ライフサイエンスコーパス: CAR

1 CAR inactivates its constitutive activity by phosphoryla

2 CAR T cells were developed that upon specific recognitio

3 CAR Tregs were specifically activated and significantly

4 CAR undergoes a conversion from inactive homodimers to a

5 CAR-19 T cells will likely become an important treatment

6 CAR-DCN or vehicle was administrated systemically until

7 CAR-T therapies for MM are at an early stage of developm

8 CAR-Ts targeting B-cell maturation antigen have demonstr

9 CARs are synthetic receptors that reprogram immune cells

10 CARs demonstrated amidation activity for various acids a

11 CARs targeting CD19 have demonstrated remarkable potency

12 sion protein complexes (e.g., occludin-ZO-1, CAR-ZO-1, and N-cadherin-ss-catenin), through a down-reg

13 To test this hypothesis, we compared 3 CAR T-cell termination strategies: (1) transiently activ

14 The maximum tolerated dose was 10(6) CAR T cells per kg, and there were no deaths or instance

15 ow the maximum tolerated dose (</= 2 x 10(6) CAR-T cells/kg).

16 e levels (2 x 10(5), 2 x 10(6), or 2 x 10(7) CAR-T cells/kg).

17 icroextraction, such as fiber coating (85mum CAR/PDMS), extraction time (2min for white and 3min for

18 In this study, we developed a CAR T cell-based immunotherapeutic strategy to target TE

19 sion rate was 93% in patients who received a CAR T-cell product and 100% in the subset of patients wh

20 oxygen sensitive subdomain of HIF1alpha to a CAR scaffold, we generated CAR T-cells that are responsi

21 We have fused a soluble TCR construct to a CAR-signalling tail and named the final product TCR-CAR.

22 A) dephosphorylates threonine 38 to activate CAR.

23 ll populations to the CD3 and CD28-activated CAR-modified T cells that we use for therapy, we followe

24 ignificantly reduce the development of acute CAR-induced lung injury.

25 study, the role of systemically-administered CAR-DCN in AAA progression and rupture was assessed in a

26 emic off-tumor toxicity, micromolar affinity CAR T cells demonstrated superior anti-tumor efficacy an

27 contraction kinetics of micromolar affinity CAR T cells.

28 cells had no disease by flow cytometry after CAR-T cells.

29 0 of 133 patients (23%) within 28 days after CAR-T-cell infusion with an infection density of 1.19 in

30 infection occurred a median of 6 days after CAR-T-cell infusion.

31 ome (CRS) severity was the only factor after CAR-T-cell infusion associated with infection in a multi

32 Treatment with BAY 11-7082 or BBG 1 h after CAR injection attenuated pulmonary membrane thickening a

33 survival (median 6.6 months follow-up) after CAR-T cell immunotherapy.

34 Results Four weeks after CAR-T cell infusion, the overall response rate (complete

35 However, the use of allogeneic CAR T cells poses a concern in that it may increase risk

36 Although CARs were expressed at higher surface levels than TCRs,

37 esized that a combination of alpha-4-1BB and CAR T-cell therapy would result in improved antitumor re

38 g that direct interaction between HAdV-5 and CAR is not required.

39 ned disruption of inhibitory checkpoints and CAR T cell therapy remains incompletely explored.

40 In vivo, we show enhanced expansion and CAR T cell antitumor efficacy, culminating in improvemen

41 , synthetic immunotherapies such as mAbs and CAR T cells demonstrate impressive effects against child

42 sk of GVHD occurring with cumulative TCR and CAR signaling.

43 ment that both the T cell receptor (TCR) and CAR be engaged to accelerate T cell exhaustion.

44 nergy of conventional anticancer therapy and CAR T cells and heralds future studies for other treatme

45 lence of AAA was similar between vehicle and CAR-DCN groups, the severity of AAA in the CAR-DCN group

46 nsitivity and signaling capacity of TCRs and CARs has been limited due to their differences in affini

47 bserved at high Ag density for both TCRs and CARs suggested a role for negative regulators in both sy

48 n proliferated in response to FVIII and ANS8 CAR Tregs were able to suppress the proliferation of FVI

49 Importantly, ANS8 CAR-transduced Tregs also were able to suppress the reca

50 III-specific chimeric antigen receptor (ANS8 CAR) using a FVIII-specific scFv derived from a syntheti

51 Transduced ANS8 CAR T cells specific for the A2 domain proliferated in r

52 We engineered an armored CAR T cell capable of constitutive secretion of IL-12, a

53 kappa light chain are under investigation as CAR targets.

54 CD19 is an attractive CAR target, which is expressed in most B cell malignanci

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

56 Autologous CAR T cells are generated from the patient's peripheral

57 We engineered a third-generation APRIL-based CAR (ACAR), which killed targets expressing either BCMA

58 17 patients (88%) with marrow disease before CAR-T cells had no disease by flow cytometry after CAR-T

59 ses showed a significant association between CAR and prognosis, regardless of the cutoff value, cutof

60 lates the intramolecular interaction between CAR's DBD and ligand-binding domain (LBD), enabling the

61 achieve a remission had a median peak blood CAR(+) cell level of 15/muL ( P = .027).

62 achieved a remission had a median peak blood CAR(+) cell level of 98/muL and those who did not achiev

63 levels were associated with high peak blood CAR(+) cell levels ( P = .001) and remissions of lymphom

64 oblastic leukemia was conducted using a CD19 CAR product of defined CD4/CD8 composition, uniform CAR

65 ide and fludarabine lymphodepletion and CD19 CAR-T cells at or below the maximum tolerated dose (</=

66 received a target dose of 2x10(6) anti-CD19 CAR T cells per kilogram of body weight after receiving

67 duction to generate PD-1 deficient anti-CD19 CAR T cells.

68 d lymphodepleting chemotherapy and anti-CD19 CAR-T cells at one of three dose levels (2 x 10(5), 2 x

69 ed CD19(+) myeloma stem cells with anti-CD19 CAR-Ts is a novel approach to MM therapy.

70 hat manufacturing a defined-composition CD19 CAR T cell identifies an optimal cell dose with highly p

71 Conclusion CD19 CAR-T cells are highly effective in high-risk patients w

72 ted patients infused with donor-derived CD19 CAR T cells after allo-HSCT.

73 cilitate safer application of effective CD19 CAR T-cell therapy.

74 CRS in 133 adult patients who received CD19 CAR T cells.

75 ys 0 to 90 in 133 patients treated with CD19 CAR-T cells in a phase 1/2 study.

76 ve T cells expressing CD28-costimulated CD19 CARs experience enhanced stimulation, resulting in the p

77 icating hematologic malignancies (e.g., CD19 CARs in leukemias).

78 ric antigen receptors (CARs) targeting CD19 (CAR-19) have potent activity against acute lymphoblastic

79 ncy against B-ALL comparable to that of CD19-CAR at biologically active doses.

80 /15) of patients receiving >/=1 x 10(6) CD22-CAR T cells per kg body weight, including 5 of 5 patient

81 to establish the clinical activity of a CD22-CAR in B-ALL, including leukemia resistant to anti-CD19

82 ted CD22(+) cell escape from killing by CD22-CAR T cells.

83 trial testing a new CD22-targeted CAR (CD22-CAR) in 21 children and adults, including 17 who were pr

84 CD30.CAR-T expansion in peripheral blood peaked 1 week after

85 CD30.CAR-Ts are safe and can lead to clinical responses in pa

86 dose levels, from 0.2 x 108 to 2 x 108 CD30.CAR-Ts/m2, were infused without a conditioning regimen.

87 blood peaked 1 week after infusion, and CD30.CAR-Ts remained detectable for over 6 weeks.

88 as discontinued at least 4 weeks before CD30.CAR-T infusion.

89 ector to express the CD30-specific CAR (CD30.CAR-Ts) encoding the CD28 costimulatory endodomain.

90 d 9 months after the fourth infusion of CD30.CAR-Ts.

91 No toxicities attributable to CD30.CAR-Ts were observed.

92 d increased activation of both CD8+ and CD4+ CAR T cells.

93 CD7 CAR T cells produced robust cytotoxicity against maligna

94 Although CD7 CAR T cells were also toxic against unedited (CD7(+)) T

95 this fratricide and enabled expansion of CD7 CAR T cells without compromising their cytotoxic functio

96 and establishes the feasibility of using CD7 CAR T cells for the targeted therapy of T-cell malignanc

97 d with increased cytokine production of CD8+ CAR T cells and increased activation of both CD8+ and CD

98 Chimeric antigen receptor-modified T cells (CAR T cells) produce proinflammatory cytokines that incr

99 Success of CAR-T cells (CAR-Ts) against leukemia and lymphoma has encouraged dev

100 h highly activated chimeric antigen T cells (CAR-Ts) and second, re-animating endogenous quiescent T

101 vides a basic framework to use a multi-chain CAR as a platform to create the next generation of smart

102 ansduction in a FX-independent manner in CHO-CAR and SKOV3-CAR cells (CHO or SKOV3 cells transfected

103 Conclusion CAR-19 T cells preceded by low-dose chemotherapy induced

104 In conclusion, CAR-transduced Tregs are a promising approach for future

105 late CAR homodimerization, thus constraining CAR in its inactive form.

106 ion of CAR DBD T38D with CAR LBD, converting CAR to the homodimer form.

107 ast, first-generation and 4-1BB-costimulated CAR T cells increased the occurrence of GVHD.

108 To date, CAR T cells have demonstrated tremendous success in erad

109 implantable biopolymer devices that deliver CAR T cells directly to the surfaces of solid tumors, th

110 Interestingly, at high Ag density, CARs also mediated greater maximal release of some cytok

111 ologous T cells that express a CD19-directed CAR (CTL019) to treat patients with diffuse large B-cell

112 mbined with administration of tumor-directed CAR T cells to control the growth of solid tumors.

113 y of cases of grade >/=4 CRS occurred during CAR T-cell dose finding.

114 Under optimal experimental conditions (DVB/CAR/PDMS fibre coating, 40 degrees C, 30min extraction t

115 improved therapeutic efficacy of Cas9-edited CAR T cells and highlights the potential of precision ge

116 n of phosphorylated DBD with the LBD enables CAR to adapt a transient monomer configuration that can

117 has high translational potential to enhance CAR T cell efficacy in several cancer types.

118 (mini-body; HDPDL1) as a strategy to enhance CAR T-cell killing.

119 here that alpha-4-1BB significantly enhanced CAR T-cell efficacy directed against the Her2 antigen in

120 1BB has a multifunctional role for enhancing CAR T-cell responses and that this combination therapy h

121 Transduction of HAdV-5 KO1 and HAdV-5/F35 (CAR binding deficient) in the presence of Rag 2(-/-) ser

122 veral target pairings hold great promise for CAR therapy of AML.

123 A549 cells, suggesting a potential role for CAR.

124 Target antigens for CARs must be expressed on malignant cells, but expressio

125 cells, and a single-chain variable fragment CAR targeting BCMA alone resulted in outgrowth of a BCMA

126 Furthermore, CAR and DeltaCAR Tregs preferentially transmigrated acro

127 d ileum ASBT and decreased liver IL-10, FXR, CAR, VDR, BSEP, MRP2, MRP3, MRP4 was also observed in AN

128 Here we present a strategy to generate CAR T-cells that are only effective locally (tumor tissu

129 astly outperforming conventionally generated CAR T cells in a mouse model of acute lymphoblastic leuk

130 of HIF1alpha to a CAR scaffold, we generated CAR T-cells that are responsive to a hypoxic environment

131 HER2-CAR VSTs were detected in the peripheral blood for up to

132 eived 1 or more infusions of autologous HER2-CAR VSTs (1 x 106/m2 to 1 x 108/m2) without prior lympho

133 Infusion of autologous HER2-CAR VSTs is safe and can be associated with clinical ben

134 with a CD28.zeta-signaling endodomain (HER2-CAR VSTs).

135 Further evaluation of HER2-CAR VSTs in a phase 2b study is warranted as a single ag

136 rus and genetically modified to express HER2-CARs with a CD28.zeta-signaling endodomain (HER2-CAR VST

137 ity compared with treatment with either HER2.CAR T cells alone or HER2.CAR T cells plus Onc.Ad.

138 t with either HER2.CAR T cells alone or HER2.CAR T cells plus Onc.Ad.

139 ated by infusion of anti-PD-L1 IgG plus HER2.CAR T cells and coadministration of Onc.Ad in an HER2(+)

140 However, combining CAd-VECPDL1 with HER2.CAR T cells enhanced antitumor activity compared with tr

141 I: 1.58-2.56, p < 0.001) indicated that high CAR yielded worse survival in different cancers.

142 Higher CAR T-cell levels in blood were associated with response

143 ing cyclophosphamide and fludarabine, higher CAR T-cell dose, thrombocytopenia before lymphodepletion

144 titumor regimens, and receipt of the highest CAR-T-cell dose (2 x 10(7) cells per kg) had a higher in

145 e of the inhibitory microenvironment and how CAR T cells can be further engineered to maintain effica

146 However, CAR T cell treatments are less effective in solid tumors

147 ion and suppression of both murine and human CAR T cells.

148 ) expression on tumor cells can render human CAR T cells (anti-CD19 4-1BBzeta) hypo-functional, resul

149 However, specific human CAR (hCAR) antagonists are limited and conflicting data

150 of the DNA-binding domain (DBD) at Thr-38 in CAR regulates this conversion.

151 have been similar to toxicities observed in CAR-T trials for leukemia.

152 to AAA rupture was significantly reduced in CAR-DCN-treated mice compared to controls.

153 ngs in this report link an important role in CAR activation that is dependent upon oxidative stress.

154 liferation marker Ki67 in tumor-infiltrating CAR T cells when combined with alpha-4-1BB.

155 -ribosyl polymerase expression and inhibited CAR-induced apoptosis.

156 ggests that the financial incentives to join CAR currently exceed the costs.

157 tatively measure the presence of PFC-labeled CAR T cells, followed by histological validation.

158 tokines), cardiac fibrosis, apoptosis, lower CAR (Coxsackievirus and adenovirus receptor) expression

159 athematical modeling demonstrated that lower CAR sensitivity could be attributed to less efficient si

160 t generation of smarter self-decision making CAR T-cells.

161 Many CARs are designed with elements that augment T cell pers

162 This DBD-LBD interaction masked CAR's dimer interface, preventing CAR homodimer formatio

163 specific chimeric antigen receptor-modified (CAR) T cells has produced impressive antitumor responses

164 rovide preclinical proof-of-concept of NKG2D CAR T-cell activity in mouse glioma models and demonstra

165 nant CAR DBD-T38D, but not nonphosphorylated CAR DBD, bound the CAR LBD peptide.

166 t for both direct and indirect activation of CAR.

167 Our results indicate rapid adoption of CAR, with registered properties covering a total of 57 M

168 Additionally, blockade of CAR with soluble HAdV-5 fiber knob inhibited mouse serum

169 ful tool to elucidate the characteristics of CAR-modified T cells, regardless of the protocol used fo

170 red with an extended C-terminus comprised of CAR homing peptide that recognizes inflamed blood vessel

171 a and lymphoma has encouraged development of CAR-T therapies for MM.

172 Patients received a single dose of CAR-19 T cells 2 days after a low-dose chemotherapy cond

173 ese devices may improve the effectiveness of CAR T cell therapy in solid tumors and help protect agai

174 These findings uncover facets of CAR immunobiology and underscore the potential of CRISPR

175 ion strategies to augment the feasibility of CAR T-cell therapy for patients with AML.

176 of a target antigen overcomes fratricide of CAR T cells and establishes the feasibility of using CD7

177 holder interviews, we quantify the impact of CAR on deforestation and forest restoration, investigati

178 e, as well as the unaddressed integration of CAR T-cell therapy into conventional anticancer treatmen

179 e, EGF signaling weakened the interaction of CAR DBD T38D with CAR LBD, converting CAR to the homodim

180 before lymphodepletion, and manufacturing of CAR T cells without selection of CD8(+) central memory T

181 ouse glioma models by promoting migration of CAR T cells to the tumor site and increased effector fun

182 (BBG) (45.5 mg/kg, i.p.) in a mouse model of CAR-induced pleurisy.

183 be conducted to explore the critical role of CAR in survival of cancer patients.

184 Success of CAR-T cells (CAR-Ts) against leukemia and lymphoma has e

185 arget antigens and restricted trafficking of CAR T cells to and impaired long-term persistence at the

186 graft transplant model, adoptive transfer of CAR Tregs alleviated the alloimmune-mediated skin injury

187 vanced-stage lymphoma in a clinical trial of CAR-19 T cells preceded by low-dose chemotherapy.

188 Our results demonstrated that the use of CAR technology is a clinically applicable refinement of

189 Mechanistic understanding of CARs was used to expand reaction scope, generating bioca

190 Concurrently, the other CAR T cells that were present in bulk donor T cell popul

191 CAR homodimer and dissociates phosphorylated CAR into its monomers, exposing the PP2A/RACK1 binding s

192 Although very potent, CAR recognition is limited to membrane antigens which re

193 To identify potential CAR targets in acute myeloid leukemia (AML), we probed t

194 The DBD-T38D-LBD interaction also prevented CAR from forming a heterodimer with RXRalpha.

195 ion masked CAR's dimer interface, preventing CAR homodimer formation.

196 Recombinant DCN fusion protein CAR-DCN was engineered with an extended C-terminus compr

197 The C-reactive protein/albumin ratio (CAR) has been shown to play a significant prognostic rol

198 efractory large B-cell lymphoma who received CAR T-cell therapy with axi-cel had high levels of durab

199 The nuclear receptor CAR (NR1I3) regulates hepatic drug and energy metabolism

200 utcome of therapy with chimeric Ag receptor (CAR)-modified T cells is strongly influenced by the subs

201 ein constitutive active/androstane receptor (CAR or NR1I3) regulates several liver functions such as

202 The constitutive androstane receptor (CAR) plays an important role in xenobiotic metabolism, e

203 h expression of a chimeric antigen receptor (CAR) derived from the huLuc63 antibody (elotuzumab) and

204 lockage (ICB) and chimeric antigen receptor (CAR) for T-cell-based adoptive cell transfer are among t

205 g a CD30-specific chimeric antigen receptor (CAR) may reduce the side effects and augment antitumor a

206 Chimeric antigen receptor (CAR) T cell therapy has shown limited efficacy for the m

207 he application of chimeric antigen receptor (CAR) T cell therapy in cancers.

208 unotherapies with chimeric antigen receptor (CAR) T cells and checkpoint inhibitors (including antibo

209 In this study, chimeric antigen receptor (CAR) T cells expressing EGFRvIII targeting transgene wer

210 Chimeric antigen receptor (CAR) T cells have been highly successful in treating hem

211 Chimeric antigen receptor (CAR) T cells have proven that engineered immune cells ca

212 CD123-redirected chimeric antigen receptor (CAR) T cells in preclinical human acute myeloid leukemia

213 Chimeric antigen receptor (CAR) T cells targeting CD19 mediate potent effects in re

214 of high-affinity chimeric antigen receptor (CAR) T cells targeting hematological cancers has yielded

215 eloped anti-TRBC1 chimeric antigen receptor (CAR) T cells, which recognized and killed normal and mal

216 to the success of chimeric antigen receptor (CAR) T-cell based therapies greatly rely on the capacity

217 Chimeric antigen receptor (CAR) T-cell therapy is an emerging immunotherapy against

218 ologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy, showed efficacy in patients with re

219 cells modified by chimeric antigen receptor (CAR) that target CD19 in B-cell cancers, although data r

220 Chimeric antigen receptor (CAR) therapy targeting CD19 has yielded remarkable outco

221 he application of chimeric antigen receptor (CAR)-modified T cells in cancer immunotherapy.

222 uman coxsackievirus and adenovirus receptor [CAR]).

223 ammed to express chimeric antigen receptors (CAR T cells) consistently produce positive results in pa

224 Chimeric antigen receptors (CAR) are clinically translatable synthetic fusion protei

225 ric TCRs or synthetic chimeric Ag receptors (CARs).

226 ave emerged: the Chimeric Antigen Receptors (CARs) and T-cell Receptor (TCR) redirection.

227 Chimaeric antigen receptors (CARs) are a class of synthetic receptors that reprogram

228 Chimeric antigen receptors (CARs) are fusion proteins incorporating antigen-recognit

229 Chimeric antigen receptors (CARs) are synthetic receptors that redirect and reprogra

230 Chimeric antigen receptors (CARs) direct tumor cell recognition of adoptively transf

231 f BCMA targeting chimeric antigen receptors (CARs) suggest antigen downregulation at relapse.

232 ified to express chimeric antigen receptors (CARs) targeting CD19 (CAR-19) have potent activity again

233 disease-specific chimeric antigen receptors (CARs), so that they can combat tumour cells once they ar

234 tibodies [mAbs], chimeric antigen receptors [CARs]).

235 imetry assays also revealed that recombinant CAR DBD-T38D, but not nonphosphorylated CAR DBD, bound t

236 ients with AML treated with CD123-redirected CAR T cells and mandates novel approaches for toxicity m

237 Carboxylic acid reductases (CARs) catalyze the reduction of a broad range of carboxy

238 using data from state-level land registries (CAR) in Para and Mato Grosso that were precursors of SIC

239 nderlying molecular mechanism that regulates CAR activation, by placing phosphorylated threonine 38 a

240 role played by antigen density in regulating CAR function.

241 of the canonical anticommutation relations (CAR) algebra.

242 ted that durable leukemia remission required CAR T-cell persistence for 4 weeks prior to ablation.

243 ong with the development of oxygen-sensitive CAR T-cells, this work also provides a basic framework t

244 that examined the association between serum CAR and overall survival in patients with cancer.

245 a FX-independent manner in CHO-CAR and SKOV3-CAR cells (CHO or SKOV3 cells transfected to stably expr

246 recognition of normal lymphocytes by SLAMF7-CAR T cells and show that they induce selective fratrici

247 however, the fratricide conferred by SLAMF7-CAR T cells spares the SLAMF7(-/low) fraction in each ce

248 Consequently, SLAMF7-CAR T cells conferred rapid cytolysis of previously untr

249 addition, a single administration of SLAMF7-CAR T cells led to resolution of medullary and extramedu

250 data illustrate the potential use of SLAMF7-CAR T-cell therapy as an effective treatment against mul

251 ody (elotuzumab) and demonstrate that SLAMF7-CAR T cells prepared from patients and healthy donors co

252 After modification with the SLAMF7-CAR, both CD8(+) and CD4(+) T cells rapidly acquired and

253 the fate and function of individually sorted CAR-modified T cell subsets after activation with CD3 an

254 Here we show that directing a CD19-specific CAR to the T-cell receptor alpha constant (TRAC) locus n

255 troviral vector to express the CD30-specific CAR (CD30.CAR-Ts) encoding the CD28 costimulatory endodo

256 e show that the expression of a CD7-specific CAR impaired expansion of transduced T cells because of

257 l growth factor (EGF) was found to stimulate CAR homodimerization, thus constraining CAR in its inact

258 i-CD19 chimeric antigen receptor-modified T (CAR-T) cell therapy in patients with chronic lymphocytic

259 rgeted chimeric antigen receptor-modified T (CAR-T)-cell immunotherapy is a novel treatment for refra

260 By coexpression of two differently tagged CAR proteins in Huh-7 cells, mouse primary hepatocytes,

261 a phase 1 trial testing a new CD22-targeted CAR (CD22-CAR) in 21 children and adults, including 17 w

262 an efficiently introduce leukaemia-targeting CAR genes into T-cell nuclei, thereby bringing about lon

263 nalling tail and named the final product TCR-CAR.

264 In addition, we demonstrate that TCR-CAR redirection was not restricted to T cells.

265 We here show that, if expressed, the TCR-CAR conserved the specificity and the functionality of t

266 Notably, the TEM8 CAR T cells targeted breast cancer stem-like cells, offs

267 Here we demonstrate that CAR undergoes homodimer-monomer conversion to regulate t

268 ancreatic cancer and melanoma, we found that CAR T cells can migrate from biopolymer scaffolds and er

269 We hypothesized that CAR T-cell depletion with optimal timing after AML eradi

270 Herein, we have observed that CAR activation resulted in increased A2AR expression and

271 imensional gel electrophoresis revealed that CAR can form a homodimer in a configuration in which the

272 Histological analysis revealed that CAR-DCN treatment significantly increased DCN and collag

273 d with bioluminescence imaging, showing that CAR T cell treatment resulted in significant tumor regre

274 Taken together, these results suggest that CAR-DCN treatment attenuates the formation and rupture o

275 This meta-analysis suggests that CAR may be a potential prognostic marker in solid cancer

276 The CAR cDNA is genetically integrated in the T cell genome.

277 but not nonphosphorylated CAR DBD, bound the CAR LBD peptide.

278 d CAR-DCN groups, the severity of AAA in the CAR-DCN group was significantly reduced.

279 ehensively explore the potential role of the CAR as a prognostic indicator in solid cancers.

280 Asp increased co-immunoprecipitation of the CAR DBD with CAR LBD in Huh-7 cells.

281 ive internalization and re-expression of the CAR following single or repeated exposure to antigen, de

282 Antagonism of the CAR represents a key strategy for studying its function

283 We further demonstrate that targeting the CAR to the TRAC locus averts tonic CAR signalling and es

284 agonistic ligand CITCO binds directly to the CAR homodimer and dissociates phosphorylated CAR into it

285 These CAR T cells are engineered to express synthetic receptor

286 and delineate the mechanisms via which these CAR T cells overcome a hostile tumor microenvironment.

287 serum protein capable of bridging HAdV-5 to CAR.IMPORTANCE The intravascular administration of HAdV-

288 otency in vitro was directly proportional to CAR affinity and ICAM-1 density.

289 n, and a reduced reproliferative response to CAR stimulation.

290 eting the CAR to the TRAC locus averts tonic CAR signalling and establishes effective internalization

291 duct of defined CD4/CD8 composition, uniform CAR expression, and limited effector differentiation.

292 ant (TRAC) locus not only results in uniform CAR expression in human peripheral blood T cells, but al

293 Upon CAR T-cell termination, we further demonstrated successf

294 We used CAR technology to redirect human polyclonal Tregs toward

295 However, treatment of solid tumors using CAR T cells has been largely unsuccessful to date, partl

296 Here, a panel of affinity-variant CARs were constructed targeting overexpressed ICAM-1, a

297 TCRs recognize peptide-HLA complexes whereas CARs typically use an Ab-derived single-chain fragments

298 d co-immunoprecipitation of the CAR DBD with CAR LBD in Huh-7 cells.

299 esults supporting treatment of lymphoma with CAR-19 T cells have been published.

300 required for effective treatment of MM with CAR-Ts.

301 eakened the interaction of CAR DBD T38D with CAR LBD, converting CAR to the homodimer form.