ライフサイエンスコーパス: coinhibitory

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

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

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

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

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

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

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

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

9 27-mediated costimulation can synergize with coinhibitory checkpoint blockade to switch off molecular

10 Although coinhibitory checkpoint blockade with anti-programmed de

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 vent the ligation of an essential regulatory coinhibitory molecule.

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

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

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

52 Coinhibitory molecules expressed by tumor cells, immune

53 Attenuating coinhibitory molecules for the treatment of cancer is ga

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

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

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

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

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

59 5 phosphorylation, and the expression of the coinhibitory molecules programmed cell death protein 1 (

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

61 Sustained signaling via these coinhibitory molecules results in functional exhaustion

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

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

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

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

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

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

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

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

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

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

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

73 Coinhibitory pathways are thought to act in later stages

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

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

76 Coinhibitory pathways in the B7-CD28 family provide crit

77 T cell coinhibitory pathways restrict the strength and duration

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

79 Tumors exploit these coinhibitory pathways to evade immune eradication.

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

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

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

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

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

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

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

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

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

89 Coinhibitory receptor CD160 was also overexpressed in pe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 Coinhibitory receptors are critical for the maintenance

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

125 The three coinhibitory receptors are cytotoxic T lymphocyte antige

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

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

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

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

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

131 Antagonistic antibodies targeting coinhibitory receptors have revolutionized the treatment

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

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

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

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

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

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

138 he contribution of several costimulatory and coinhibitory receptors.

139 cular signature defined by the expression of coinhibitory receptors.

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

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

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

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

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

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

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

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

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

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

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

151 These coinhibitory signals limit the strength and duration of

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

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

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

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

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

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

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