ライフサイエンスコーパス: CAR

1 CAR macrophages (CAR-Ms) demonstrated antigen-specific p

2 CAR T cells administered ICV also traffic from the CNS i

3 CAR T cells that target uPAR extend the survival of mice

4 CAR-NKT cells expanded in vivo, localized to tumors and,

5 CAR-T cell expansion in vivo was cell dose dependent.

6 CAR-T cell therapy is effective for hematologic malignan

7 CAR-T cells costimulated with 4-1BB or ICOS persist in x

8 CAR-T cells have shown encouraging activity against recu

9 19-CAR-ML NK cells controlled lymphoma burden in vivo and i

10 Furthermore, 19-CAR-ML NK cells generated from lymphoma patients exhibit

11 The 19-CAR and ML responses were synergistic and CAR specific a

12 hance the kinetics of tumor killing of 4-1BB CAR-T cells or SHP1 to tune down cytokine release of CD2

13 ll persistence even in the context of 28zeta CAR activation, which indicates distinct prosurvival sig

14 naling differences between BBzeta and 28zeta CARs, they demonstrate the necessary and nonredundant ro

15 continuity or architecture, or on any Day 3 CAR measure.

16 nts of cellular therapy (Allo, 35; Auto, 37; CAR T, 5; median time from cellular therapy, 782 days; I

17 sequentially tested in the trial (50 x 10(6) CAR(+) T cells [one or two doses], 100 x 10(6) CAR(+) T

18 100 x 10(6) CAR(+) T cells, and 150 x 10(6) CAR(+) T cells), which were administered as a sequential

19 R(+) T cells [one or two doses], 100 x 10(6) CAR(+) T cells, and 150 x 10(6) CAR(+) T cells), which w

20 /- 3.8%) and treated patients with 3 x 10(6) CAR-NKT cells per square meter of body surface area afte

21 of three doses (1x10(5), 1x10(6), or 1x10(7) CAR-NK cells per kilogram of body weight) after lymphode

22 A CAR designated FHVH33-CD8BBZ contains a fully human heav

23 tes in a checkpoint, capable of triggering a CAR constriction delay through the SIN pathway to ensure

24 report that T and NK cells transduced with a CAR that recognizes the surface marker, CD147, also know

25 In addition, CAR altered sterol metabolism in all animals analyzed, w

26 Response consolidation with additional CAR T-cell infusions includes pembrolizumab to improve t

27 abundant-reticular (CAR) cell subsets (Adipo-CAR and Osteo-CAR) differentially localize to sinusoidal

28 stent insults to their immune function after CAR-T-cell infusion.

29 K patient developed acute pancreatitis after CAR-T therapy.

30 However, allogeneic CAR T cells may cause life-threatening graft-versus-host

31 These improved allogeneic CAR-T cell products will pave the way for further breakt

32 Nevertheless, the use of allogeneic CAR T cells from donors has many potential advantages ov

33 ing step forward for the field of allogeneic CAR T cells, and UCART19 offers the opportunity to treat

34 nt sources of T cells for optimal allogeneic CAR-T cell therapy and describe the different technologi

35 based on gene editing, to produce allogeneic CAR T cells with limited potential for graft-versus-host

36 ges, are promising alternatives to alphabeta CAR-T adoptive therapy.

37 ells and the FDC reservoir in vitro Although CAR-T cells eliminated CD4(+) T cells that express HIV,

38 minutes on each subsequent day (Day 1-3) and CAR measurement indices were derived: awakening cortisol

39 .CONCLUSIONIn this series of Allo, Auto, and CAR T recipients, we report overall favorable clinical o

40 We hypothesized that ML differentiation and CAR engineering would result in complementary improvemen

41 ibody engineering, antibody humanization and CAR-T cell therapy.

42 ing T-cell-mediated anti-tumour immunity and CAR T-cell therapy against solid tumours.

43 treatment using immune check inhibitors and CAR (chimeric antigen receptor) T-cell therapy serve as

44 studying the overlapping function of PXR and CAR.

45 19-CAR and ML responses were synergistic and CAR specific and required immunoreceptor tyrosine-based

46 We demonstrated recipient anti-CAR T-cell responses against a murine single-chain varia

47 ial strategy that may allow for dual-antigen CAR T-cell targeting.

48 association with cortical nodes that act as CAR precursors.

49 We assessed CAR-T cell cytotoxicity using a carboxyfluorescein succi

50 er the levels and distribution of cohesin at CARs, changing the pattern of positioned loops.

51 MIS-SHP1 phosphatase complex that attenuates CAR-CD3zeta phosphorylation.

52 dly progressive disease and where autologous CAR-T-cell therapy is unavailable.

53 The sr39tk gene did not affect B7H3 CAR T-cell functionality and in vitro and in vivo studie

54 and ganciclovir-mediated destruction of B7H3 CAR T cells incorporating a mutated version of the HSV1-

55 models showed no significant effect on B7H3 CAR T-cell antitumor activity.

56 n and hindered the persistence of CD28-based CAR-T cells and changing this asparagine to phenylalanin

57 ignaling in promoting the survival of BBzeta CAR T cells, which likely underlies the engraftment pers

58 tiple myeloma, but improvements in anti-BCMA CARs are needed.

59 fragment (scFv) used clinically in anti-BCMA CARs.

60 ogic adverse events, as they occurred before CAR-NKT cell infusion, and no dose-limiting toxicities w

61 Taken together, the BCMA/CS1 bispecific CAR presents a promising treatment approach to prevent a

62 Median peak blood CAR-positive cell levels were higher among patients with

63 These drawbacks can be circumvented by CAR-T cells targeting tumour-specific driver gene mutati

64 To specifically study signal transduction by CARs, we developed a cell-free, ligand-based activation

65 Levels of CAR, CAR metabolites, sterols, and oxysterols were measured i

66 ic-gated (log) GPC3-synNotch-inducible CD147-CAR to target HCC.

67 s support the therapeutic potential of CD147-CAR-modified immune cells for HCC patients.

68 CD19 CAR T-cell therapy with concurrent ibrutinib was well to

69 rial of T cells expressing the new anti-CD19 CAR Hu19-CD828Z (NCT02659943).

70 vestigated the role of perforin in anti-CD19 CAR T cell efficacy and HLH-like toxicities in a syngene

71 lymphocytic leukaemia treated with anti-CD19 CAR T cells and identify factors associated with differe

72 Various anti-CD19 CAR T-cell constructs have been trialled and responses v

73 or neurotoxicity between different anti-CD19 CAR T-cell constructs.

74 rs occurred after 51% of evaluable anti-CD19 CAR T-cell treatments.

75 f T cells expressing FMC63-28Z, an anti-CD19 CAR tested previously by our group, which contains murin

76 ector expressing genes that encode anti-CD19 CAR, interleukin-15, and inducible caspase 9 as a safety

77 al, we administered HLA-mismatched anti-CD19 CAR-NK cells derived from cord blood to 11 patients with

78 Since CD19 CAR is insensitive to serum IgG, we designed various com

79 CAR constructs in order to maintain the CD19 CAR T cell efficacy, but with IGK CAR target selectivity

80 (IPs) and blood of patients undergoing CD19 CAR-T immunotherapy.

81 Using CD19 CAR as a model, we report that, similar to the endogenou

82 fraction of patients who received anti-CD22 CAR T cells also experienced biphasic inflammation, with

83 In the largest experience of CD22 CAR T-cells to our knowledge, we provide novel informati

84 clinical outcomes and report on unique CD22 CAR T-cell toxicities and toxicity mitigation strategies

85 Here, we develop CD229 CAR T cells that are highly active in vitro and in vivo

86 In addition, while CD229 CAR T cells target normal CD229(high) T cells, they spar

87 r SHP1 to tune down cytokine release of CD28 CAR-T cells.

88 apsed or refractory HL and administered CD30.CAR-Ts after lymphodepletion with either bendamustine al

89 nfusion of two components (CD8(+) and CD4(+) CAR(+) T cells) at equal target doses.

90 Perforin contributed to both CD8+ and CD4+ CAR T cell cytotoxicity but was not required for in vitr

91 RNA sequencing (scRNA-seq) to profile CD8(+) CAR-T cells from infusion products (IPs) and blood of pa

92 ukemia cell lines are readily killed by CD83 CAR T cells.

93 Human CD83 CAR T cells are a promising cell-based approach to preve

94 Thus, the use of human CD83 CAR T cells for GVHD prevention and treatment, as well a

95 ccur after chimeric antigen receptor T cell (CAR T cell) infusion and represent a therapeutic challen

96 mples from chimeric antigen receptor T cell (CAR-T cell) therapy patients without washing away excess

97 r chimeric antigen receptor-modified T-cell (CAR-T-cell) therapy are limited.

98 In this study, negatively charged CAR-NPs and positively charged polyethylenimine (PEI)-co

99 tively charged polyethylenimine (PEI)-coated CAR-(PEI)NPs were formulated by nanoprecipitation method

100 Our results demonstrate that a combinatorial CAR approach can improve target selectivity and efficacy

101 serum IgG, we designed various combinatorial CAR constructs in order to maintain the CD19 CAR T cell

102 4-1BB-costimulated CAR (BBzeta) T cells exhibit longer persistence after ad

103 adoptive transfer than do CD28-costimulated CAR (28zeta) T cells.

104 uture evaluation in other CD28-costimulatory CARs in an effort to improve durable antitumor effects.

105 In 2 animals with declining CAR T cells, rhesusized anti-programmed cell death prote

106 ated in vitro activation, perforin-deficient CAR T cells produced higher amounts of proinflammatory c

107 Thus, a murine model of perforin-deficient CAR T cells recapitulated late-onset inflammatory toxici

108 ) and its effector, MAPK Sty1, downregulates CAR assembly in S. pombe when its integrity becomes comp

109 to the CAR T cell product, we developed Dual-CAR T cells that simultaneously expressed both 4-1BB/CD3

110 enhanced therapeutic potency of a novel Dual-CAR T cell product with the potential to effectively tre

111 of antitumor immunity, but promoting durable CAR T cell responses remains challenging.

112 ell deconstruction of gene regulation during CAR-T therapy, leading to the discovery of cellular fact

113 se studies have observed the nuances of each CAR T cell product, including variability in manufacturi

114 l types are therefore required for effective CAR-based therapies.

115 ntrast, the synapse formed by 4-1BB-encoding CAR recruits the THEMIS-SHP1 phosphatase complex that at

116 e integration of lentiviral vectors encoding CAR that direct tumor cell killing.

117 oints after infusion.CONCLUSIONSB-engineered CAR T cells expand and persist in pediatric and adult B-

118 ions in the costimulatory domain may enhance CAR-T cell persistence, warranting future evaluation in

119 ment of neurological disorders, and enhanced CAR T/NK cell immunotherapy.

120 In the presence of Epo, EpoRm-CAR T cells had greater ex vivo expansion than CAR T cel

121 re sufficient to preferentially expand EpoRm-CAR T cells, yielding a significantly higher antileukemi

122 dyl ester (CFSE) release assay and evaluated CAR-T cell activation through interferon gamma (IFN-gamm

123 nt blockade triggered expansion of exhausted CAR T cells and concordantly lowered viral loads to unde

124 se formation, nor actin remodeling following CAR activation.

125 mutations might not be ideal candidates for CAR use, especially if they are nursing, pregnant or pla

126 with CAR T cell persistence, especially for CAR T cells that target CD19(+) hematologic malignancies

127 data, we create a 'targetable landscape' for CAR cell therapies based on 13,206 proteins and RNAs acr

128 imaging reporter and as a suicide switch for CAR T cells.

129 Furthermore, CAR elevated toxic oxysterols in the brain of maternally

130 a or lambda, we designed a second-generation CAR targeting Igkappa, IGK CAR.

131 Three cycles of HER2 CAR T cells given after lymphodepleting chemotherapy ind

132 However, CAR T cells can induce substantial toxic effects, and th

133 t inflammatory toxicities occurring in human CAR T cell recipients, providing therapeutically relevan

134 Here, we demonstrate that human CAR-T cells polarized and expanded under a Th9-culture c

135 treated with CAR T cells without ibrutinib, CAR T cells with concurrent ibrutinib were associated wi

136 second-generation CAR targeting Igkappa, IGK CAR.

137 n the CD19 CAR T cell efficacy, but with IGK CAR target selectivity.

138 selection of the apheresis product improved CAR T-cell manufacturing feasibility as well as heighten

139 cytotoxic T cell-mediated killing, improving CAR T cell therapy.

140 lity of these antibodies was demonstrated in CAR format.

141 atment approach to prevent antigen escape in CAR-T cell therapy against MM, and the vertically integr

142 ral genomes at the single-cell resolution in CAR-T cells.

143 f concept of targeting TF as a new target in CAR-NK immunotherapy for effective treatment of TNBC and

144 ical to define the identity of an individual CAR-T cell and simultaneously chart where the CAR-T vect

145 cer drugs and genetic mechanisms influencing CAR T-cell cytotoxicity.

146 The infused CAR-NK cells expanded and persisted at low levels for at

147 eral tyrosine kinase inhibitors that inhibit CAR T-cell cytotoxicity by impairing T-cell signaling tr

148 ier that delivers in vitro-transcribed (IVT) CAR or TCR mRNA for transiently reprograming of circulat

149 nt mice were exposed to vehicle or 0.2 mg/kg CAR from E12 to E19.

150 The clinical study of PD-L1 CAR haNKs is warranted.

151 PD-L1 CAR haNKs reduced levels of macrophages and other myeloi

152 ch as IL-1beta and IL-18 and concurrent late CAR T cell expansion characterized the HLH-like syndrome

153 LogCD147-CAR selectively kills dual antigen (GPC3(+)CD147(+)), bu

154 CAR macrophages (CAR-Ms) demonstrated antigen-specific phagocytosis and t

155 Thus, CD4-MBL CAR-T cells are unable to eliminate the FDC-associated H

156 CD4-MBL CAR-T cells were unresponsive to cell-free HIV or concen

157 We also measured CAR bioaccessibility by using an in vitro model.

158 o acid substitution in CD28-based mesothelin CAR-T cells results in improved persistence and function

159 up-regulated in type 1 diabetic Akita mice; CAR spontaneously accumulates in the nucleus and activat

160 In humanized mouse models, CAR-Ms were further shown to induce a pro-inflammatory t

161 mission which is consolidated with four more CAR T-cell infusions without lymphodepletion.

162 Moreover, CAR preferably interacted with phosphomimetically mutate

163 Moreover, CAR-modified T cells expanded with the engineered IL-10

164 unosuppressive agents was prohibited in most CAR-T trials effectively excluding patients with prior s

165 MP and succinate and engineered three mutant CARs with enhanced activity against 6-ACA.

166 , we discuss the innovative designs of novel CAR T cell products that are being developed to increase

167 We created 8 novel CARs using anti-CMV neutralizing antibody sequences, whi

168 Therapies using NPM1c CAR-T cells for the treatment of NPM1c(+)HLA-A2(+) AML m

169 tional assays for quantifying the ability of CAR T cells to sense and respond to soluble ligands are

170 anced the in vitro antimicrobial activity of CAR against Escherichia coli, Listeria monocytogenes, Sa

171 eceptor (CAR) improved antitumor activity of CAR-T cells.

172 and opportunities for novel applications of CAR-T therapy for the treatment of both haematological m

173 ll modifications, redosing or combination of CAR T cells directed against different targets, and decr

174 RB sequencing shows that clonal diversity of CAR-T cells is highest in the IPs and declines following

175 odifications to the costimulatory domains of CAR-T cells can enable longer persistence and thereby im

176 patients were infused with a single dose of CAR T cells.

177 pring, and tested the biochemical effects of CAR in human serum samples.

178 We assessed the effects of CAR on maternally exposed Dhcr7(+/-) and wild-type mouse

179 sociated antigen enables robust expansion of CAR T cells in an antigen-sparse environment.

180 c approach is often limited by the extent of CAR-T cell expansion in vivo.

181 ty in the cellular and molecular features of CAR T cell infusion products contributes to variation in

182 receptor (CAR) T cells offer a novel form of CAR-T-cell product that is available for immediate clini

183 antigen engagement triggers the formation of CAR microclusters that transduce downstream signaling.

184 recruit and potentiate the functionality of CAR T cells.

185 indings are important for the improvement of CAR-T cell-based immunotherapy for human cancers.

186 Levels of CAR, CAR metabolites, sterols, and oxysterols were measu

187 s underwent leukapheresis for manufacture of CAR(+) T cells (liso-cel), of whom 269 patients received

188 ies, suggesting a link between mechanisms of CAR T-cell cytotoxicity and cancer genetics.

189 tically investigated druggable mechanisms of CAR T-cell cytotoxicity using >500 small-molecule drugs

190 late kinetics, metabolism and persistence of CAR-T cells, and the mechanisms governing these differen

191 esponse might serve as an early predictor of CAR T cell efficacy.

192 t interfere with CAR assembly or the rate of CAR constriction, but did delay the onset of constrictio

193 Controlled release of CAR from PLA nanoparticles (NPs) could improve its antim

194 al. report favorable ZUMA-2 trial results of CAR T cells for patients with relapsed and refractory ma

195 The rapidity of commercial utilization of CAR-T-cell therapy has created a largely unexplored gap

196 pha bridging the PBREM and OARE orchestrates CAR and HNF4alpha to form active chromatin complex durin

197 ular (CAR) cell subsets (Adipo-CAR and Osteo-CAR) differentially localize to sinusoidal and arteriola

198 re consistent with those reported with other CAR T-cell therapies.

199 ross-presentation, that CD40L-overexpressing CAR T cells elicit an impaired antitumor response in the

200 e stimulatory effect of CD40L-overexpressing CAR T cells on innate and adaptive immune cells, and pro

201 e a rationale for using CD40L-overexpressing CAR T cells to improve immunotherapy responses.

202 In breast and lung cancer patients, CAR-T cells targeting the tumor-associated antigen recep

203 weeks to generate GBOs and 5-7 d to perform CAR T cell co-culture using this protocol.

204 However, coexpression of endogenous TCR plus CAR led to superior persistence of T cells and significa

205 lls: pre CAR-T-cell infusion, immediate post CAR-T-cell infusion, and long-term follow-up.

206 nts receiving CD19-targeted CAR-T cells: pre CAR-T-cell infusion, immediate post CAR-T-cell infusion,

207 e rich sequence (BRS) of CD3epsilon promoted CAR-T persistence via p85 recruitment.

208 iven by a cell polarity kinase that promotes CAR assembly in the correct time and place.

209 ProVA CAR in carrots with the highest concentrations also prov

210 as to enhance provitamin A carotenoid (proVA CAR) concentrations and bioaccessibility in carrots by m

211 This strategy provides CARs with Tn-peptide specificities, all based on a singl

212 rbital via constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha).

213 effective, but a chimeric antigen receptor (CAR) approach would provide a feasible method for broad

214 o express a PD-L1 chimeric antigen receptor (CAR) haNKs killed a panel of human and murine head and n

215 second-generation chimeric antigen receptor (CAR) improved antitumor activity of CAR-T cells.

216 man CD83-targeted chimeric antigen receptor (CAR) T cell for GVHD prevention.

217 BACKGROUNDChimeric antigen receptor (CAR) T cell immunotherapy has resulted in complete remis

218 oint blockade and chimeric antigen receptor (CAR) T cell therapeutic modalities.

219 Chimeric antigen receptor (CAR) T cell therapy has shown promise in hematologic mal

220 nical response to chimeric antigen receptor (CAR) T cell therapy is correlated with CAR T cell persis

221 Chimeric antigen receptor (CAR) T cell therapy works by mechanisms distinct from th

222 ovel HIV-specific chimeric antigen receptor (CAR) T cell to target both HIV-infected CD4(+) T cells a

223 Chimeric antigen receptor (CAR) T cells are potent drivers of antitumor immunity, b

224 ogeneic anti-CD19 chimeric antigen receptor (CAR) T cells offer a novel form of CAR-T-cell product th

225 ents treated with chimeric antigen receptor (CAR) T cells or bispecific T cell engager (BiTE) antibod

226 Chimeric antigen receptor (CAR) T cells represent a potent new approach to treat ha

227 Anti-CD19 chimeric antigen receptor (CAR) T cells showed significant antileukemic activity in

228 ed the utility of chimeric antigen receptor (CAR) T cells, expressing the CD4 ectodomain to confer sp

229 tumor activity of chimeric antigen receptor (CAR) T cells.

230 tegies to monitor chimeric antigen receptor (CAR) T-cell biodistribution and proliferation harbor the

231 Innovations in chimeric antigen receptor (CAR) T-cell immunotherapies are at the forefront of new

232 s, CD19-directed, chimeric antigen receptor (CAR) T-cell product.

233 Anti-CD19 chimeric antigen receptor (CAR) T-cell therapy has shown remarkable activity in pat

234 Anti-CD19 chimeric antigen receptor (CAR) T-cell therapy has shown remarkable clinical effica

235 elevant models of chimeric antigen receptor (CAR) T-cell-induced cytokine release syndrome.

236 Chimeric antigen receptor (CAR) therapy is a promising immunotherapeutic strategy f

237 antibody 237 as a chimeric antigen receptor (CAR) to mediate recognition of mouse tumor cells that be

238 ss a GD2-specific chimeric antigen receptor (CAR) with interleukin-15 in children with relapsed or re

239 Chimeric antigen receptor (CAR)-expressing T cells targeting B-cell maturation anti

240 uding those using chimeric antigen receptor (CAR)-modified T cells, to solid tumors requires combinat

241 Chimeric antigen receptor (CAR)-T cell immunotherapy is highly effective against B

242 (2020) develop chimeric antigen receptor (CAR)-T cells targeting uPAR, a novel senescent-cell mark

243 Chimeric antigen receptor (CAR)-T immunotherapy has yielded impressive results in s

244 third generation Chimeric Antigen Receptors (CAR) T cells demonstrating specific cytolytic activity.

245 Anti-CD19 chimeric antigen receptors (CARs) are artificial fusion proteins that cause CD19-spe

246 trials employing chimeric antigen receptors (CARs), no comprehensive survey of their scope, targets a

247 he Csk-recruiting ITAM of CD3epsilon reduced CAR-T cytokine production whereas the basic residue rich

248 6-ACA and HMD by carboxylic acid reductases (CARs) and transaminases (TAs), which involves two rounds

249 d sleep and the cortisol awakening response (CAR), depending on whether it was experienced or just an

250 demonstrate that Cxcl12-abundant-reticular (CAR) cell subsets (Adipo-CAR and Osteo-CAR) differential

251 bination with a second-generation retroviral CAR transduction including a 4-1BB costimulatory domain

252 mporal coordination between actomyosin ring (CAR) constriction with membrane ingression and septum sy

253 a single scFv scaffold, that allows the same CAR to be tested for toxicity in mice and efficacy again

254 3-28Z; axicabtagene ciloleucel uses the same CAR.

255 blish the therapeutic potential of senolytic CAR T cells for senescence-associated diseases.

256 Their observation suggests that sequential CAR T-cell targeting strategies may be safe and effectiv

257 and ex vivo culture system for CD19-specific CAR T cells.

258 mphoma model without affecting CD19-specific CAR T-cell antitumor activity.

259 , which are then eradicated by CD19-specific CAR-T cells in immunodeficient and immunocompetent mouse

260 Whether HIV-specific CAR-T cells can recognize and eliminate the follicular d

261 st study to show expansion of virus-specific CAR T cells in infected, suppressed hosts, and delay/con

262 oluminescence and PET imaging of B7H3-sr39tk CAR T cells confirmed complete tumor ablation with intra

263 persistence of chimeric antigen receptor T (CAR-T) cells is a key characteristic associated with lon

264 Chimeric antigen receptor-T (CAR-T) cell therapies can eliminate relapsed and refract

265 Compared to IL2-polarized (T1) cells, T9 CAR-T cells secrete IL9 but little IFN-gamma, express ce

266 d expanded under a Th9-culture condition (T9 CAR-T) have an enhanced antitumor activity against estab

267 agement for patients receiving CD19-targeted CAR-T cells: pre CAR-T-cell infusion, immediate post CAR

268 In comparison to CAR T cells, p40-Td CAR T cells showed improved antitumor capacity in vitro,

269 R T cells had greater ex vivo expansion than CAR T cells and killed CD19+ leukemic cells more effecti

270 Together, these data show that CAR T cells can bypass LAT for a subset of downstream si

271 The CAR used was FMC63-28Z; axicabtagene ciloleucel uses the

272 , we determined the crystal structure of the CAR substrate-binding domain in complex with AMP and suc

273 t treatment, possible standardization of the CAR-T cell product, time for multiple cell modifications

274 In combination with TAs, the CAR L342E protein showed 50-75% conversion of 6-ACA to H

275 ovides further evidence to indicate that the CAR is a marker of anticipation and not recovery.

276 We further demonstrated that the CAR synapse can be engineered to recruit either LCK to e

277 Differential signaling through the CAR costimulatory domain can alter the T cell metabolism

278 Through iterative improvements to the CAR T cell product, we developed Dual-CAR T cells that s

279 netics, making variable contributions to the CAR-T cell pool after infusion.

280 AR-T cell and simultaneously chart where the CAR-T vector integrates into the genome.

281 e engraftment persistence observed with this CAR design.

282 Thus, CAR engineering of ML NK cells enhanced responses agains

283 In comparison to CAR T cells, p40-Td CAR T cells showed improved antitumo

284 Embryonic exposure to CAR significantly increased levels of 7-DHC in all organ

285 high net state of immunosuppression prior to CAR-T-cell infusion coupled with unique acute and persis

286 Key challenges relating to CAR T cells include severe toxicities, restricted traffi

287 rtant mediator of cancer cell sensitivity to CAR T-cell cytotoxicity, with potential for pharmacologi

288 urther advances are required for solid tumor CAR therapy.

289 By providing direct access to tumours, CAR-T-cell-loaded micropatterned nitinol thin films can

290 Two CAR T-cell therapies, tisagenlecleucel and axicabtagene

291 tion of AA to HMD (via 6-ACA), the wild type CAR was combined with the L342E variant and two differen

292 Upon CAR-mediated in vitro activation, perforin-deficient CAR

293 ciated cytokines, despite equivalent in vivo CAR T-cell expansion.

294 ptor (CAR) T cell therapy is correlated with CAR T cell persistence, especially for CAR T cells that

295 BP did not interfere with CAR assembly or the rate of CAR constriction, but did de

296 Compared with CLL patients treated with CAR T cells without ibrutinib, CAR T cells with concurre

297 enetically engineered human macrophages with CARs to direct their phagocytic activity against tumors.

298 f proinflammatory cytokines compared with WT CAR T cells.

299 In addition, CD28-YMFM CAR-T cells exhibited reduced T cell differentiation and

300 ing clearance of ATRT xenografts, B7-H3.BB.z-CAR T cells administered intracerebroventricularly or in