ライフサイエンスコーパス: coinhibitory

1 Laminins alpha4 and alpha5 are coinhibitory and costimulatory ligands for human and mou

2 eron (IFN-I) signaling, and a diverse set of coinhibitory and costimulatory molecules during CD4(+) T

3 cell activation can be profoundly altered by coinhibitory and costimulatory molecules.

4 A highly complex network of coinhibitory and costimulatory receptors regulates the o

5 The CD28 family is comprised of coinhibitory and costimulatory receptors.

6 B7-DC is highly homologous to a coinhibitory B7 family member, B7-H1, which also binds P

7 m conditional Rictor(-/-) mice exhibit lower coinhibitory B7-H1 molecule expression independently of

8 expression of costimulatory (CD80, CD86) and coinhibitory (B7-H1) molecules on mDCs.

9 Here, we found that the coinhibitory cell surface receptor programmed death 1 (P

10 CD28 and CTLA-4 are major costimulatory and coinhibitory cell surface signaling molecules interactin

11 27-mediated costimulation can synergize with coinhibitory checkpoint blockade to switch off molecular

12 Although coinhibitory checkpoint blockade with anti-programmed de

13 PD-1/PD-L1 is a major coinhibitory checkpoint pathway that modulates immune es

14 In this study, we analyzed T-cell coinhibitory/costimulatory genes across more than 1100 s

15 reatic Tregs had increased expression of the coinhibitory counter-receptor T-cell immunoreceptor with

16 ulatory CSSMs that promote the response, and coinhibitory CSSMs that inhibit the response, are requir

17 the contribution of costimulatory (CD28) and coinhibitory (CTLA-4, PD-1) receptors on MP T cell homeo

18 timulatory interactions, which preserves the coinhibitory CTLA4-CD80/86 interactions and the function

19 We evaluated Eomes and coinhibitory cytotoxic T lymphocyte antigen-4 (CTLA4) ex

20 Antibody modulation of T-cell coinhibitory (e.g., CTLA-4) or costimulatory (e.g., 4-1B

21 atory potential of CD28 while exploiting the coinhibitory effects of CTLA-4.

22 effects in the diagnostic stage and minimal coinhibitory effects on normal cells.

23 n this reductionist system, costimulatory or coinhibitory engagement mainly elicits generic responses

24 We hypothesized that B7-H3, a coinhibitory factor, is expressed by primary breast canc

25 ir viability, led to increased expression of coinhibitory factors CTLA-4, PD-1, and Blimp-1, and decr

26 these findings demonstrate a cell-intrinsic coinhibitory function of FcgammaRIIB in regulating CD8(+

27 tion both in vitro and in vivo, validating a coinhibitory function of PD-1H.

28 derstanding of the mechanisms underlying the coinhibitory functions of CTLA-4, PD-1, PD-L1:B7-1 and P

29 t knowledge of the mechanisms underlying the coinhibitory functions of pathways in the B7-CD28 family

30 pleting monoclonal antibody specific for the coinhibitory immunoglobulin receptor, B and T lymphocyte

31 xic T-lymphocyte antigen 4 (CTLA4) encodes a coinhibitory immunoreceptor that is a key regulator of s

32 cell-death 1 (PDCD1) are two genes encoding coinhibitory immunoreceptors that harbor polymorphisms w

33 1 ligand 1), and TNFRSF14, which impede the coinhibitory interactions between the neoplastic B- and

34 report that rapamycin treatment modulates EC coinhibitory ligand expression and alters cytokine/chemo

35 d ectopically expressed PD-1H functions as a coinhibitory ligand for T cell responses.

36 y of proteins and has been shown to act as a coinhibitory ligand on APCs that suppress T cell respons

37 oral arteries revealed low expression of the coinhibitory ligand programmed death ligand-1 (PD-L1) co

38 wever, relative to other known costimulatory/coinhibitory ligands (e.g., CD86, CD80, PD-L1), the phys

39 Crosstalk between costimulatory and coinhibitory ligands are a prominent node of immune cell

40 owing immune attack, solid tumors upregulate coinhibitory ligands that bind to inhibitory receptors o

41 cells, promoted expression of exhaustion and coinhibitory markers on T cells, and synergized with CTL

42 unique structural features may contribute to coinhibitory mechanisms.

43 soluble form of T cell exhaustion associated coinhibitory molecule 3, sTim-3, is shed from the surfac

44 of GECs induces the expression of the T cell coinhibitory molecule B7-H1 on GECs.

45 T cell responses by way of expression of the coinhibitory molecule B7-H4, and may provide fundamental

46 SC revealed that activated HSC expressed the coinhibitory molecule B7-H4.

47 we demonstrate that signals delivered by the coinhibitory molecule B7-homologue 1 (B7-H1) via a B7-ho

48 the endogenous T cell repertoire through the coinhibitory molecule B7H1.

49 g cells showed reduced surface levels of the coinhibitory molecule CD200R.

50 imulation of dendritic cells mediated by the coinhibitory molecule CTLA-4 induced nuclear localizatio

51 Our results pinpoint the coinhibitory molecule CTLA4 as an immunological checkpoi

52 clinical models predict that blockade of the coinhibitory molecule cytotoxic T lymphocyte-associated

53 d regulatory T cell frequency, and augmented coinhibitory molecule expression on donor CD4(+) T cells

54 s PD-1H on both T cells and APCs serves as a coinhibitory molecule for T cell activation and provide

55 PD-1H is a recently identified cell surface coinhibitory molecule of the B7/CD28 immune modulatory g

56 iral infections shows that expression of the coinhibitory molecule PD-1 predicts CD8+ antiviral T-cel

57 me circumstances, such as the absence of the coinhibitory molecule PD-1, additional hits are required

58 omparatively high relative expression of the coinhibitory molecule PD-L1, and the elevated frequency

59 ng cells also express enhanced levels of the coinhibitory molecule programmed cell death ligand 1 (PD

60 human Ag-specific CD8(+) T cells acquire the coinhibitory molecule programmed death ligand 1 (PD-L1)

61 mphocyte attenuator (BTLA, CD272) is a novel coinhibitory molecule structurally and functionally rela

62 Programmed death-1 ligand 1 (PD-L1) is a coinhibitory molecule that negatively regulates multiple

63 study, we examined the role of the putative coinhibitory molecule TIGIT and show that loss of TIGIT

64 e identified Foxp3(+) T cells expressing the coinhibitory molecule TIGIT as a distinct Treg cell subs

65 rogrammed death-1 homolog (PD-1H), an immune coinhibitory molecule, is highly expressed in blasts fro

66 vent the ligation of an essential regulatory coinhibitory molecule.

67 We found that unlike other coinhibitory molecules (CTLA-4, LAG-3, TIM-3), PD-1 was

68 revealed the expansion of B cells expressing coinhibitory molecules (PD-1, PD-L1, TIM-1, VISTA, CTLA-

69 we review factors controlling LIP, including coinhibitory molecules and other attenuators of TCR sign

70 ) cells are characterized by upregulation of coinhibitory molecules and reduced polyfunctionality.

71 The roles of other coinhibitory molecules and their individual contribution

72 analysis revealed that clustering of MHC and coinhibitory molecules are indispensable for the inhibit

73 Coinhibitory molecules expressed by tumor cells, immune

74 Attenuating coinhibitory molecules for the treatment of cancer is ga

75 The transfer of functionally active coinhibitory molecules from APCs onto human CD8(+) T cel

76 heir expression of various costimulatory and coinhibitory molecules in a manner that was dependent on

77 atory molecules and attenuated expression of coinhibitory molecules necessary for higher T cell activ

78 no difference in levels of costimulatory and coinhibitory molecules on precursor myeloid DC between t

79 population that expressed high levels of the coinhibitory molecules PD-1, Lag-3, and TIGIT, thereby l

80 High protein expression of coinhibitory molecules PD1, CTLA4, and LAG3, accompanied

81 5 phosphorylation, and the expression of the coinhibitory molecules programmed cell death protein 1 (

82 nisms by which HIV-1 induces upregulation of coinhibitory molecules remain to be fully elucidated.

83 Sustained signaling via these coinhibitory molecules results in functional exhaustion

84 T5 capacity CD8+ T cells and the increase in coinhibitory molecules were correlated.

85 presentation, drive heightened expression of coinhibitory molecules, and promote tumor survival after

86 memory phenotype with minimal expression of coinhibitory molecules, and they were polyfunctional bas

87 Today, a variety of coinhibitory molecules, including cytotoxic T lymphocyte

88 on of STAT5 and have increased expression of coinhibitory molecules, processes which were correlated

89 (STAT)5 phosphorylation and upregulation of coinhibitory molecules.

90 Therefore, manipulation of coinhibitory networks is an attractive adjuvant immunoth

91 nhances T cell function, serving as either a coinhibitory or costimulatory receptor depending on the

92 o studies indicate that Grx4 and Fra2 act as coinhibitory partners that inactivate the transcriptiona

93 signals, the CD27-CD70 axis may represent a coinhibitory pathway for this immunoregulatory T cell po

94 This unique human T-cell coinhibitory pathway may afford unique strategies for th

95 ressive viral factor, induces the PD-1/PD-L1 coinhibitory pathway on human dendritic cells (DCs).

96 y virus type 1 (HIV-1) Tat on the PD-1/PD-L1 coinhibitory pathway on human monocyte-derived dendritic

97 se results provide the first evidence that a coinhibitory pathway plays a critical role in regulating

98 ch conditions is dependent on the PD-1/PD-L1 coinhibitory pathway.

99 we discuss the immunoregulatory functions of coinhibitory pathways and their translation to effective

100 Coinhibitory pathways are thought to act in later stages

101 Advances in understanding T cell coinhibitory pathways have stimulated a new era of immun

102 gands (PD-L1 and HLA-DR), demonstrating that coinhibitory pathways impede CAR T-cell persistence in t

103 In this review, we discuss the influence of coinhibitory pathways in suppressing autologous and allo

104 Coinhibitory pathways in the B7-CD28 family provide crit

105 ced concurrent activation of multiple T cell coinhibitory pathways is an effective way to induce self

106 T cell coinhibitory pathways restrict the strength and duration

107 t cause chronic infections can exploit these coinhibitory pathways to establish an immunosuppressive

108 Tumors exploit these coinhibitory pathways to evade immune eradication.

109 de of co-stimulation pathways and agonism of coinhibitory pathways, in order to achieve the delicate

110 viral immunity by altering costimulatory and coinhibitory pathways, selective targeting of VIP signal

111 esting the implication of other Tat-mediated coinhibitory pathways.

112 ction is associated with induction of T-cell coinhibitory pathways.

113 such as interleukin-12, while downregulating coinhibitory PD-L1 molecule.

114 (HLA-A2) alongside costimulatory CD80 and/or coinhibitory programmed death ligand 1 (PD-L1).

115 show that engagement of the newly discovered coinhibitory receptor B and T lymphocyte attenuator (BTL

116 ongyloides ratti induced upregulation of the coinhibitory receptor B and T lymphocyte attenuator (BTL

117 this capacity, including cancer vaccines and coinhibitory receptor blockade, have demonstrated clinic

118 ell activation, with increased proportion of coinhibitory receptor BTLA(+) T cells and Tim-3(+) NK ce

119 Coinhibitory receptor CD160 was also overexpressed in pe

120 Furthermore, blockade of the coinhibitory receptor CTL-associated antigen 4 (CTLA-4)

121 have an increased propensity to express the coinhibitory receptor CTLA-4 and this correlates with vi

122 The T cell coinhibitory receptor CTLA-4 has been implicated in the

123 is study we examined the contribution of the coinhibitory receptor cytotoxic T lymphocyte antigen-4 (

124 at a small population of mTECs expressed the coinhibitory receptor cytotoxic T lymphocyte-associated

125 ination treatment were further improved when coinhibitory receptor cytotoxic T-lymphocyte-associated

126 rring downstream of TCR and costimulatory or coinhibitory receptor engagement.

127 Despite high coinhibitory receptor expression in the Tc17 cell cluste

128 how that type 1 interferon (IFN-I) regulates coinhibitory receptor expression on human T cells, induc

129 We also describe heterogeneity of Tr1 cell coinhibitory receptor expression that has implications f

130 The identification of unique TFs controlling coinhibitory receptor expression under IFN-I response ma

131 The coinhibitory receptor expression was linked to altered I

132 ere, we determined that PD-1H functions as a coinhibitory receptor for CD4(+) T cells.

133 Thus, CEACAM1 acted as a coinhibitory receptor for G-CSFR regulating granulopoies

134 the B and T lymphocyte attenuator (BTLA), a coinhibitory receptor for T cells, suppresses, while blo

135 The coinhibitory receptor lymphocyte activation gene 3 (LAG-

136 y reveals the crucial function of PD-1H as a coinhibitory receptor on alloreactive T cells and its fu

137 Here, we show that CD31 is a key coinhibitory receptor on stimulated DCs, favoring the de

138 cell activation, identifying HVEM/BTLA as a coinhibitory receptor pair.

139 product of programmed cell death 1 (PDCD1), coinhibitory receptor PD-1, was expressed at a higher pe

140 First, signaling via PD-1H coinhibitory receptor potently arrests alloreactive dono

141 usly, we demonstrated the involvement of the coinhibitory receptor programmed death-1 (PD-1) in suppr

142 The coinhibitory receptor programmed death-1 (PD-1) maintain

143 exhausted with heightened expression of the coinhibitory receptor programmed death-1 (PD-1).

144 These analyses revealed that the coinhibitory receptor T cell Ig and ITIM domain (TIGIT)

145 which is mediated, in part, by the membrane coinhibitory receptor T cell immunoglobulin mucin domain

146 Here we identify TIGIT as a coinhibitory receptor that critically limits antitumor a

147 ITIM domain (TIGIT) is a recently identified coinhibitory receptor that is found on the surface of a

148 Programmed cell death-1 (PD-1) is a coinhibitory receptor that suppresses T cell activation

149 ression of the signature cytokine IL-21, the coinhibitory receptor TIGIT and the transcriptional repr

150 ule secretion by preferentially engaging the coinhibitory receptor TIGIT.

151 , TIGIT+ Tregs upregulated expression of the coinhibitory receptor TIM-3 in tumor tissue, and TIM-3 a

152 Programmed death 1 (PD-1) protein, a T-cell coinhibitory receptor, and one of its ligands, PD-L1, pl

153 lymphocyte attenuator (BTLA), a CD28 family coinhibitory receptor, in hapten-induced CHS, BTLA-defic

154 recently shown that the murine cell surface coinhibitory receptor, PD-1, has a role in septic morbid

155 pendent and have increased expression of the coinhibitory receptor, programmed death 1, resulting in

156 Costimulatory and coinhibitory receptor-ligand pairs on T cells and APC co

157 nase ADAM10, producing a soluble form of the coinhibitory receptor.

158 ion to costimulatory signals, B7/CD28 family coinhibitory receptor/ligands that modulate immune respo

159 gulatory T cells (Tregs), T cells expressing coinhibitory receptors (CD38, PD-1, and PD-1/TIM-3), and

160 derate, and severe disease, we observed that coinhibitory receptors (e.g., PD-1, CTLA-4, TIM-3, VISTA

161 ns of SARS-CoV-2-reactive T cells expressing coinhibitory receptors and examine the immunogenicity of

162 temporal kinetics that control expression of coinhibitory receptors and IFN-I response genes, with SP

163 unctions are mediated by local expression of coinhibitory receptors and immunosuppressive mediators t

164 In C57BL/6 mice, CD4 T cells upregulate coinhibitory receptors and lose effector cytokine produc

165 n, which is characterized by upregulation of coinhibitory receptors and loss of T cell function.

166 nce mechanisms, including regulation through coinhibitory receptors and suppression by regulatory T c

167 Coinhibitory receptors are critical for the maintenance

168 d Tregs is crucial, as therapies that target coinhibitory receptors are currently at the forefront of

169 The three coinhibitory receptors are cytotoxic T lymphocyte antige

170 curred independently of STAT6 and the T cell coinhibitory receptors B7-DC and B7-H1, two receptors th

171 Thus, multiple coinhibitory receptors can affect the development of HIV

172 Expression of the coinhibitory receptors CD160 and CD244 on circulating CD

173 This review outlines how the coinhibitory receptors CTLA-4 (cytotoxic T-lymphocyte an

174 immunomodulatory antibodies targeting T cell coinhibitory receptors CTLA-4 and PD-1 (programmed death

175 e a high frequency of cells that express the coinhibitory receptors CTLA-4 and PD-1, two subsets prev

176 Although inhibition of T cell coinhibitory receptors has revolutionized cancer therapy

177 Antagonistic antibodies targeting coinhibitory receptors have revolutionized the treatment

178 Understanding the function of coinhibitory receptors in effector T cells and Tregs is

179 To further investigate the role of coinhibitory receptors in the beryllium-induced immune r

180 Mechanistically, T reg cells and coinhibitory receptors maintained long-term viral sanctu

181 Expression of coinhibitory receptors on circulating CD4(+) and CD8(+)

182 Importantly, the expression of coinhibitory receptors on T cells recognizing SARS-CoV-2

183 Dual blockade of the PD-1 and TIGIT coinhibitory receptors on T cells shows promising early

184 Cancers exploit coinhibitory receptors on T cells to escape tumor immuni

185 ng antimyeloma activity, while inhibition of coinhibitory receptors PD-1 and CTLA-4 had no effect.

186 totoxic granule release, and coexpression of coinhibitory receptors PD-1 and TIM-3.

187 Although Gal-9 was coexpressed with other coinhibitory receptors such as TIGIT, CD160, CD39, and V

188 terplay of B cell dysregulation, implicating coinhibitory receptors, IL-6, and kynurenine in impaired

189 he contribution of several costimulatory and coinhibitory receptors.

190 nt of human CD4+ T cells expressing multiple coinhibitory receptors.

191 ough expression of a compensatory network of coinhibitory receptors.

192 R (killer cell immunoglobulin-like receptor) coinhibitory receptors.

193 production of TNF and IL2 and expression of coinhibitory receptors.

194 f IFNgamma, TNF, IL2, and high expression of coinhibitory receptors.

195 cular signature defined by the expression of coinhibitory receptors.

196 The key coinhibitory role exerted by CD31 on DCs highlighted by

197 These data are consistent with a coinhibitory role for mouse BTNs, including BTN1A1, the

198 ogrammed death-1 (PD-1) transmits a critical coinhibitory signal to T cells to negatively regulate im

199 Numerous studies indicate that coinhibitory signaling hampers the clinical benefit of c

200 ce that B and T lymphocyte attenuator (BTLA) coinhibitory signaling is required to temper early infla

201 T cell Ig and mucin domain protein-3 (TIM-3) coinhibitory signaling on activation of naive and memory

202 Our results illuminate a novel role for 2B4 coinhibitory signaling on CD4(+) T cells in mediating im

203 istinct TCR Vbeta subtypes, dysregulation of coinhibitory signaling pathways, and dysfunctional Tregs

204 through GITR suppressed conversion, whereas coinhibitory signaling via programmed death 1 ligand (PD

205 40L-OX40, CD155/CD112-DNAM-1) and subsequent coinhibitory signals (eg, CD80/CD86-CTLA4, PDL1/2-PD1, C

206 An excess of coinhibitory signals has been proposed to drive the T-ce

207 These coinhibitory signals limit the strength and duration of

208 To better understand how costimulatory and coinhibitory signals might be integrated, we profiled th

209 age or memory differentiation nor blocked by coinhibitory signals or missing inflammatory stimuli.

210 timulatory signals can be counterbalanced by coinhibitory signals such as the checkpoint molecule VIS

211 by altering the balance of costimulatory and coinhibitory signals these cells receive.

212 une responses by delivering costimulatory or coinhibitory signals through their ligands.

213 equirements in CD28 costimulatory and CTLA-4 coinhibitory signals to control naive and memory T cells

214 ntigen, and the net sum of costimulatory and coinhibitory signals transmitted via ligation of these m

215 costimulation while sparing CTLA-4 and PD-L1 coinhibitory signals.

216 ion while sparing CTLA-4 and PD-L1-dependent coinhibitory signals.

217 tinct from those expressing the KLRG1+TIGIT+ coinhibitory signature at the single-cell level.

218 In contrast, a coinhibitory signature, with an increased frequency of K

219 ly memory T cells, rather than activation or coinhibitory signatures, could distinguish the relapse.