8(+) TILs, Foxp3(+) Tregs, and PD-1(+) TILs were strongly associated with favorable prognosis.

7 s in CD8(+)PD-1(+) compared with CD8(+)PD-1- TIL populations.

8 than single-positive (PD-1(+) or CTLA-4(+)) TIL, including an inability to proliferate and secrete e

9 .3-0.8]; and brisk, 0.3 [0.5-0.7] [vs absent TILs]), and anatomic site other than scalp/neck (0.1 [0.

10 uence of the bisphosphonate tiludronic acid (TIL) on periodontitis.

11 BMC feeder cells in the REP or the activated TIL expressed 4-1BB ligand.

12 t can be concluded that locally administered TIL solution (1 mg/kg body weight) reduced alveolar bone

13 ulation suppressed TIL expansion and altered TIL cytokine production.

14 e HPR motif, which is highly conserved among TIL proteins, extends over as short stretch of eight ami

15 ggest that the HPR motif may directly anchor TILs to cell membranes, favoring in this way further con

16 ent in tumor cells (32% vs 7%, P = .003) and TILs (47% vs 18%, P = .008) after adjusting for the age

17 able prognostic factor in breast cancer, and TILs may synergize with chemotherapy and immune checkpoi

18 that CD3-engaging bsAbs can induce apoptotic TIL depletion followed by rapid tumor regrowth, reminisc

19 Arabidopsis TIL (AtTIL) is considered the ortholog of human ApoD, a

20 or (IL-36R) knockout mice exhibit attenuated TILs after UUO.

21 procure tumour tissue to generate autologous TIL cultures, which then underwent large scale ex-vivo e

22 a single intravenous infusion of autologous TILs and high-dose interleukin-2 [720 000 IU/kg] every 8

23 t describing adoptive transfer of autologous TILs to mediate objective tumour regression in patients

24 detected no significant association between TIL values and progression-free survival (adjusted HR 0.

25 95% CI, 0.5 to 1.0) and 50% less with brisk TIL grade (HR, 0.5; 95% CI, 0.3 to 0.9) relative to TIL

26 mor cells that were recognized by three bulk TIL lines from three individuals with melanoma that were

27 rs may not be the in vitro expansion of bulk TILs, but the ability to select and enrich for tumor-rea

28 complex-binding algorithm for recognition by TILs.

29 gression in tumor volume due to enhanced CAR TIL infiltrate, decreased susceptibility to tumor-induce

30 er, our results indicate that CD8(+)CD103(+) TIL, freshly isolated from NSCLC specimens, display tran

31 his study, we show that an enhanced CD103(+) TIL subset correlates with improved early stage NSCLC pa

32 CD3(+) TILs were composed of 57% CD4(+) (82% TEM and 20% Tregs)

33 increased proliferation of CD8(+) and CD4(+) TIL and cytokine production in response to stimulation w

34 hese inhibitory receptors, CD8(+) and CD4(+) TIL that did express these receptors had higher levels o

35 ng inhibitor of p38 pY323(+), reduced CD4(+) TIL production of TNF-alpha, IL-17A, IL-10 and secondary

36 d IFNgamma expression on intratumoral CD4(+) TILs and a reduced accumulation of Tregs and CD11b(+)/Gr

37 Thus, TCR-mediated activation of CD4(+) TILs results in alternative p38 activation and productio

38 and loss of Th1 effector functions on CD4(+) TILs, such as CD40L and IFNgamma expression.

39 n vivo, only cells expanded from PD-1(+) CD8 TILs contained tumor progression, and their efficacy was

40 The fold expansion of PD-1(+) CD8 TILs was 10 times lower than that of PD-1(-) cells, sugg

41 e most upregulated genes in both CD4 and CD8 TILs were PMCH, ETV1, and TNFRSF9.

42 f tumor-reactive T cells present in bulk CD8 TILs before expansion, only T-cell products derived from

43 ed PD-1(+), but not from PD-1(-) or bulk CD8 TILs, specifically recognized tumor cells.

44 r specificity of cells derived from bulk CD8 TILs.

45 restore/enhance the effector function of CD8 TILs and thus improve the antitumor efficacy of current

46 The effector function of CD8 TILs could not be rescued in mice lacking intact type I

47 Double-positive (PD-1(+)CTLA-4(+)) CD8(+) TIL had characteristics of more severe dysfunction than

48 l-to-mesenchymal transition (EMT) and CD8(+) TIL immunosuppression, two key drivers of cancer progres

49 o be a clear link established between CD8(+) TIL density and frameshift mutations in colorectal cance

50 cific CD8(+) TIL, compared with other CD8(+) TIL.

51 mor-associated antigen (TAA)-specific CD8(+) TIL, compared with other CD8(+) TIL.

52 dysfunctional tumor antigen-specific CD8(+) TIL.

53 We found that CD8(+) TIL density correlated positively with the total number

54 We found that CD8(+) TIL up-regulate 4-1BB expression early during the REP af

55 ion of TA-specific CD8(+) T cells and CD8(+) TILs in melanoma patients and suggest that dual TIGIT an

56 f both TA-specific CD8(+) T cells and CD8(+) TILs.

57 08:02-restricted T cell receptor from CD8(+) TILs that targeted the KRAS(G12D) hotspot driver mutatio

58 t drives a dysfunctional phenotype in CD8(+) TILs.

59 ortantly, 48 hours after irradiation, CD8(+) TILs showed brighter expression of CD137 and PD1, thereb

60 Moreover, CD8(+) TILs from patients exhibited downregulation of the costi

61 evaluated unique phenotypic traits of CD8(+) TILs and TCR beta chain (TCRbeta) clonotypic frequency i

62 uring tumor progression regardless of CD8(+) TILs' antigen specificity.

63 B and LAG-3 was seen on a majority of CD8(+) TILs, but not in lymphoid organs.

64 s demonstrate that PD-1 expression on CD8(+) TILs also accurately identifies the repertoire of clonal

65 lobulin and mucin domain 3 (TIM-3) on CD8(+) TILs identified the autologous tumor-reactive repertoire

66 T cells, and that PD-1 expression on CD8(+) TILs is not always associated with repeated Ag encounter

67 High frequencies of CD3(+) or CD8(+) TILs, Foxp3(+) Tregs, and PD-1(+) TILs were strongly ass

68 metabolic switch partially preserves CD8(+) TILs' effector functions, although co-inhibitor expressi

69 Thus, functional virus-specific CD8(+) TILs could skew the results of prognostic or diagnostic

70 Virus-specific CD8(+) TILs migrated into cutaneous melanoma lesions during acu

71 These data suggest that CD8(+) TILs can reflect an individual's immune status, rather t

72 mouse melanoma models, we report that CD8(+) TILs enhance peroxisome proliferator-activated receptor

73 munofluorescence analysis showed that CD8(+) TILs expressing high Kv1.3 preferentially localized in t

74 r Cell, Zhang et al. demonstrate that CD8(+) TILs reprogram under hypoxic and hypoglycemic conditions

75 Although it is generally assumed that CD8(+) TILs will be tumor-associated Ag (TAA) specific, it is u

76 promoting FA catabolism improves the CD8(+) TILs' ability to slow tumor progression.

77 PD-1(-)TIGIT(+), and PD-1(+)TIGIT(-) CD8(+) TILs had similar functional capacities ex vivo, suggesti

78 Fewer HR+ tumors demonstrated CD8+ TIL (43%; range, 30%-73%).

79 21, IL-22, TNF-alpha or IL-6 does not change TIL-derived supernatant-driven STAT3 and NF-kB activatio

80 lockade delays tumor growth without changing TIL metabolism or functions.

81 Methods to characterize TIL biology are increasingly important, and the authors

82 udies in this cancer subtype should consider TILs as a stratification factor and investigate whether

83 ed for binding to tumor digests and cultured TILs used for the treatment of patients.

84 interpretation of prognostic and diagnostic TIL assays.

85 skew the results of prognostic or diagnostic TIL assays.

86 I cancer patients tested (9% of 188 distinct TIL cultures) and in 9 of 10 melanoma patients (43% of 2

87 of 10 melanoma patients (43% of 246 distinct TIL cultures).

88 s depleted in patients with highly divergent TIL repertoires.

89 Notably, gene expression induced during TIL hypofunction more closely resembled self-tolerance t

90 arkers defining tumor-specific dysfunctional TILs, and PD-1 alone is not sufficient.

91 of cytokine production by the dysfunctional TILs, with only limited changes in gene expression and c

92 seven patients responded to CD8(+)-enriched TILs (35% v 20%; not significant).

93 the evidence indicates that CD8(+)-enriched TILs are not more potent therapeutically and they are mo

94 unselected young TILs versus CD8(+)-enriched TILs.

95 ssociation between PD-L1 protein expression, TILs, and clinicopathological features were determined.

96 microenvironment and in vitro culture of FL TILs could restore cytokine signaling in the PD-1(hi) su

97 c, because tonsil T cells were similar to FL TILs.

98 rable lesions for at least 5 years following TIL treatment.

99 (84%) of 808 participants were evaluable for TILs, including 519 (77%) archival samples, 155 (23%) fr

100 Sections were scored for TILs on hematoxylin-eosin (H&E)-stained sections, and im

101 Four TIL-derived TCRs exhibited strong selection for peptides

102 re analyzed and CD3(+), CD8(+), and FOXP3(+) TIL densities were quantitated.

103 ells were detected at low frequency in fresh TIL cultures shortly after extraction from the tumor.

104 However, T cells from TILs show a functional switch compared with those from L

105 esions and assess their impact on gammadelta TIL recruitment in vivo.

106 The majority of 481 evaluable cancers had TILs (sTILs, 80%; iTILs, 15%).

107 bset of viral-negative tumors exhibited high TILs and PD-L1 expression, corresponding with the higher

108 Expression of PD-L1 was correlated with high TILs using both E1L3N (P = .007) and SP142 (P = .02).

109 astuzumab, and pertuzumab or placebo, higher TIL values are significantly associated with improved ov

110 astuzumab, and pertuzumab or placebo, higher TIL values are significantly associated with improved ov

111 However, TILs show an overall hydrophilic character and do not co

112 regression of metastatic melanoma; however, TILs are a heterogeneous population, and there are no ef

113 cer can occur after a single infusion of HPV-TILs.

114 pillomavirus (HPV) E6 and E7 reactivity (HPV-TILs).

115 uppressive effects of Tregsin vitro In human TIL cultures, MK-4166 induced phosphorylation of NFkappa

116 spite being drastically lower in other human TILs and in many human peripheral blood populations.

117 ore set of genes that defined hypofunctional TIL; these data comprise the first molecular profile of

118 This may greatly improve TIL persistence and anti-tumor activity in vivo after ad

119 optive transfer of these T cells may improve TIL therapy for melanoma and permit its broader applicat

120 a monoclonal expansion of the Vh7 family in TIL-B, also present in a tumor-associated LN.

121 ly, the presence of these regulatory ILCs in TIL cultures corresponded with a striking reduction in t

122 s of memory (e.g., long-term persistence) in TIL that are characteristically exhausted and senescent

123 presence of this CD56(+)CD3(-) population in TIL cultures was associated with reduced T cell numbers,

124 0% reduction in functional Kv1.3 channels in TILs as compared with peripheral blood T cells from pair

125 Upregulation of TNF-alpha expression in TILs strongly correlated with an increase in the total a

126 f 138) were positive for PD-L1 expression in TILs, defined as greater than 5% positive immunohistoche

127 efective Kv1.3 channels and Ca(2+) fluxes in TILs may contribute to reduced immune surveillance in HN

128 3.77 (3.50-4.22) years, every 1% increase in TILs was associated with a 3% decrease in the rate of an

129 PD-1 was overexpressed in TILs (81% vs 28%; P < .001) and peritumoral lymphocytes

130 ainst TIM3, LAG3, or CTLA4 further increased TIL functions.

131 tion of hRT and anti-PD-1 strongly increased TIL numbers, and even very large tumors were completely

132 pression on stromal (sTILs) and intratumoral TILs.

133 gnaling in renal tubulointerstitial lesions (TILs), a major prognostic feature of renal inflammation

134 n, we isolate tumor-infiltrating leukocytes (TILs) and lamina propria mononuclear cells (LPMCs) from

135 for studying tumor-infiltrating leukocytes (TILs) in 23 cancer types profiled by The Cancer Genome A

136 nsists of 2 domains, trypsin-inhibitor-like (TIL') and E', of which the TIL' domain lacks extensive s

137 We provide evidence that links TIL abundance and therapeutic outcome to the regulation

138 proposed role in protecting membrane lipids, TILs have been reported to be associated to cell membran

139 Temperature-induced lipocalins (TILs) play an essential role in the response of plants t

140 chips thin-coated with tailored ionic liquid TIL 1.

141 d is associated with patients exhibiting low TIL divergence and is depleted in patients with highly d

142 Lower TIL grade for NRAS+ melanoma suggests it has a more immu

143 ained tumour samples had significantly lower TIL values than did archival samples (10.00% [95% CI 5.0

144 egrin on lung tumor-infiltrating lymphocyte (TIL) clones in promoting specific TCR-mediated epithelia

145 -3.3]), lower tumor-infiltrating lymphocyte (TIL) grade (nonbrisk, 0.5 [0.3-0.8]; and brisk, 0.3 [0.5

146 can increase tumor-infiltrating lymphocyte (TIL) numbers.

147 In tumor-infiltrating B lymphocytes (TIL-B), both switched memory cells and plasmablasts were

148 We isolated tumor-infiltrating lymphocytes (TIL) and intra-hepatic lymphocytes.

149 ionship with tumor-infiltrating lymphocytes (TIL) and PD-L1 IHC expression.

150 e status of T-cell-infiltrating lymphocytes (TIL) and PD-L1 in MCC tumors.

151 increase in tumor-infiltrating lymphocytes (TIL) and T cells, as revealed by real-time imaging in vi

152 Tumor-infiltrating lymphocytes (TIL) are potent mediators of an antitumor response.

153 lly modified tumor-infiltrating lymphocytes (TIL) by inhibitory receptors (IR), namely PD1.

154 (ACT) using tumor-infiltrating lymphocytes (TIL) can induce tumor regression in up to 50% or more of

155 xhaustion of tumor-infiltrating lymphocytes (TIL) correlated with expression of PD-1 ligands by tumor

156 tic value of tumor-infiltrating lymphocytes (TIL) expressing CD3, Foxp3, or NKp46 (NCR1) in a cohort

157 e found that tumor-infiltrating lymphocytes (TIL) expressing PD-1 can recognize autologous tumor cell

158 nstrate that tumor-infiltrating lymphocytes (TIL) from a patient with metastatic cholangiocarcinoma c

159 ironment and tumor-infiltrating lymphocytes (TIL) in a B-RafV600E/Pten-driven murine model of melanom

160 transfer of tumor-infiltrating lymphocytes (TIL) in a randomized fashion.

161 pression of tumour-infiltrating lymphocytes (TIL) is a common feature of advanced cancer, but its bio

162 presence of tumor-infiltrating lymphocytes (TIL) is a favorable prognostic factor in breast cancer,

163 g autologous tumor-infiltrating lymphocytes (TIL) results in complete regression of advanced cancer i

164 r density of tumor-infiltrating lymphocytes (TIL) than other colorectal cancers.

165 lt in CD8(+) tumor-infiltrating lymphocytes (TIL) with a hypofunctional phenotype incapable of tumor

166 d autologous tumor-infiltrating lymphocytes (TIL), we show how MHC class II expression on melanoma ce

167 portion of tumor-infiltrating T lymphocytes (TIL) (n = 24, Mann-Whitney p = 0.047).

168 relates of tumor-infiltrating T lymphocytes (TIL) in squamous cell carcinoma (SCC), using a systems b

169 naive and tumor-infiltrating T lymphocytes (TIL).

170 ucing CD4(+) tumor-infiltrating lymphocytes (TILs) and aggressive disease.

171 presence of tumor infiltrating lymphocytes (TILs) and five-year-event-free-survival were examined.

172 h autologous tumor-infiltrating lymphocytes (TILs) and high-dose interleukin-2 (IL-2) administered to

173 we evaluated tumor-infiltrating lymphocytes (TILs) and immunologically relevant genes in the neoadjuv

174 valuation of tumor-infiltrating lymphocytes (TILs) and PD-1 and PD-L1 expression was performed in 63

175 es of CD8(+) tumor-infiltrating lymphocytes (TILs) and used genetic perturbations to identify a disti

176 dicates that tumor-infiltrating lymphocytes (TILs) are associated with clinical outcomes and may pred

177 suggest that tumor-infiltrating lymphocytes (TILs) are associated with disease-free (DFS) and overall

178 that CD8(+) tumor-infiltrating lymphocytes (TILs) are correlated with positive prognoses in cancer p

179 ificities of tumor-infiltrating lymphocytes (TILs) are not well understood.

180 transfer of tumor-infiltrating lymphocytes (TILs) can mediate cancer regression in patients with met

181 transfer of tumor-infiltrating lymphocytes (TILs) can mediate regression of metastatic melanoma; how

182 autologous tumour-infiltrating lymphocytes (TILs) could mediate regression of metastatic uveal melan

183 ts receiving tumor-infiltrating lymphocytes (TILs) for metastatic melanoma reveals a substantial subs

184 strated that tumor-infiltrating lymphocytes (TILs) from 9 out of 10 patients with metastatic gastroin

185 hat inhibits tumor-infiltrating lymphocytes (TILs) from high-grade serous tumors, defined their suppr

186 s and CD8(+) tumor-infiltrating lymphocytes (TILs) from patients with melanoma, and these TIGIT-expre

187 Tumor infiltrating lymphocytes (TILs) have been associated with favorable prognosis in m

188 rtion of the tumor-infiltrating lymphocytes (TILs) in claudin-low tumors, and Tregs isolated from tum

189 antities of tumour-infiltrating lymphocytes (TILs) in primary HER2-positive breast cancer are associa

190 presence of tumor-infiltrating lymphocytes (TILs) indicates an endogenous antitumor response, immune

191 presence of tumor-infiltrating lymphocytes (TILs) is a favorable prognostic factor in breast cancer,

192 presence of tumor-infiltrating lymphocytes (TILs) is associated with improved outcomes in human epid

193 Tumor-infiltrating lymphocytes (TILs) possessed higher VJ-independent diversity than non

194 urvival with tumor-infiltrating lymphocytes (TILs) present in primary melanomas, it is uncertain whet

195 valuation of tumor-infiltrating lymphocytes (TILs) relies on histopathological measurements with limi

196 ty in CD8(+) tumor-infiltrating lymphocytes (TILs) that recognize a model tumor antigen and have feat

197 Tumor-infiltrating lymphocytes (TILs) were scored in hematoxylin-eosin slides using curr

198 or cells and tumor-infiltrating lymphocytes (TILs) with PD-L1 expression, intensities of expression,

199 linked with tumor-infiltrating lymphocytes (TILs), and a repressed CSC metagene signature.

200 abundance of tumor-infiltrating lymphocytes (TILs), and expression of the immune checkpoints were inv

201 h increased tumour infiltrating lymphocytes (TILs), however, MAPK activity is required for T cells fu

202 toxic CD8(+) tumor-infiltrating lymphocytes (TILs), leading to a major delay in breast cancer and mel

203 nally active tumor-infiltrating lymphocytes (TILs), the tumor specificity of these TILs, and the corr

204 How tumor-infiltrating T lymphocytes (TILs) adapt to the metabolic constrains within the tumor

205 ransferred tumor-infiltrating T lymphocytes (TILs) that mediate complete regression of metastatic mel

206 eated with hRT alone, accompanied by massive TIL apoptosis.

207 The MeTIL signature measured TIL distributions in a sensitive manner and predicted su

208 The median TIL value was 10% (IQR 5-30).

209 FAS as an additional cause of bsAb-mediated TIL depletion.

210 esult of melanoma was 30% less with nonbrisk TIL grade (hazard ratio [HR], 0.7; 95% CI, 0.5 to 1.0) a

211 regions observed in bystander, nonexhausted TILs and in acutely restimulated CD8(+) T cells, we defi

212 In support of these observations, TILs from these mice released higher levels of IFN-gamma

213 lyses the effects of local administration of TIL on ligature-induced periodontitis in rats.

214 hat the main challenge to the development of TIL adoptive cell transfer for metastatic GI cancers may

215 experimental periodontitis and the dosage of TIL may influence its anti-inflammatory and antiresorpti

216 logic inhibition of Akt enables expansion of TIL with the transcriptional, metabolic, and functional

217 on therapies to boost anti-tumor function of TIL specifically against tumor cells.

218 protein expression and analyze any impact of TIL-expressed genes on outcome.

219 cer with no, intermediate, or high levels of TIL and assess variations in lymphocytic cell subsets ac

220 Conclusions and Relevance: The magnitude of TIL is variable within and between breast cancer subtype

221 indicates that the backbone malleability of TIL' is important for its biological activity.

222 ylation markers to identify a methylation of TIL (MeTIL) signature that recapitulates TIL evaluations

223 nhibition results in enhanced persistence of TIL after adoptive transfer into an immunodeficient anim

224 herapy may be limited by poor persistence of TIL after adoptive transfer.

225 The molecular profile of TIL was further dissected to determine the extent of ove

226 As suggested by the molecular profile of TIL, protein expression of inhibitory receptor LAG-3 was

227 onstrated MHC class I-mediated reactivity of TIL against autologous tumor in 5 of 7 GI cancer patient

228 functions and the prognosis significance of TIL subpopulations in non-small cell lung carcinoma (NSC

229 After adoptive transfer of TIL containing about 25% mutation-specific polyfunctiona

230 ssion on CD8(+) cells suggested that 0-3% of TILs expanded from GI cancer metastases were tumor-react

231 also present between beta-strands 5 and 6 of TILs.

232 potential association between the ability of TILs to mediate durable regressions and their ability to

233 , in addition to enhancing the activation of TILs, MK-4166 may attenuate the Treg-mediated suppressiv

234 ter than did histopathological assessment of TILs or gene expression-based immune markers, respective

235 haracterization of immune cell complexity of TILs and LPMCs reveals no differences in the percentages

236 2197 and E1199 were evaluated for density of TILs in intraepithelial (iTILs) and stromal compartments

237 mately 16% of cancers showing no evidence of TILs.

238 y, we compared the phenotype and function of TILs derived from liver and lung metastases from patient

239 We seek to validate the prognostic impact of TILs in primary TNBCs in two adjuvant phase III trials c

240 median (interquartile range [IQR]) level of TILs was 12.5% (5.0%-30.0%), with levels lower in hormon

241 For the pCR end point, levels of TILs greater than 5% were associated with higher pCR rat

242 Levels of TILs were examined for their associations with efficacy

243 y in patients with low to moderate levels of TILs.

244 ted with high neoantigen loads and number of TILs, which is counterbalanced by overexpression of PD-1

245 We evaluated levels of percentage of TILs using hematoxylin-eosin-stained core biopsy section

246 The presence of TILs at diagnosis is an independent, positive, prognosti

247 ity as represented by baseline quantities of TILs in patients with advanced HER2-positive breast canc

248 To investigate the role of TILs, particularly cytotoxic CD8+ T cells, in the predic

249 RC and show that the culture supernatants of TILs, but not of LPMCs, potently enhance the growth of h

250 motif open the possibility that targeting of TILs to cell membranes could be mediated by interaction

251 ufficient for the intracellular targeting of TILs.

252 ucts as the primary immunological targets of TILs from melanomas.

253 Herein, we review recent clinical trials of TILs and antigen receptor gene therapy for advanced canc

254 ribution of reduced Kv1.3 and Ca(2+) flux on TIL effector function in head and neck cancer (HNC).

255 to a flexible, positively charged region on TIL', which is supported by the rigid scaffold of the TI

256 orphan" T cell receptors (TCRs) expressed on TILs from human colorectal adenocarcinoma.

257 se TILs, and the correlation between patient TILs and long-term survival.

258 ts recognized by effective melanoma-reactive TILs remain elusive.

259 of TIL (MeTIL) signature that recapitulates TIL evaluations and their prognostic value for long-term

260 June 7, 2013, and Sept 9, 2016, and received TIL therapy.

261 IL-36R knockout UUO mice, also reduced renal TIL formation in UUO mice.

262 ing contributes to the pathogenesis of renal TILs through the activation of the NLRP3 inflammasome an

263 s and urine samples from patients with renal TILs correlated with renal function impairment.

264 anced survival capability of CD8(+) post-REP TIL when re-cultured in the absence or presence of cytok

265 ide a rationale for the use of PD-1-selected TILs in ACT.

266 ated the antitumor activity of PD-1-selected TILs in vivo In two mouse models of solid tumors, we sho

267 he first molecular profile of tumor-specific TIL that are naturally responding and represent a polycl

268 ific TILs, in sharp contrast to TAA-specific TILs in the same tumors.

269 entification and isolation of tumor-specific TILs without previous knowledge of their antigen specifi

270 Virus-specific TILs developed independently of viral Ag in the tumor an

271 orrelate with dysfunction for virus-specific TILs, in sharp contrast to TAA-specific TILs in the same

272 justed for age, sex, site, AJCC tumor stage, TIL grade, and study center.

273 oint Committee on Cancer (AJCC) tumor stage, TIL grade, and study center.

274 umab did not differ significantly by stromal TIL value for either progression-free survival (pinterac

275 ariate Cox regression models fitting stromal TILs as a continuous variable (per 10% increment).

276 aluated before random assignment for stromal TILs and lymphocyte-predominant BC (LPBC).

277 erall survival, each 10% increase in stromal TILs was significantly associated with longer overall su

278 We assessed the quantity of stromal TILs in prospectively collected tumour samples and inves

279 Increased levels of stromal TILs predicted pCR in univariable (P < .001) and multiva

280 demonstrated that this population suppressed TIL expansion and altered TIL cytokine production.

281 he collective impact of pathways suppressing TIL function, we compared genome-wide mRNA expression of

282 Here the authors show that TILs activity following MEK inhibition can be enhanced b

283 ellular localization studies have shown that TILs are targeted to a variety of cell membranes and org

284 Three of the TIL TCRs were specific for non-mutated self-antigens, tw

285 ch is supported by the rigid scaffold of the TIL' and E' domain beta sheets.

286 Furthermore, surface-charge mapping of the TIL'E' structure reveals a potential mechanism for the e

287 n-inhibitor-like (TIL') and E', of which the TIL' domain lacks extensive secondary structure, is stri

288 cytes (TILs), the tumor specificity of these TILs, and the correlation between patient TILs and long-

289 This TIL subset also displays increased activation-induced ce

290 In EP-TIL0.1, EP-TIL0.3, and EP-TIL1, TIL solutions of 0.1, 0.3, and 1 mg/kg body weight, resp

291 ls, and addition of anti-NKp46 antibodies to TIL cultures abrogated the ability of these regulatory I

292 de (HR, 0.5; 95% CI, 0.3 to 0.9) relative to TIL absence, adjusted for age, sex, site, and AJCC tumor

293 n primary melanomas, it is uncertain whether TILs provide prognostic information beyond existing mela

294 rences in survival for malignancies in which TILs were not known to have a prognostic value.

295 e primary end point of DFS, association with TIL scores was determined by fitting proportional hazard

296 Compared with TIL that did not express these inhibitory receptors, CD8

297 e fraction of CDR3 reads was associated with TILs fraction, tumor purity, adaptive immunity gene expr

298 s responded to therapy with unselected young TILs (according to Response Evaluation Criteria in Solid

299 ctively assigned to receive unselected young TILs versus CD8(+)-enriched TILs.

300 ure studies should focus on unselected young TILs.