ライフサイエンスコーパス: inhibitory receptor

1 ession of the programmed cell death 1 (PD-1) inhibitory receptor.

2 tive signals received through activating and inhibitory receptors.

3 and associated with coexpression of multiple inhibitory receptors.

4 iated with reduced binding to its respective inhibitory receptors.

5 or CD112, and has co-varied expression with inhibitory receptors.

6 ly due to residual binding to the respective inhibitory receptors.

7 thogen molecular mimicry of host ligands for inhibitory receptors.

8 e the host immune system by targeting immune inhibitory receptors.

9 of multiple additional co-stimulatory and co-inhibitory receptors.

10 nd could be sculpted by blockade of specific inhibitory receptors.

11 ulated genes and ligands for multiple T cell inhibitory receptors.

12 that had downregulated PD-1 as well as other inhibitory receptors.

13 ceptor without coexpressing any allospecific inhibitory receptors.

14 of activation markers and downregulation of inhibitory receptors.

15 ct to downregulation by MHC class I-specific inhibitory receptors.

16 he sensitivity of IL-15 transpresentation to inhibitory receptors.

17 pecific T cells, and increased expression of inhibitory receptors.

18 onal impairment and upregulation of numerous inhibitory receptors.

19 CD8(+) T cells induce expression of multiple inhibitory receptors.

20 enome encodes more than 300 potential immune inhibitory receptors.

21 ot thymic Tregs with increased expression of inhibitory receptors.

22 ponses, independently of blockade of NK cell inhibitory receptors.

23 cells through integration of activation and inhibitory receptors.

24 gagement of the TCR and one or more of these inhibitory receptors.

25 i and regulates the surface level of NK-cell inhibitory receptors.

26 we used chimeric antibodies specific for DC inhibitory receptor 2 (DCIR2) or DEC-205 to target self-

27 We found that self-specific inhibitory receptors affected NK cell precursor survival

28 Inhibitory receptors also promote NK cell tolerance and

29 r T cells, a decrease in the coexpression of inhibitory receptors, an improved Ag-specific CD8(+) T c

30 memory B cells (AMB), which express multiple inhibitory receptors and activation markers, and are hyp

31 Atypical MBCs express an array of inhibitory receptors and B cell receptor (BCR) signaling

32 unction, including migration, costimulation, inhibitory receptors and cytokines, via multiple repress

33 control, CD4+ T cells quickly downregulated inhibitory receptors and differentiated into long-lived

34 and cytokine production, high expression of inhibitory receptors and distinct transcriptional profil

35 ss of effector functions, high expression of inhibitory receptors and distinct transcriptional progra

36 CD8(+) T cells expressed elevated levels of inhibitory receptors and exhibited transcriptomic exhaus

37 ted effector function, high co-expression of inhibitory receptors and extensive transcriptional chang

38 al infection through the interaction between inhibitory receptors and human leukocyte antigen (HLA) l

39 ulation and characterized by upregulation of inhibitory receptors and loss of effector function.

40 et cell recognition, where the engagement of inhibitory receptors and MHC class I molecules attenuate

41 highly similar expression pattern of killer inhibitory receptors and other candidate molecules in NK

42 levels were strongly correlated with various inhibitory receptors and that high SLAMF7 expression was

43 T cells and characterized the expression of inhibitory receptors and the presence of the parasite in

44 These cells did not coexpress other inhibitory receptors and were able to proliferate in res

45 higher expression of the programmed death 1 inhibitory receptor, and blockade of this receptor incre

46 nts an evolutionarily conserved pDC-specific inhibitory receptor, and is required to prevent spontane

47 ed cytokine production, high coexpression of inhibitory receptors, and advanced cellular differentiat

48 are NK1.1(+) (CD161(+) in human), express NK-inhibitory receptors, and express the promyelocytic leuk

49 ate the CD8(+) T cell subsets, expression of inhibitory receptors, and functionality of T cells in CC

50 t, precedes the expression of MHC-I-specific inhibitory receptors, and is modulated in an education-d

51 main molecule 3 (Tim-3), which are potent co-inhibitory receptors, and their persistent expression of

52 TAT3 phosphorylation, expression of multiple inhibitory receptors, and transcription factors associat

53 CD4 T cells following blocking of different inhibitory receptors, and we confirmed our results in a

54 ppressive mechanism involving IL-10, NK cell inhibitory receptors, and, unexpectedly, engagement of t

55 ination or therapeutic strategies.IMPORTANCE Inhibitory receptors are important for limiting damage b

56 ncer cells despite expressing high levels of inhibitory receptors are unknown.

57 an array of germ line-encoded activating and inhibitory receptors, as well as modulating coreceptors.

58 wo KIR3DL1 alleles encoding highly expressed inhibitory receptors associated with protection from PD

59 notype including the increased expression of inhibitory receptors, associated with an elevated consti

60 an tissue, a decrease in the density of this inhibitory receptor at the cell surface.

61 se IRAP ligands increase the density of this inhibitory receptor at the plasma membrane, they also po

62 Studies have shown that blocking inhibitory receptors augments CD8 T cell functionality i

63 F ligands, LIGHT and LTa; the immunoglobulin inhibitory receptor, B and T lymphocyte attenuator (BTLA

64 The CD300a inhibitory receptor belongs to the CD300 family of cell

65 ied a pan anti-MHC-I mAb that blocks NK cell inhibitory receptor binding at a site distinct from the

66 PD-1 inhibitory receptor blockade partially reversed T cell u

67 he ability to reinvigorate Tex cells through inhibitory receptor blockade, such as alphaPD-1, highlig

68 olecule in GC-derived lymphomas, engages the inhibitory receptor BTLA on Tfh cells and loss of HVEM l

69 V-specific CD8(+) T cells expressed the PD-1 inhibitory receptor, but also expressed several costimul

70 and functions due to its interaction with NK inhibitory receptors, but its exact role in NK cells is

71 Most CD33-related Siglecs function as inhibitory receptors, but the ability of Siglec-8 to sti

72 rolled by the balance between activating and inhibitory receptors, but the expression of these recept

73 enes, including the upregulation of numerous inhibitory receptors by lung TCD8.

74 s their ability to engage several classes of inhibitory receptors by their specific ligands, includin

75 g T cell activation by stimulating a natural inhibitory receptor called leukocyte-associated Ig-like

76 antibodies specific for the PD-1 and CTLA-4 inhibitory receptors can induce durable responses in a w

77 IgE and a high-affinity glycan ligand of the inhibitory receptor CD33 (CD33L) to targeted mast cells

78 gen and a high-affinity glycan ligand of the inhibitory receptor CD33 profoundly suppressed IgE-media

79 Compared with TIL that did not express these inhibitory receptors, CD8(+) and CD4(+) TIL that did exp

80 ciently inhibiting surface expression of the inhibitory receptor CD94/NK group 2 member A (NKG2A) thr

81 er (NK) cell activity via ligation of the NK inhibitory receptor CD94/NKG2A.

82 mice, an effect enhanced by blockade of the inhibitory receptor CD96 or CpG-oligonucleotide treatmen

83 s part of a module that contains multiple co-inhibitory receptors (checkpoint receptors), which are c

84 cell responses associated with a decrease in inhibitory receptor coexpression, which could serve as b

85 e of advanced differentiation, and increased inhibitory receptor coexpression.

86 by expression of a narrower range of T cell inhibitory receptors compared with CD8+ T cells, with in

87 lation expressed elevated levels of multiple inhibitory receptors concomitant with the reduced functi

88 In vitro Ab blockade revealed that multiple inhibitory receptors contribute to TCD8 impairment induc

89 Since inhibitory receptors control NK-cell activation and are

90 The inhibitory receptor CTLA4 and the transcription factor H

91 ell as CD25(+) CD4(+) T cells expressing the inhibitory receptor CTLA4.

92 effector and proliferation programs through inhibitory receptor, cytotoxic-T-lymphocyte-associated p

93 While inhibitory receptors dampen cellular activation by recog

94 type associated with increased expression of inhibitory receptors, decreased functional capacity, and

95 ilibrium of signaling through activating and inhibitory receptors dictates whether a given NK cell wi

96 Blockade of inhibitory receptors differentially affected cytokine pr

97 In chronic HIV infection, inhibitory receptor distribution differed markedly betwe

98 Together, these results show that inhibitory receptor distribution on HIV-specific CD4 T c

99 lls selects for the induction of appropriate inhibitory receptors during development, which NK cells

100 (IFPs) to enhance ACT efficacy, combining an inhibitory receptor ectodomain with a costimulatory endo

101 Coengagement of inhibitory receptors, either KIR2DL1 or CD94-NKG2A, did

102 cellular domain of LAIR1, a collagen-binding inhibitory receptor encoded on chromosome 19, was insert

103 main of LAIR1, an immunoglobulin superfamily inhibitory receptor encoded on chromosome 19.

104 T cell Ig and ITIM domain (TIGIT) is an inhibitory receptor expressed by activated T cells, Treg

105 We discuss here the role of TIGIT, an inhibitory receptor expressed by lymphocytes, in limitin

106 immunoglobulin and ITIM domain (TIGIT) is an inhibitory receptor expressed on the surface of natural

107 Inhibitory receptors expressed by T cells mediate tolera

108 The majority of Siglecs are inhibitory receptors expressed in immune cells that bind

109 SHIP1 is recruited to a large number of inhibitory receptors expressed on invariant NK (iNKT) ce

110 d higher cytokine release per cell and lower inhibitory receptor expression (PD-1, CTLA-4, and the ap

111 n subjects with Down syndrome, whereas their inhibitory receptor expression (programmed cell death 1

112 oral T cell exhaustion by modulating several inhibitory receptor expression and exhaustion-associated

113 ung TCD8s from VLP-vaccinated mice exhibited inhibitory receptor expression and functional impairment

114 ing was associated with a marked increase in inhibitory receptor expression and with T cells that wer

115 The identification of EECs marked by inhibitory receptor expression at tumor sites will enabl

116 We uncovered differences in inhibitory receptor expression depending on the CD4 T ce

117 ype, but retained the capacity to upregulate inhibitory receptor expression in peripheral sites.

118 Our results show that inhibitory receptor expression on CD4 T cells is linked

119 ng of chronic diseases where constitutive co-inhibitory receptor expression on T cells dampens effect

120 beneficial anti-tumor immunity by modulating inhibitory receptor expression on tumor-infiltrating lym

121 We therefore determined and compared inhibitory receptor expression patterns of 2B4, CTLA-4,

122 iation phenotypes, transcription factor, and inhibitory receptor expression revealed progression of C

123 K cell development or NK cell-activating and inhibitory receptor expression yet, as in humans, did de

124 nfection promotes apoptosis, activation, and inhibitory receptor expression, and interferon-insensiti

125 ses on T cell lineage, T cell activation and inhibitory receptor expression, and myeloid immunosuppre

126 Thus, serum HBsAg correlates with inhibitory receptor expression, HBV-specific CD4(+) T ce

127 terns and significantly lower frequencies of inhibitory receptor expression, i.e., PD-1 and coexpress

128 ss of effector functions, high and sustained inhibitory receptor expression, metabolic dysregulation,

129 inhibition of IL-12 production, rather than inhibitory receptor expression, was responsible for inhi

130 Additional loss of the inhibitory receptor FcgammaRIIb in Siglec-G(-/-) mice do

131 The inhibitory receptor FcgammaRIIB is expressed on human an

132 The inhibitory receptor FcgammaRIIB plays a central role in

133 recruitment to the phospho-ITIM motif of the inhibitory receptor FcgammaRIIB.

134 mally at 5 d post-infection (dpi), while the inhibitory receptor (FcgammaRIIB) remained highly elevat

135 caffold that we here show binds low-affinity inhibitory receptors (FcRL5, FcgammaRIIb, and DC-SIGN) w

136 y is limited by their expression of dominant inhibitory receptors for human leukocyte antigen (HLA) c

137 h active celiac disease, and without loss of inhibitory receptors for NK cells.

138 tolerance also occurs for NK cells that lack inhibitory receptors for self-MHC I, and for all NK cell

139 y using Cal-Light to drive expression of the inhibitory receptor halorhodopsin (eNpHR), which respond

140 In recent years, a number of inhibitory receptors have been connected to the immune c

141 Inhibitory receptors have been extensively described for

142 itory checkpoint receptors, including B cell inhibitory receptors, have important functions in regula

143 surface expression of the human pDC-specific inhibitory receptor Ig-like transcript 7.

144 state cancer cells induced the expression of inhibitory receptor (ILT2/LILRB1) and downregulated the

145 stigate the impact of licensing through this inhibitory receptor in precursor and mature NK cells.

146 ogrammed cell death-1 (PD-1) is an essential inhibitory receptor in T cells.

147 occur in cancer, highlighting the role of co-inhibitory receptors in contributing to this process whi

148 We investigated the role of these immune inhibitory receptors in driving immune impairments in pa

149 The expression of inhibitory receptors, including NKG2A and inhibitory kil

150 Activating and inhibitory receptors, including NKG2A, NKG2D, KIR2DL1, K

151 Impaired lung TCD8 upregulated multiple inhibitory receptors, including PD-1, lymphocyte activat

152 icroenvironment, and increased expression of inhibitory receptors, including programmed cell death pr

153 MHC I-binding inhibitory receptors, including those belonging to the L

154 e IL2Rbeta chain on CD8(+) T cells restrains inhibitory receptor induction, in particular 2B4 and Tim

155 Siglec-7 is an inhibitory receptor (IR) expressed on human blood eosino

156 fied tumor-infiltrating lymphocytes (TIL) by inhibitory receptors (IR), namely PD1.

157 and CD56(dim)CD57(-)KIR(-)NKG2A(-) (lacking inhibitory receptors; IR(-)) human NK cells by quantifyi

158 e focus has shifted to targeting alternative inhibitory receptors (IRs) and suppressive mechanisms wi

159 Although immunotherapeutics targeting the inhibitory receptors (IRs) CTLA-4, PD-1 or PD-L1 have ma

160 e that balancing of immune responses through inhibitory receptors is an important quality control che

161 IRPalpha(+) CD8(+) T cells, expression of co-inhibitory receptors is counterbalanced by expression of

162 uggests that the regulation of expression of inhibitory receptors is uncoupled from the loss of effec

163 man cells expressing HLA class I ligands for inhibitory receptors KIR2DL1, KIR2DL2/3, or CD94-NKG2A w

164 ecular profile of TIL, protein expression of inhibitory receptor LAG-3 was differentially regulated t

165 y inducing high expression of the checkpoint inhibitory receptors LAG-3 and PD-1.

166 s were used, cells expressing or lacking the inhibitory receptor leukocyte immunoglobulin-like recept

167 ms for suppressing T-cell activation via the inhibitory receptor leukocyte-associated immunoglobulin-

168 wed that this protection was mediated by the inhibitory receptor LILRB1, whose expression was upregul

169 on-like profile, with expression of multiple inhibitory receptors, limited cytokine production, and r

170 d and stressed cells(1) using activating and inhibitory receptors, many of which interact with HLA cl

171 port an important and physiological role for inhibitory receptor-mediated regulation of CD4+ T cells

172 sue of Blood, Alvarez et al describe a novel inhibitory receptor-mediated role for unlicensed natural

173 is vital for the organization of proteins at inhibitory receptors, molybdenum cofactor biosynthesis a

174 MHC molecule HLA-E, which interacts with the inhibitory receptor NKG2A expressed by NK and highly dif

175 on of activation receptors NKp30, NKp46, and inhibitory receptor NKG2A on blood NK cells reduced duri

176 receptor CX3CR1 on CD56(bright) NK cells and inhibitory receptor NKG2A on CD56(dim) NK cells, compare

177 ducated NK cells and increased expression of inhibitory receptor NKG2A/CD94 on terminally differentia

178 NK cells expressing the inhibitory receptor NKG2A/CD94 recognize and respond to

179 icron-scale reorganization of activating and inhibitory receptors occurs at the surface of human macr

180 er functions as a coreceptor for KIR3DL1, an inhibitory receptor of NK cells that is specific for cer

181 MHC-IB genes, several of which interact with inhibitory receptors of NK cells.

182 Thus, although inhibitory receptors often cause T cell exhaustion and v

183 We now show that signal inhibitory receptor on leukocytes-1 (SIRL-1) attenuates

184 f signal regulatory protein (SIRP)-alpha, an inhibitory receptor on macrophages, or of its ligand CD4

185 rotein alpha (SIRPalpha), which serves as an inhibitory receptor on macrophages.

186 ne, they also potentiate the effects of this inhibitory receptor on seizure activity.

187 Programmed cell death protein 1 (PD-1) is an inhibitory receptor on T lymphocytes that is critical fo

188 These strategies include blockade of immune-inhibitory receptors on activated T cells; for example,

189 eloped against CTLA-4 and PD-1, block immune-inhibitory receptors on activated T-cells, amplifying th

190 However, the prevalence of inhibitory receptors on CD4 T cells and their relative i

191 -specific lung TCD8 expressing three or more inhibitory receptors on day 14 postinfection.

192 We assessed the expression of inhibitory receptors on HIV-specific CD4 T cells and the

193 BACKGROUND & AIMS: Ligand binding to inhibitory receptors on immune cells, such as programmed

194 Many Siglecs function as inhibitory receptors on innate and adaptive immune cells

195 ) T cells was associated with an increase in inhibitory receptors on monocytes in Amish, but not Hutt

196 support the hypothesis that upregulation of inhibitory receptors on T cells during P. vivax malaria

197 ts with AAH caused over expression of immune inhibitory receptors on T cells via Toll-like receptor 4

198 upregulate coinhibitory ligands that bind to inhibitory receptors on T cells.

199 n affects the expression of diverse types of inhibitory receptors on the axon and dendrites of mouse

200 s II on DCs also resulted in upregulation of inhibitory receptors on Tregs, reduced body weight, and

201 We suggest that inhibitory receptors operate as two distinct functional

202 omain mediate binding to the adhesion and co-inhibitory receptor P-selectin glycoprotein ligand-1 (PS

203 mechanisms by which antibody blockade of the inhibitory receptor PD-1 (anti-PD-1) reinvigorates T cel

204 apply this technology to tune the T-cell co-inhibitory receptor PD-1 and to explore how antigen expr

205 imprinting of the epigenetic program of the inhibitory receptor PD-1 occurs during the effector phas

206 circulating CD8(+) T cells which express the inhibitory receptor PD-1, as well as the cytolytic prote

207 Expression of PD-L1, the ligand for T-cell inhibitory receptor PD-1, is one key immunosuppressive m

208 bpopulations showed higher expression of the inhibitory receptor PD-1.

209 xpressing CD8(+) T cells often coexpress the inhibitory receptor PD-1.

210 CD8 TILs with high expression of activating/inhibitory receptors PD-1 and LAG-3 (denoted PD-1(hi)) t

211 intratumoral CD8(+) T cells coexpressing the inhibitory receptors PD-1 and Tim-3 from patients with r

212 mour-infiltrating lymphocytes expressing the inhibitory receptors PD-1 and TIM3 exhibited similar pro

213 flow cytometry to quantify expression of the inhibitory receptors PD-1, hepatitis A virus cellular re

214 er proportion of CD8(+) T cells coexpressing inhibitory receptors (PD-1/CTLA4) than HCV-negative LT,

215 ed IL-35 promoted the expression of multiple inhibitory receptors (PD1, TIM3, LAG3), thereby facilita

216 cells, patient-derived ALL cells express the inhibitory receptors PECAM1, CD300A and LAIR1 at high le

217 In the case of MHC class I-specific inhibitory receptors, phosphorylation of cytosolic tyros

218 Costimulatory and inhibitory receptors play a key role in regulating immun

219 ediated by human, but not by mouse TIGIT, an inhibitory receptor present on all human NK cells and on

220 Further, inhibitory receptors present in the TME can inhibit T ce

221 these patients express high levels of immune inhibitory receptors, produce lower levels of interferon

222 ics of the inhibitory synapse mediated by an inhibitory receptor, programed death protein-1, and the

223 (+) regulatory T cells and expression of the inhibitory receptor programmed cell death -1 PD-1 on CD4

224 and cancer have sustained expression of the inhibitory receptor programmed cell death 1 (PD-1).

225 liver, where CD8(+) T-cell expression of the inhibitory receptor programmed cell death 1 increased 25

226 after HMPV infection expressed levels of the inhibitory receptor programmed death 1 (PD-1) similar to

227 various immune responses by engaging the co-inhibitory receptor programmed death-1.

228 Progenitors lacking the inhibitory receptors programmed death-1 (PD-1) and T cel

229 stimulator, interleukin 7 receptor), whereas inhibitory receptors (programmed cell death protein 1 an

230 ptation: transcriptional upregulation of the inhibitory receptor Ptch1, transcriptional downregulatio

231 R KO mice had increased expression of T cell inhibitory receptors, reduced expression of chemokine re

232 Since PD-1 is a major inhibitory receptor regulating T cell dysfunction during

233 acellular mechanism for functional tuning by inhibitory receptors remains unclear.

234 t with restoration of NK cell activating and inhibitory receptor repertoire to normal healthy donor l

235 essed this mutant Ly49A exhibited an altered inhibitory receptor repertoire.

236 playing the highest and lowest prevalence of inhibitory receptors, respectively.

237 k mechanisms by which negative selection and inhibitory receptors restrain TCR signaling to enforce b

238 of TIGIT and PD-1, the coexpression of those inhibitory receptors should be considered when evaluatin

239 une evasion through its interaction with the inhibitory receptor sialic-acid-binding Ig-like lectin 1

240 Here, we studied the inhibitory receptor Siglec-11 that shows uniquely human

241 ith Siglec-7 ligands, thereby recruiting the inhibitory receptor Siglec-7 expressed on the NK cell su

242 D47 molecule is known to be a ligand for the inhibitory receptor signal regulatory protein alpha and

243 ated protein CD47, which is a ligand for the inhibitory receptor signal regulatory protein alpha, is

244 The inhibitory receptor signal regulatory protein-alpha (SIR

245 a model where the balance of activating and inhibitory receptor signaling in NK cells selects for th

246 ctor function, and cell differentiation with inhibitory receptor signaling that may be exploited to e

247 ation of CD47, a ligand for the myeloid cell inhibitory receptor SIRPalpha, from tumor cells by genet

248 Recent translation of knowledge about inhibitory receptors such as CTLA-4 and PD-1 into the ca

249 Blocking the function of inhibitory receptors such as PD-1, CTLA-4, 2B4, Tim-3, a

250 ine secretion and up-regulated expression of inhibitory receptors such as PD-1.

251 ses to limit immunopathology by upregulating inhibitory receptors such as programmed cell death 1 (PD

252 r molecules and upregulate the expression of inhibitory receptors such as programmed cell-death 1 (PD

253 leted TST cells did not upregulate genes for inhibitory receptors (such as Pdcd1, Entpd1, Havcr2, Cd2

254 Co-inhibitory receptors, such as CTLA-4 and PD-1, have an i

255 concerted actions of activating FcgammaR and inhibitory receptors, such as FcgammaRIIb and SIRPalpha.

256 e CNS revealed increased expression of other inhibitory receptors, such as Pd1 and Tim3, and decrease

257 al killer (NK) cell function is regulated by inhibitory receptors, such as the family of killer immun

258 inding affinities of the PD-1-PD-L1/PD-L2 co-inhibitory receptor system, and discovered an unexpected

259 daptive NK cells express lower levels of the inhibitory receptor T-cell Ig and ITIM domain (TIGIT), w

260 The inhibitory receptor T-cell immunoglobulin and mucin doma

261 Expression levels of the inhibitory receptor, T cell immunoglobulin and ITIM doma

262 review immunoregulatory mechanisms, such as inhibitory receptors, T regulatory cells, and the anti-i

263 The next wave of co-inhibitory receptor targets that are being explored in c

264 Our data thus implicate CD160 as a co-inhibitory receptor that delivers antigen-dependent sign

265 PD-1 is an inhibitory receptor that has a major role in T cell dysf

266 which is encoded by Klrc1, is a lectin-like inhibitory receptor that is expressed as a heterodimer w

267 Ig-like receptor B is a cell surface immune-inhibitory receptor that is expressed by eosinophils and

268 Tim-3 is a co-inhibitory receptor that is expressed on IFN-g-producing

269 ed cell death protein 1 (PD-1) is a critical inhibitory receptor that limits excessive T cell respons

270 PD-1 is an inhibitory receptor that regulates T cell function, but

271 Siglec-8 is a human immune-inhibitory receptor that, when engaged by specific self-

272 In this regard, several co-inhibitory receptors that are preferentially expressed b

273 NK cells possess inhibitory receptors that are responsible for self-MHC c

274 hereby maintained inhibition of NK cells via inhibitory receptors that bind HLA-C and HLA-E.

275 Many NK cells express inhibitory receptors that bind self-MHC class I (MHC I)

276 is has provided impetus to identify other co-inhibitory receptors that could be exploited to enhance

277 ke receptor B2 (LILRB2) are widely expressed inhibitory receptors that interact with a diverse set of

278 he tumor microenvironment (TME), blockade of inhibitory receptors that limit NK cell functions, and t

279 via stochastically expressed MHC-I-specific inhibitory receptors that prevent NK cell activation via

280 wn as PD ligand 1 [PDL1]) and galectin-9-are inhibitory receptors that regulate the balance between p

281 ceptor DNAX accessory molecule (DNAM)-1, the inhibitory receptor TIGIT, and the CD96 receptor with bo

282 ific antigen-presenting cell subsets and the inhibitory receptor Tim-3 may contribute to CD8(+) T cel

283 ed than those of WT mice and upregulated the inhibitory receptor Tim-3.

284 rating lymphocytes coexpressed PD-1 with the inhibitory receptors TIM-3, CTLA-4, LAG-3, and TIGIT, bu

285 tion-associated system: the complex of human inhibitory receptor TIM3 (hTIM3) and its ligand phosphat

286 TORC1 signaling also decreased expression of inhibitory receptors TIM3 and PD-1, as well as partially

287 Here we show that P. falciparum uses immune inhibitory receptors to achieve immune evasion.

288 However, how NK cells determine which inhibitory receptors to express on their cell surface du

289 cells organize signaling from activating and inhibitory receptors to form a lytic synapse.

290 netic technology - artificial excitatory and inhibitory receptors - to modulate neuronal activity in

291 y ligands, and enhanced engagement of T cell inhibitory receptors, upon antigen presentation, by thes

292 The expression of the CD300a inhibitory receptor was significantly reduced on cells f

293 Marked induction of checkpoint inhibitory receptors was also observed on the surface of

294 granzyme B and perforin and those expressing inhibitory receptors was higher in symptomatic patients

295 activation molecule families and a number of inhibitory receptors were identified as hubs for viral p

296 unction also as the main ligands for NK cell inhibitory receptors, which prevent NK cells from killin

297 Programmed cell death-1 (PD-1) is an inhibitory receptor with an essential role in maintainin

298 us myeloid immune cells and classified as an inhibitory receptor with the potential to mediate tyrosi

299 ecognition of alloantigens by activating and inhibitory receptors with shared specificity is uncharac

300 ocyte-activation gene 3 (LAG-3) is an immune inhibitory receptor, with major histocompatibility compl