ライフサイエンスコーパス: TIL

1 TIL correlated moderately ( approximately 0.50) with PD1

2 TIL density profiles across the IZ are used to compute a

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

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

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

6 es in the transcriptional profile of PD-1(-) TILs.

7 are required to accurately estimate absolute TIL numbers.

8 ulation suppressed TIL expansion and altered TIL cytokine production.

9 Although TIL-tumor cell couples readily formed, couple stability

10 c, and epigenetic regulation of Trm cell and TIL development and function is largely undefined.

11 0 was specifically required for Trm cell and TIL development and polyfunctionality.

12 ts into the local regulation of Trm cell and TIL function.

13 metabolic regimen that promoted Trm cell and TIL gene signatures associated with tissue residency and

14 hanistically, Bhlhe40 sustained Trm cell and TIL mitochondrial fitness and a functional epigenetic st

15 sociated with complete cancer regression and TIL persistence and a terminally differentiated CD39-pos

16 Both tumor and TIL analyses were evaluated by using three convolutional

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

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

19 L5 expression prevented Cxcl9 expression and TILs loss, and attenuated tumor growth in mice through I

20 generate combined maps of cancer regions and TILs in routine diagnostic breast cancer whole slide tis

21 The test for interaction between RT and TILs was not statistically significant (P = .317).

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

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

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

25 effector functions among APC and autologous TILs.

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

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

28 adoptive T-cell transfer (ACT) of autologous TILs.

29 In multivariable analyses, automated TIL scores show an independent association with disease-

30 Therefore, the open source, automated TIL scoring is an independent prognostic marker in melan

31 m 2 institutions, we show that the automated TIL scoring algorithm separates patients into favorable

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

33 our findings imply that an interplay between TIL, charged membrane lipids, BAR domain, and SH3 domain

34 DAC inhibits tumor growth and increases both TILs and a subset of tumor-infiltrating M2-polarized mac

35 e analysis showed that patients with a brisk TIL score had improved melanoma-specific survival than t

36 Compared to bystander TILs, TSA-reactive TILs possess a distinct T cell recept

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

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

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

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

41 We found that CD4(+) TILs from one patient recognized mutated C-terminal bind

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

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

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

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

46 r specificity of cells derived from bulk CD8 TILs.

47 therapy was administered after PD-1(hi) CD8 TILs had become reduced in frequency and/or function.

48 y and/or functional capacity of PD-1(hi) CD8 TILs in tumor-bearing sepsis survivors, checkpoint block

49 development of sepsis-induced lesions in CD8 TILs.

50 Direct ex vivo analysis of CD8 TILs from CLP hosts showed decreased proliferation, IFN-

51 septic environment reduced the number of CD8 TILs with high expression of activating/inhibitory recep

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

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

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

55 Dysfunctional CD8(+) TILs possess canonical epigenetic and transcriptional fe

56 Consequently, progenitor exhausted CD8(+) TILs are better able to control tumor growth than are te

57 Exhausted CD8(+) TILs include a subpopulation of 'progenitor exhausted' c

58 Conditional deletion of the GR in CD8(+) TILs improved effector differentiation, reduced expressi

59 dogenous steroid hormone signaling in CD8(+) TILs promotes dysfunction, with important implications f

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

61 Bulk and single-cell RNA profiles of CD8(+) TILs after combined Tim-3+PD-1 blockade in preclinical m

62 murine tumors, a large proportion of CD8(+) TILs had decreased surface expression of CD226 and exhib

63 moting BLIMP1-dependent exhaustion of CD8(+) TILs that limits effective anti-tumor immunity.

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

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

66 ssociated transcriptomic signature of CD8(+) TILs.

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

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

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

70 dysfunctional phenotype, TSA-reactive CD8(+) TILs possess substantial capabilities of proliferation a

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

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

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

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

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

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

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

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

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

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

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

82 um(2) represented by a covalently conjugated TIL region from the beta1-adrenergic receptor.

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

84 mma in TILs was correlated with high-density TILs; and IFN-gamma in tumor cells was correlated with a

85 of T-cell subset and pathologist-determined TIL score.

86 interpretation of prognostic and diagnostic TIL assays.

87 skew the results of prognostic or diagnostic TIL assays.

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 sociated myeloid cells,v leading to enhanced TIL expansion and function.

93 Progenitor exhausted TILs can respond to anti-PD-1 therapy, but terminally ex

94 anti-PD-1 therapy, but terminally exhausted TILs cannot.

95 nd differentiate into 'terminally exhausted' TILs.

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

97 e40 expression, and Bhlhe40 was critical for TIL reinvigoration following anti-PD-L1 blockade.

98 (84%) of 808 participants were evaluable for TILs, including 519 (77%) archival samples, 155 (23%) fr

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

100 Four TIL-derived TCRs exhibited strong selection for peptides

101 on of cases with high-density CD4(+)FOXP3(+) TILs by FOXP3:CD4 ratio enables refinement of prognostic

102 Low density of stromal CD4(+)FOXP3(+) TILs within TCe and IF was identified as an independent

103 ets mediating ACT response are distinct from TIL subsets enriched for antitumor reactivity.

104 To address this, we generated TIL cultures from patients with primary bladder cancer a

105 Altogether, 670 (71%) of patients had TILs less than 10%.

106 d features of dysfunction, whereas CD226(hi) TILs were highly functional.

107 0.42; 95% CI, 0.29 to 0.61; P < .001), high TILs (HR, 0.61; 95% CI, 0.39 to 0.96, P = .033) grade (3

108 0.24 to 0.58; P < .001) but not in the high TILs group (HR, 0.58; 95% CI, 0.28 to 1.19; P = .138).

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

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

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

112 had improved survival, likely due to higher TIL and M1 macrophage infiltration as well as lower intr

113 ble and poor prognosis cohorts, where higher TILs scores were associated with favorable prognosis.

114 have generally low and spatially homogenous TIL burdens, although a small proportion exhibit higher

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 g exhausted tumor-infiltrating ilymphocytes (TILs).

119 o the development of metabolic exhaustion in TIL.

120 l inter- and intra-tumoural heterogeneity in TIL burden within a retrospective cohort of primary LMS

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

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

123 This correlation was seen also in TILs isolated from HNSCC patients.

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

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

126 nistically, reduced mitochondrial fitness in TILs was induced by the coordination of T cell receptor

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

128 d stromal content, and high BA; IFN-gamma in TILs was correlated with high-density TILs; and IFN-gamm

129 Increases in TILs and CD8+ T cell proportions in response to NAC are

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

131 terface, reduced Ca(2+) signaling, increased TIL locomotion, and impaired tumor cell killing.

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

133 ation IL-2 reduces toxicity while increasing TILs that potentiate combined cancer therapies.

134 Local PD-1 signaling inhibited TIL Bhlhe40 expression, and Bhlhe40 was critical for TIL

135 To provide insight into TIL-based immunotherapy, we studied a successful case of

136 pression on stromal (sTILs) and intratumoral TILs.

137 D' with its TIL' and E' modules projects away from D3.

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

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

140 Effector- and memory-precursor-like TILs contained tumor-antigen-specific cells, exhibited p

141 Tumor-reactive stem-like TILs were capable of self-renewal, expansion, persistenc

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

143 percentage infiltration of stromally located TILs (sTILs) that were quantified in the same manner in

144 h the proline-rich third intracellular loop (TIL) of various G-protein-coupled receptors (GPCRs), and

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

146 l categorisation of tumours with high or low TIL burden, but that many more cores (>=11) are required

147 eased HLA expression was associated with low TIL density, pronounced stromal content, and high BA; IF

148 RT was significantly beneficial in the low TILs group (HR, 0.37; 95% CI, 0.24 to 0.58; P < .001) bu

149 st that patients with breast cancer with low TILs may derive a larger benefit from RT regarding the r

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

151 ession caused tumor-infiltrating lymphocyte (TIL) desertification, whereas forced CCL5 expression pre

152 e immune cell tumor-infiltrating lymphocyte (TIL) score for correlation with melanoma patient outcome

153 rgoing either tumor infiltrating lymphocyte (TIL)-based or anti- programmed death 1 (PD1) immunothera

154 e transfer of tumor-infiltrating lymphocyte (TIL)-based therapies.

155 nd abundance (tumor infiltrating lymphocyte, TIL, burden).

156 tion between tumor-infiltrating lymphocytes (TIL) and cancer cells for metabolic resources often rend

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

158 to attack by tumor infiltrating lymphocytes (TIL) and macrophages.

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

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

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

162 activity in tumor-infiltrating lymphocytes (TIL) induces cellular senescence and limits tumor suppre

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

164 en tumor and tumor-infiltrating lymphocytes (TIL) is increasingly important in both basic science and

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

166 ) and CD8(+) tumor-infiltrating lymphocytes (TIL), PD1 expression, and tumor necrosis while slowing t

167 panded human tumor-infiltrating lymphocytes (TIL), proliferating TILs, and in vitro differentiated ne

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

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

170 reactivate tumor-infiltrating T lymphocytes (TIL), for example, by cytokines or immune checkpoint blo

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

172 se of CD8(+) tumor-infiltrating lymphocytes (TILs) after checkpoint blockade therapy.

173 ector CD8(+) tumor-infiltrating lymphocytes (TILs) after interaction with target tumor cells.

174 function of tumor-infiltrating lymphocytes (TILs) and resistance to immunotherapy.

175 rboring more tumor infiltrating lymphocytes (TILs) and up-regulation of inflammatory signatures predi

176 Tumor-infiltrating lymphocytes (TILs) are an important histopathologic feature of colore

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

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 ssessment of tumor infiltrating lymphocytes (TILs) as a prognostic variable in melanoma has not seen

181 d autologous tumor-infiltrating lymphocytes (TILs) can mediate complete regression of certain human c

182 uency of CD8 tumor-infiltrating lymphocytes (TILs) concomitant with an increased tumor burden.

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

184 function of tumor-infiltrating lymphocytes (TILs) for treating cancer patients with adoptive cell th

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

186 bundance of tumour infiltrating lymphocytes (TILs) has been shown to be a key prognostic indicator in

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

188 e of stromal tumor infiltrating lymphocytes (TILs) have not been studied.

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

190 tic value of tumor-infiltrating lymphocytes (TILs) in early-stage triple negative breast cancer (TNBC

191 elevance of tumour-infiltrating lymphocytes (TILs) in leiomyosarcoma (LMS), a subtype of soft tissue

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

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

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

195 ilution from tumor-infiltrating lymphocytes (TILs) permitted functional validation regarding neoantig

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

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

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

199 f endogenous tumor-infiltrating lymphocytes (TILs) that recognize cancer neoantigens.

200 splenic and tumor-infiltrating lymphocytes (TILs) was impaired and associated with enhanced tumor gr

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

202 tribution of tumor-infiltrating lymphocytes (TILs) within the tumor microenvironment provides strong

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

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

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

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

207 ivo expanded tumor-infiltrating lymphocytes (TILs).

208 usted CD8(+) tumor-infiltrating lymphocytes (TILs).

209 ional CD8(+) tumor-infiltrating lymphocytes (TILs).

210 rograms with tumor-infiltrating lymphocytes (TILs).

211 xpression on tumor-infiltrating lymphocytes (TILs); however, the underlying mediators and mechanisms

212 lial/stromal tumor-infiltrating lymphocytes (TILs; CD3(+)/CD4(+)/CD8(+)/CD4(+)FOXP3(+)/IL-17A(+)) wer

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

214 ognized by tumor-infiltrating T lymphocytes (TILs) from eight melanoma patients for all their class I

215 ctivity of tumor-infiltrating T lymphocytes (TILs).

216 ntly higher prognostic value than the manual TIL score (p = 0.0024).

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

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

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

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

221 Therefore, anionic lipids can modulate TIL/SH3 domain binding.

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

223 do not respond to immunotherapy with ACT of TIL or immune checkpoint blockade.

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

225 The impact of TIL phenotypes on clinical success of TIL-ACT is current

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

227 However, the current methods of TIL analysis are subjective and open to variability in i

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

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

230 An automated method for quantification of TIL abundance has the potential to facilitate better str

231 novel method for objective quantification of TIL abundance in OSCC histology images.

232 red to provide an accurate representation of TIL burden in a full tissue section.

233 act of TIL phenotypes on clinical success of TIL-ACT is currently unclear.

234 PD-1 thus contributes to the suppression of TIL function by inducing a state of impaired subcellular

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

236 ithm for image-based automated assessment of TILs on hematoxylin-eosin stained sections in melanoma.

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

238 this study was to analyze the association of TILs with the effect of postoperative RT on ipsilateral

239 is motivated by the biological definition of TILs as tumour infiltrating lymphocytes, with the added

240 evels and more heterogeneous distribution of TILs.

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

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

243 r survival outcomes based on the presence of TILs in colon cancer.

244 es and facilitate improved quantification of TILs.

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

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

247 This study shows that high values of TILs in the primary tumor independently seem to reduce t

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

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

250 state (CD39(+)CD69(+)) associated with poor TIL persistence.

251 ue microarrays (TMA) in studies that profile TIL burden is attractive but given the potential for int

252 nfiltrating lymphocytes (TIL), proliferating TILs, and in vitro differentiated neurons, suggesting a

253 The proposed TIL abundance (TILAb) score is calculated by first segme

254 o date has shown whether neoantigen-reactive TILs can be found in bladder tumors.

255 studies have identified neoantigen-reactive TILs from several types of cancer, no study to date has

256 is finding suggests that neoantigen-reactive TILs reside in bladder cancer, which may help explain th

257 Most antitumor neoantigen-reactive TILs were found in the differentiated CD39(+) state.

258 Compared to bystander TILs, TSA-reactive TILs possess a distinct T cell receptor (TCR) repertoire

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 novel immunogradient indicators that reflect TIL gradient towards the tumor.

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

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

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

265 ysis with IBTR as dependent variable and RT, TILs, subtype, age, and grade as independent variables,

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

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

268 hese findings suggest that TILs and specific TIL subsets serve as prognostic biomarkers for colorecta

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

270 ool of CD39(-) stem-like neoantigen-specific TILs that was lacking in ACT nonresponders.

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

272 strating that the majority of tumor-specific TILs after anti-PD-1 treatment have TCRs not identified

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

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

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

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

277 Stromal TILs were assessed on whole-section hematoxylin-eosin-st

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

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

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

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

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

283 factor VIII binds not only to the N-terminal TIL' domain of D' distal from D3 but also extends across

284 We observed that TIL recruits endophilin to membranes composed of 95 mol%

285 Furthermore, we show that TIL electrostatically interacts with membranes composed

286 These data suggest that TIL subsets mediating ACT response are distinct from TIL

287 We found that TILs accumulated depolarized mitochondria as a result of

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

289 These findings suggest that TILs and specific TIL subsets serve as prognostic biomar

290 can be facilitated through detection of the TIL of activated GPCRs in addition to binding to anionic

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

292 Four T cell receptors (TCRs) made up the TIL infusion and recognized two KRAS-G12D neoantigens, a

293 the specificity, on average, of 12.2% of the TILs recognizing a mean of 3.1 shared antigen-derived ep

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

295 nd cutaneous melanoma that do not respond to TIL therapy or immune checkpoint blockade.

296 ls and a public data set consisting of tumor/TIL maps for 1090 invasive breast cancer images from The

297 More importantly, endophilin recruited via TIL tubulates vesicles and gets sorted onto highly curve

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

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

300 produces epigenome remodeling events within TIL resulting from loss of the histone methyltransferase