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 ulated genes and ligands for multiple T cell inhibitory receptors.

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

4 ceptor without coexpressing any allospecific inhibitory receptors.

5 and associated with coexpression of multiple inhibitory receptors.

6 of activation markers and downregulation of inhibitory receptors.

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

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

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

10 onal impairment and upregulation of numerous inhibitory receptors.

11 cannot replace Qa-1 as a ligand for NK cell inhibitory receptors.

12 gh combinatorial signals from activating and inhibitory receptors.

13 iated with reduced binding to its respective inhibitory receptors.

14 functions may be regulated by activating or inhibitory receptors.

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

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

17 thogen molecular mimicry of host ligands for inhibitory receptors.

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

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

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

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

22 tive signals received through activating and inhibitory receptors.

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

24 ct DC subpopulations via targeting Abs to DC inhibitory receptor 2 (DCIR2, clone 33D1) or to DEC205 w

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

26 from a gene recombination event between the inhibitory receptor allele KIR3DL1*001 and the activatin

27 Inhibitory receptors also promote NK cell tolerance and

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

29 rs in spite of high surface expression of an inhibitory receptor and in contrast to the immunodominan

30 Paired Ig-like type 2 receptor (PILR)alpha inhibitory receptor and its counterpart PILRbeta activat

31 ssed immunoglobulin-like transcript 4 (ILT4) inhibitory receptor and that this expression was induced

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

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

34 ereas atypical MBCs expressed high levels of inhibitory receptors and had low TNF-alpha responses.

35 to eliminate cancer but is held in check by inhibitory receptors and ligands.

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

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

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

39 The interaction between clonally distributed inhibitory receptors and their activating counterparts o

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

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

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

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

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

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

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

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

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

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

50 activating receptor rather than through the inhibitory receptor as classically proposed.

51 surface expression of phenotypic markers and inhibitory receptors, as well as in vivo cytotoxicity an

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

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

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

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

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

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

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

59 MHC-I-specific inhibitory receptors both block activation signals and t

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

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

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

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

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

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

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

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

68 usters account for 5% of the total number of inhibitory receptor clusters on principal neurons.

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

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

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

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

73 Since inhibitory receptors control NK-cell activation and are

74 The inhibitory receptor CTLA4 and the transcription factor H

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

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

77 While inhibitory receptors dampen cellular activation by recog

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

79 Blockade of inhibitory receptors differentially affected cytokine pr

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

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

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

83 kade demonstrated that PD-1 was the dominant inhibitory receptor early after reinfection.

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

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

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

87 , virus-infected, or transformed cells, most inhibitory receptors engage MHC class I, preventing NK c

88 Programmed cell death 1 (PD-1) is an inhibitory receptor expressed by activated T cells that

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

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

91 lymphocyte-associated antigen 4 (CTLA-4), an inhibitory receptor expressed by T lymphocytes, has emer

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

93 Inhibitory receptors expressed by T cells mediate tolera

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

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

96 y the constellation of co-stimulatory and co-inhibitory receptors expressed on the cell surface.

97 MHC class I D(k) and Ly49G2 (G2) inhibitory receptor-expressing NK cells are essential to

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

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

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

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

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

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

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

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

106 There is an unclear relationship between inhibitory receptor expression on T cells and their abil

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

108 hesis was accompanied by the upregulation of inhibitory receptor expression on the T cells, and ex vi

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

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

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

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

113 The inhibitory receptor FcgammaRIIB is expressed on human an

114 The inhibitory receptor FcgammaRIIB plays a central role in

115 Interestingly however, expression of the inhibitory receptor FcgammaRIIb was also modestly increa

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

117 exes by stimulating the up-regulation of the inhibitory receptor FcgammaRIIB.

118 phylaxis and whether this occurs through the inhibitory receptor FcgammaRIIb.

119 on CCR7 and increased in the absence of the inhibitory receptor FcgammaRIIB.

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

121 Rs are activating and controlled by a single inhibitory receptor, FcgammaRIIB (CD32B), which also reg

122 immune complexes are controlled by a single inhibitory receptor, FcgammaRIIb (CD32b).

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

124 Indeed, engagement of this D1-like inhibitory receptor following binding with DA suppresses

125 Reduced MHC-I expression or a lack of inhibitory receptors for MHC-I results in diminished NK

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

127 onsiveness between NK cells with and without inhibitory receptors for self-MHC ("licensing").

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

129 otoxic T lymphocyte antigen-4 (CTLA-4) is an inhibitory receptor found on immune cells.

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

131 Even though expression of inhibitory receptors has been reported on neutrophils, t

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

133 Inhibitory receptors have been extensively described for

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

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

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

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

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

139 is study, we tested the roles of the BCR and inhibitory receptors in controlling the expression of Et

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

141 -cell tolerance to define the roles of these inhibitory receptors in regulating CD8(+) T-cell toleran

142 The GABAA receptors are the major inhibitory receptors in the brain and are localized at b

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

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

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

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

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

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

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

150 between their extracellular domains, NK cell inhibitory receptors killer Ig-like receptor (KIR) 2DL2*

151 vestigated the expression and function of an inhibitory receptor, killer cell lectin-like receptor su

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

153 sed effector functions and expression of the inhibitory receptor KLRG1.

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

155 show decreased expression of the generalized inhibitory receptor leukocyte Ig-like receptor subfamily

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

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

158 Several inhibitory receptors limit the magnitude and duration of

159 nship between T-cell location, expression of inhibitory receptors, maturation, and viral control usin

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

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

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

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

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

165 f CTCL cells, induced expression of the cell-inhibitory receptor of CD80, CD152 (CTLA-4), impairs gro

166 ts demonstrate that siglec-E functions as an inhibitory receptor of neutrophils via positive regulati

167 activation is regulated by costimulatory and inhibitory receptors, of which both B and T lymphocyte a

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

169 lymphocyte attenuator (BTLA) functions as an inhibitory receptor on gd T cells and suggest that disru

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

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

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

173 In this study, we identify Sirpa encoding an inhibitory receptor on myeloid cells as a gene in the in

174 nal-regulatory protein alpha (SIRPalpha), an inhibitory receptor on myeloid cells that gives a "don't

175 immunoglobulin-like lectin 5 (Siglec-5), an inhibitory receptor on phagocytes.

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

177 nstrating the crucial role of Siglec-G as an inhibitory receptor on this cellular subset.

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

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

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

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

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

183 Siglec-7 and -9 are MHC class I-independent inhibitory receptors on human NK cells that recognize si

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

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

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

187 Blockade of inhibitory receptors on T cells in Stx11-deficient mice

188 ent clinical trials showed that targeting of inhibitory receptors on T cells induces durable response

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

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

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

192 oliferation, and increased expression of the inhibitory receptor PD-1 in CMV-specific CD4(+) T lympho

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

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

195 by signals through the exhaustion-associated inhibitory receptor PD-1, suggesting that induction of e

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

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

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

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

200 more impaired and more highly expressed the inhibitory receptors PD-1, LAG-3, and 2B4 than primary T

201 Despite increased expression of the inhibitory receptors PD1, CD160, and CD244 on total CD8(

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

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

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

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

206 ain a specific subset of both activating and inhibitory receptors, potentially imbuing them with a di

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

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

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

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

211 exhaustion of CD8+ T cells that express the inhibitory receptor programmed cell death 1 (PD-1).

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

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

214 Blockade of inhibitory receptor programmed cell death protein 1 (PD-

215 previously showed that the engagement of the inhibitory receptor programmed death (PD)-1 on HIV-1-spe

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

217 The inhibitory receptor programmed death-1 (PD-1) constrains

218 The inhibitory receptor programmed death-1 (PD-1) has been s

219 ed upregulation of surface expression of the inhibitory receptor programmed death-1 (PD-1), but surpr

220 ute viral lower respiratory infection by the inhibitory receptor programmed death-1 (PD-1).

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

222 In all 6 tumors studied, expression of the inhibitory receptors programmed cell death 1 (PD-1; also

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

224 toma in mice initiated by deletion of the Hh inhibitory receptor Ptch1.

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

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

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

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

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

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

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

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

233 which can engage the myelomonocytic lineage inhibitory receptor Siglec-9, thereby evading immunosurv

234 Thus, the loss of the inhibitory receptor Siglec-G led to a moderate exacerbat

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

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

237 The inhibitory receptor signal regulatory protein-alpha (SIR

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

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

240 This NK cell education, which is mediated by inhibitory receptors specific for MHC-I molecules, chang

241 ell population, defined by the expression of inhibitory receptors specific for self-MHC class I molec

242 Inhibitory receptors such as CD22 can downmodulate autor

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

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

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

246 hich infiltrating T cells are "exhausted" by inhibitory receptors such as PD-1.

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

248 ronic infections and cancer via signaling by inhibitory receptors such as programmed cell death-1 (PD

249 l signals within the tissue by expression of inhibitory receptors such as programmed death 1 that lim

250 stromal lymphopoietin receptors, as well as inhibitory receptors, such as CD300a, FcgammaRIIb, and e

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

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

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

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

255 The inhibitory receptor T-cell immunoglobulin and mucin doma

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

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

258 T cells from liver express different inhibitory receptors than T cells from blood, independen

259 ction and lower expression of PD-1 and other inhibitory receptors than TCD8s from HMPV-infected mice.

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

261 fects of programmed cell death 1 (PD1), a co-inhibitory receptor that impairs T-cell function and is

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

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

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

265 KIR3DL1 is a polymorphic inhibitory receptor that modulates NK cell activity thro

266 KIR3DL1 is a highly polymorphic inhibitory receptor that recognizes a diverse array of H

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

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

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

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

271 NK cells express an array of activating and inhibitory receptors that determine NK cell responses up

272 erbalanced by a number of membrane-localized inhibitory receptors that limit B cell activation and pl

273 nsing, is a complex process mediated through inhibitory receptors that recognize self.

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

275 differentiated based on their expression of inhibitory receptors; these correlate with their memory

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

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

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

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

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

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

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

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

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

285 Binding of NK cell inhibitory receptors to MHC class I (MHC-I) confers incr

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

287 alone is insufficient for TCD8 impairment or inhibitory receptor upregulation, but that viral Ag-indu

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

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

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

291 mphocytes were extracted; T-cell markers and inhibitory receptors were quantified for total and virus

292 uman cell lines showed that TLR10 acts as an inhibitory receptor when forming heterodimers with TLR2;

293 erminants: mature NK cells acquire primarily inhibitory receptors, whereas CD8(+) T cells attain a sp

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

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

296 t of the surface Ig-like transcript 2 (ILT2) inhibitory receptor with its preferential ligand HLA-G i

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

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

299 Natural killer (NK) cells express inhibitory receptors with varied binding affinities to s

300 ng capacity of pDCs is regulated by specific inhibitory receptors, yet none of the known receptors ar