ライフサイエンスコーパス: PD-L2

1 th receptor-1 (PD-1) and its ligands (PD-L1, PD-L2).

2 ll death protein 1 (PD-1) ligands, PD-L1 and PD-L2.

3 cancer target PD-1 and its ligands PD-L1 and PD-L2.

4 etween the two known PD-1 ligands, PD-L1 and PD-L2.

5 press high levels of PD-1 ligands, PD-L1 and PD-L2.

6 cules, CD16/32, ICAM-1, as well as PD-L1 and PD-L2.

7 onocyte-derived AAMs up-regulated Raldh2 and PD-L2.

8 b mRNA, whereas lung dendritic cells express PD-L2.

9 its interactions with its ligands, PD-L1 and PD-L2.

10 n interaction with its two ligands, PD-L1 or PD-L2.

11 n of T cells: CD115, CD124, CD80, PD-L1, and PD-L2.

12 upon interacting with its ligands PD-L1 and PD-L2.

13 ace receptor binds to two ligands, PD-L1 and PD-L2.

14 PD-1 receptor and its two ligands PD-L1 and PD-L2.

15 ted by the PD ligand (PD-L) PD-L1 but not by PD-L2.

16 only inflammatory macrophages to up-regulate PD-L2.

17 ) MBCs expressed MBC subset markers CD80 and PD-L2.

18 els of programmed death ligand 1 (PD-L1) and PD-L2.

19 cket formation and alter PD-1's affinity for PD-L2.

20 firmed EBV miR-BHRF1-2-5p bound to PD-L1 and PD-L2 3'UTRs to reduce PD-L1/L2 surface protein expressi

21 We report that programmed death ligand 2 (PD-L2), a known ligand of PD-1, also binds to repulsive

22 Furthermore, adoptive transfer of PD-L1(+)/PD-L2(+) AAMvarphis into EAE induced mice reduced diseas

23 PD-L2 abundance exceeded PD-L1 in over half the specimen

24 d and -purified proteins, we found that W110(PD-L2) acts as an "elbow" that helps shorten PD-L2 engag

25 nds of the binding face as the source of the PD-L2 affinity advantage.

26 rgence of placental mammals, suggesting that PD-L2-affinity tuning was part of the alterations to the

27 PD-L1/PD-L2 alterations are a defining feature of cHL.

28 n assay to evaluate CD274/PD-L1 and PDCD1LG2/PD-L2 alterations in 108 biopsy specimens from patients

29 nature, and prognostic significance of PD-L1/PD-L2 alterations in cHL remain undefined.

30 In cHL, chromosome 9p24.1/PD-L1/PD-L2 alterations increase the abundance of the PD-1 lig

31 ith cancer cells harboring genomic PD-L1 and PD-L2 amplification in the second.

32 S-L expression, and IL-4 treatment increased PD-L2 and B7-H3 expression and decreased ICOS-L expressi

33 PD-L2 and BMP-2/4 bind to distinct sites on RGMb.

34 f primary OASC were immunostained for PD-L1, PD-L2 and CD8.

35 of PD-L1 tended to express higher levels of PD-L2 and CD8.

36 lografts, as blocking PD-L1 or PD-1, but not PD-L2 and cytotoxic T-lymphocyte antigen 4, abrogated lo

37 a tryptophan (W110(PD-L2)) that is unique to PD-L2 and has been assumed to fit snuggly into a pocket

38 lips et al. explore the distinct features of PD-L2 and identify a specific evolutionary event linked

39 Importantly, PC-reactive B-1 cells expressed PD-L2 and irradiated chimeras demonstrated that B cell-i

40 Only 9 (50%) tumors expressed PD-L2 and it was at a low level.

41 s increased graft EC expression of PD-L1 and PD-L2 and reduced subsequent infiltration of allogeneic

42 Both tumors stained diffusely for PD-L2 and showed sparse PD-L1 staining.

43 ressed high constitutive levels of PD-L1 and PD-L2 and that PD-L2 overexpression inhibited neoantigen

44 nto the differential roles of host PD-L1 and PD-L2 and their associated cellular and metabolic mechan

45 e B7 family (ICOS ligand (ICOSL), PD-L1, and PD-L2) and the TNF/TNFR families (OX40 ligand (OX40L), C

46 gand 1 (PD-L1), programmed death 1 ligand 2 (PD-L2), and the butyrophilin family member butyrophilin-

47 RSV infection up-regulated PD-L1, PD-L2, and B7-H3 expression on all cells and ICOS-L expr

48 entified between tissue expression of PD-L1, PD-L2, and CD8.

49 d PD-1 ligand loci, CD274/PD-L1 and PDCD1LG2/PD-L2, and copy number-dependent increased expression of

50 latency genes, cell of origin (COO), PD-L1, PD-L2, and EBV miRs.

51 ces in gene and surface expression of PD-L1, PD-L2, and major histocompatibility class II (MHC-II).

52 of PD-1 engagement by its ligands, PD-L1 and PD-L2, and of PD-L1 binding to B7-1 requires quantitativ

53 of programmed cell death 1 ligand 1 (PD-L1), PD-L2, and other checkpoint genes.

54 ICOSL, PD-L1, PD-L2, and OX40L also are expressed on APCs such as dend

55 on T cells and its ligands (PD-1:PD-L1, PD-1:PD-L2, and PD-L1:B7.1), expressed on other cells in the

56 the abundance of the PD-1 ligands, PD-L1 and PD-L2, and promote their induction through Janus kinase

57 LR4 on human CMFs upregulates PD-L1, but not PD-L2, and reinforces CMF-mediated suppression of CD4(+)

58 ic markers, programmed death-ligand (PD-L)1, PD-L2, and the tryptophan degrading enzyme, IDO.

59 the abundance of the PD-1 ligands, PD-L1 and PD-L2, and their further induction through Janus kinase

60 esion molecules, including CSF2, CD40, PD-L1/PD-L2, and VCAM1.

61 ly higher levels of the PRMT1 targets PD-L1, PD-L2, and VISTA than those with the CC genotype.

62 Programmed death-ligand 1 (PD-L1) and PD-L2 are B7 family members expressed on several cell ty

63 PD-L1 (programmed death ligand 1) and PD-L2 are cell-surface glycoproteins that interact with

64 The PD-1 ligands PD-L1 and PD-L2 are commonly expressed on the surface of cells, wh

65 and preceding studies confirm that PD-L1 and PD-L2 are expressed in a high percentage of OASCs.

66 Human PD-L1 and PD-L2 are expressed on immature dendritic cells (iDC) an

67 We also observed that both PD-L1 and PD-L2 are independently required on donor cells to achie

68 PD-L1 and PD-L2 are ligands for PD-1, a costimulatory molecule tha

69 Programmed death ligand 1 (PD-L1) and PD-L2 are ligands for PD-1; the former is ubiquitously e

70 Programmed death-1 ligand (PD-L)1 and PD-L2 are ligands for programmed death-1 (PD-1), a membe

71 PD-L1 and PD-L2 are ligands for the inhibitory receptor programmed

72 These findings suggest that PD-L1 and PD-L2 are nonredundant aspects of the natural protective

73 programmed death-1 (PD-1) ligands PD-L1 and PD-L2 are recurrently observed.

74 PD-L1 and PD-L2 are the ligands for PD1 and are differentially reg

75 1 (PD-1) receptor and its ligands, PD-L1 and PD-L2, are a co-inhibitory pathway that contributes to t

76 ion and gain of high expression of PD-L1 and PD-L2 as well as co-stimulatory molecules.

77 entify the immunoregulatory genes, PD-L1 and PD-L2, as key targets at the 9p24.1 amplification peak i

78 tion between PD-1 and its ligands, PD-L1 and PD-L2, at the time of alphaGalCer treatment prevented th

79 tor to its ligands, B7-H1 (PD-L1) and B7-DC (PD-L2), attenuates T cell activation, reduces IL-2 and I

80 e and irradiated chimeras reconstituted with PD-L2(-/-) B cells had significantly higher levels of IL

81 B1a cells, particularly the PD-L2(+) B1a cell subset, are enriched with autoantigen-

82 family members, ICOS ligand, PD-L1 (B7-H1), PD-L2 (B7-DC), B7-H3, and B7-H4 (B7x/B7-S1) are expresse

83 of PD-1 with its ligands, PD-L1 (B7-H1) and PD-L2 (B7-DC), enhances autoimmune disease in several an

84 and inhibitory costimulatory markers (PD-L1, PD-L2, B7-H3, and B7-H4) were increased in E3 DCs.

85 estigate programmed death-1 ligand (PD-L) 1, PD-L2, B7-H3, and inducible costimulatory ligand (ICOS-L

86 interacts with its ligands, PD-L1/B7-H1 and PD-L2/B7-DC, on other cells, and delivers inhibitory sig

87 raction is entropically driven, whereas PD-1/PD-L2 binding has a large enthalpic component.

88 to the 3-fold smaller dissociation rate for PD-L2 binding.

89 yeast surface display to select for enhanced PD-L2 binding.

90 Because PD-L2 binds to both PD-1, which inhibits antitumor immun

91 PD-L2 binds to PD-1 with 3-fold stronger affinity compar

92 G35-55 developed chronic persistent EAE, and PD-L2 blockade in the chronic phase exacerbated EAE, whe

93 rotein (PLP) peptide 139-151, both PD-L1 and PD-L2 blockade markedly enhanced EAE severity.

94 PD-1 or PD-L1 but not PD-L2 blockade rapidly precipitated diabetes in prediabe

95 coprotein (MOG) peptide 35-55, PD-L1 but not PD-L2 blockade significantly increased EAE incidence.

96 rediabetic NOD mice immunized with PLP48-70, PD-L2 blockade worsened EAE but did not induce diabetes,

97 PD-1 or PD-L1 deficiency, and PD-1 but not PD-L2 blockade, unleashed insulin-specific T follicular

98 PD-L1, but not PD-1 or PD-L2, blockade accelerated MHC class II-mismatched skin

99 PD-1/PD-L1, but not PD-1/PD-L2, blockade markedly accelerated GVHD-induced lethal

100 Administration of PD-L1 or PD-L2 blocking Abs prior to mild or moderate kidney IRI

101 Interestingly, PD-L2 but not PD-L1 blockade in WT animals also resulted

102 r of Ly6C(+) monocytes gave rise to PD-L1(+)/PD-L2(+), but not PD-L1(+)/PD-L2(-) cells in T. crassice

103 monocytes and GM-CSF-dependent FcgammaRIII(+)PD-L2(+)CD209a(+) moDCs but generated iNOS(+) macrophage

104 ubset acted as a precursor for FcgammaRIII(+)PD-L2(+)CD209a(+), GM-CSF-dependent moDCs but was distal

105 monocytes differentiated into FcgammaRIII(+)PD-L2(-)CD209a(-)iNOS(+) macrophages upon microbial stim

106 In this article, we show that, together, PD-L2 (CD273), CD80, and CD73 define at least five pheno

107 eficient in PD-L2 (Pdcd1lg2(-/-)), PD-L1 and PD-L2 (Cd274(-/-)Pdcd1lg2(-/-)) or PD-1 (Pdcd1(-/-)) had

108 L1]), CD273 (programmed cell death-2 ligand [PD-L2]), CD275 (inducible costimulator ligand [ICOS-L]),

109 luding programmed cell death ligand (PD-L)1, PD-L2, CD40, CD80, CD86, and inducible T cell costimulat

110 Immunohistochemical staining for PD-L1, PD-L2, CD8, and p16 was performed and graded in a standa

111 Memory subsets defined by PD-L2, CD80, and CD73 are biologically distinct from one

112 r respective ligands (PD-1 ligand 1 [PD-L1], PD-L2, CD80, and CD86) on MDSCs.

113 rise to PD-L1(+)/PD-L2(+), but not PD-L1(+)/PD-L2(-) cells in T. crassiceps-infected mice, demonstra

114 SLs and PTLs also have frequent 9p24.1/PD-L1/PD-L2 CNAs and additional translocations of these loci,

115 zed the binding affinities of the PD-1-PD-L1/PD-L2 co-inhibitory receptor system, and discovered an u

116 l structures of the human triple-mutant PD-1/PD-L2 complex and the apo triple-mutant PD-1 variant at

117 was found to express B7H1 (PD-L1) and B7DC (PD-L2) constitutively, and this expression was up-regula

118 vors inhibition, and indicate that PD-L1 and PD-L2 contribute to the poor stimulatory capacity of iDC

119 alterations of 9p24.1/CD274(PD-L1)/PDCD1LG2(PD-L2) contribute to robust PD-L1 and PD-L2 expression b

120 Importantly, in TCGA datasets, PD-L2 correlated with worse clinical outcomes in glioma

121 PD-L2 CPS >=1 was present in 60%, while only 20% had PD-

122 Naive PD-L2-deficient (PD-L2(-/-)) mice produced significantly

123 Experiments with PD-L2-deficient mice showed that PD-L2 expression on non

124 ed death 1 (PD-1) and its ligands, PD-L1 and PD-L2, deliver inhibitory signals that regulate the bala

125 However, ocular cell-expressed PD-L1 and PD-L2 did not induce T-cell apoptosis.

126 In conclusion, PD-L1 and PD-L2 differentially regulate the susceptibility and chr

127 with anti-PD-1 and anti-PD-L1, but not anti-PD-L2, displayed bigger lesions with significantly lower

128 Blocking PD-L1, but not PD-L2, during direct priming of naive T cells by infecte

129 nce of these two opposing features, the W110(PD-L2) "elbow" and a C-D region "latch." Interestingly,

130 PD-L2) acts as an "elbow" that helps shorten PD-L2 engagement with PD-1 and therefore lower affinity.

131 Thus, OX40L and PD-L2 expressed on DCs differentially regulate cytokine

132 lls, IFN-gamma treatment increased PD-L1 and PD-L2 expression and decreased B7-H3 and ICOS-L expressi

133 that GATA2 is sufficient to drive PD-L1 and PD-L2 expression and is necessary for PD-L2 expression.

134 CD1LG2(PD-L2) contribute to robust PD-L1 and PD-L2 expression by HRS cells.

135 an ocular cells were evaluated for PD-L1 and PD-L2 expression by RT-PCR and flow cytometry.

136 egulation depends on TLR4 and STAT1, whereas PD-L2 expression depends on IL-4R alpha and STAT6.

137 trinsic mechanisms of constitutive PD-L1 and PD-L2 expression in brain tumors.

138 .4 [12.2] years) detected increased PD-1 and PD-L2 expression in high-risk cSCC.

139 ng may influence interpretation of PD-L1 and PD-L2 expression in ocular adnexal tumors.

140 PRMT1 deletion in mice reduced PD-L1 and PD-L2 expression in tumors and reduced the efficiency of

141 Thus, B-1 cell-intrinsic PD-L2 expression inhibits IL-5 production by T cells and

142 Assessment of immune-infiltration by PD-L2 expression is a promising tool with which to help

143 We found that in some tumor types, PD-L2 expression is more closely linked to Th1/IFNG expr

144 FN-gamma treatment alone increased PD-L1 and PD-L2 expression on all cells and decreased B7-H3 expres

145 PD-1 expression on T cells and PD-L2 expression on B cells controlled T(FH) cell and PC

146 Here we have shown that higher PD-L2 expression on blood dendritic cells, from Plasmodi

147 PD-L1 and PD-L2 expression on human CMFs was determined using West

148 ls also differentially up-regulate PD-L1 and PD-L2 expression on inflammatory macrophages.

149 n supressed MHCII on DCs, enhanced PD-L1 and PD-L2 expression on MHCII(lo) DCs, and skewed the Treg-T

150 iments with PD-L2-deficient mice showed that PD-L2 expression on non-T cells was critical for respira

151 programmed cell death 1 ligand 1 (PD-L1) and PD-L2 expression on target DCs, and the ability of Tregs

152 bone marrow chimeras demonstrate that PD-L1/PD-L2 expression only on antigen-presenting cells is ins

153 chimeras demonstrated that B cell-intrinsic PD-L2 expression regulated PC-specific Ab production.

154 ons between clinical responses and PD-L1 and PD-L2 expression status were evaluated in TCGA datasets

155 The degree of PD-L1 and PD-L2 expression was also associated with the area in mi

156 PD-L1 and PD-L2 expression was assessed by flow cytometry and qRT-

157 e patients with adverse outcomes; therefore, PD-L2 expression was chosen to distinguish immune infilt

158 Although PD-L2 expression was detectable by flow cytometry on 3 o

159 f CXCR5(+)PD-1(HIGH) Tfh were increased, but PD-L2 expression was downregulated on B cells, possibly

160 Whereas PD-L2 expression was limited to hematopoietic cells, hem

161 PD-L1 and PD-L2 expression were graded with both the combined posi

162 Both PD-L1 and PD-L2 expression were upregulated in the spleen, liver,

163 Mice had reduced PD-L1 and PD-L2 expression when PRMT1 was specifically deleted in

164 demonstrated a high prevalence of PD-L1 and PD-L2 expression, treatment-induced expansion of T cells

165 ighly sensitive to the dynamics of PD-L1 and PD-L2 expression.

166 L1 and PD-L2 expression and is necessary for PD-L2 expression.

167 n in dendritic cells did not alter PD-L1 and PD-L2 expression.

168 istinguish immune infiltration(HI) (ie, high PD-L2) FL biopsies from immune infiltration(LO) (ie, low

169 PD-L1) and programmed cell death 1 ligand 2 (PD-L2) has been shown to predict tumor response to these

170 PD-L1 and PD-L2 have overlapping functions in inhibiting interleuk

171 To investigate whether PD-L1 and PD-L2 have synergistic or unique roles in regulating T c

172 ed Death-1 Ligand 1 or 2 molecules (PD-L1 or PD-L2) have suggested additional receptors for these B7

173 ed death 1 (PD-1) and its ligands, PD-L1 and PD-L2, have emerged as critical inhibitory signaling pat

174 y immunotherapy target proteins PD-1, PD-L1, PD-L2, IDO1, LAG3, TIM3, ICOSLG, VISTA, GITR, and CD40 i

175 Murine CLL cells highly expressed PD-L1 and PD-L2 in all organs, with high PD-L1 expression in the s

176 Expression of PD-1 and its ligands PD-L1 and PD-L2 in chronic rhinosinusitis with nasal polyps (CRSwN

177 dendritic cells, colocalized with PD-L1 and PD-L2 in cSCC lesions.

178 nent role for inhibitory molecules PD-L1 and PD-L2 in peripheral tolerance has been proposed.

179 PD-L1 expression differs from PD-L2 in that PD-L1 is expressed on activated T cells, p

180 Expression of PD-L1 and PD-L2 in the cSCC microenvironment was defined.

181 Expression of PD-L1 and PD-L2 in the cSCC microenvironment.

182 These cells uniquely expressed MGL2 and PD-L2 in the metastatic microenvironment and preferentia

183 be useful to decrease inhibitory effects of PD-L2 in the microenvironment.

184 of PD-1 and PD-1 pathway ligands (PD-L1 and PD-L2) in the tumor microenvironment.

185 or beta, interleukin 10, and PD-1 (and PD-L1/PD-L2) in tolerant skin grafts and increased expression

186 B7 family ligands, B7-H1 (PD-L1) and B7-DC (PD-L2), in early fate decisions of CD8 T cells.

187 n of prognostic immune biomarkers, PD-L1 and PD-L2, in invasive ocular surface squamous neoplasia.

188 he role of the known PD-1 ligands, PD-L1 and PD-L2, in kidney IRI.

189 eptor and its ligands, B7-H1/PD-L1 and B7-DC/PD-L2, in maintaining an immunosuppressive tumor microen

190 xpression of PD-1 and its ligands, PD-L1 and PD-L2, in multiple tissues during the course of chronic

191 on the basis of their expression of CD80 and PD-L2, independently of isotype, identified MBC subsets

192 Blockade of the RGMb-PD-L2 interaction markedly impaired the development of r

193 Binding of PD-L2 is accompanied by formation of a prominent pocket

194 ng via programmed death ligand-1 (PD-L1) and PD-L2 is crucial for maintaining peripheral tolerance.

195 cell lines as well as resident macrophages, PD-L2 is most significantly inducible only on inflammato

196 In contrast, PD-L2 is not expressed on inflammatory macrophages but c

197 e show that the 3-fold affinity advantage of PD-L2 is the consequence of these two opposing features,

198 rotein 1 (PD-1) and the PD-1 ligands (PD-L1, PD-L2) is essential for malignant Hodgkin Reed-Sternberg

199 We demonstrate that PD-L1, but not PD-L2, is constitutively expressed at high levels by the

200 gagement of its inhibitory ligands, PD-L1 or PD-L2, is of particular interest due to recent successes

201 had concordant alterations of the PD-L1 and PD-L2 loci (polysomy, 5% [five of 108]; copy gain, 56% [

202 nd efficacy of nivolumab and to assess PD-L1/PD-L2 locus integrity and protein expression.

203 PD-L2 mAb blockade of wild-type B-1 cells in culture sig

204 and STAT5 inhibition blunted the effects of PD-L2 mAb blockade on B-1 cells.

205 PD-L2 mAb blockade significantly increased IL-5(+) T cel

206 CD80(+)PD-L2(+) MBCs differentiated rapidly into AFCs but did n

207 e germinal centers (GCs); conversely, CD80(-)PD-L2(-) MBCs generated few early AFCs but robustly seed

208 activated monocyte-derived F4/80(int)CD206(+)PD-L2(+)MHCII(+) macrophages into macrophages with a tis

209 ages with a tissue-resident F4/80(hi)CD206(-)PD-L2(-)MHCII(-)UCP1(+) phenotype in the peritoneal cavi

210 addition to increased PC-specific IgM, naive PD-L2(-/-) mice and irradiated chimeras reconstituted wi

211 PD-L2(-/-) mice had significantly increased PC-specific

212 This afforded PD-L2(-/-) mice with selectively enhanced protection aga

213 enerated mice lacking PD-L1 and PD-L2 (PD-L1/PD-L2(-/-) mice) and compared them to mice lacking eithe

214 ulating IgG and IgG deposits in glomeruli in PD-L2(-/-) mice, but not PD-L1(-/-) mice.

215 enal pathology was similar in PD-L1(-/-) and PD-L2(-/-) mice, our findings suggest that kidney diseas

216 d CD8(+) T cells in PD-L1(-/-) mice, but not PD-L2(-/-) mice.

217 Naive PD-L2-deficient (PD-L2(-/-)) mice produced significantly more PC-reactive

218 arphis, based on the expression of PD-L1 and PD-L2 molecules, resulting upon T. crassiceps infection.

219 lated that of HLA class I, B7-H3, PD-L1, and PD-L2, molecules that might limit NK cell function.

220 h (PD)-1 molecule and its ligands (PD-L1 and PD-L2), negative regulatory members of the B7 family, pl

221 Programmed death-ligand (PD-L)1 and PD-L2, newer B7 superfamily members, are implicated in t

222 early onset diabetes that develops in PD-L1/PD-L2(-/-) non-obese diabetic mice.

223 t correlate with the expression of PD-L1 and PD-L2 on dendritic cells and macrophages in lymphoid tis

224 chemical staining did not show expression of PD-L2 on either normal or inflamed ocular tissues.

225 Blockade of PD-L1 and/or PD-L2 on migratory LCs (mLCs) and DDCs enhanced T-cell a

226 gands reverses upon maturation and PD-L1 and PD-L2 on mLC function to inhibit T-cell responses.

227 ced, indirectly, the expression of PD-L1 and PD-L2 on monocytes/macrophages in PBMC.

228 lation of the inhibitory molecules PD-L1 and PD-L2 on rapa-ECs.

229 y-number gains of CD274 (PD-L1) and PDC1LG2 (PD-L2) on chromosome 9p24.1.

230 ing the costimulatory family molecule B7-DC (PD-L2) on DC up-regulating IL-12 production, homing to l

231 ed expression of the PD-1 ligands, PD-L1 and PD-L2, on BAL CD14+ cells compared with blood was also s

232 ed death-1 (PD-1) with its ligands PD-L1 and PD-L2 or by the interaction of PD-L1 with B7-1.

233 In contrast, no effect on the expression of PD-L2 or PD-1 molecules was detected.

234 ) in mice lacking PD-L1 (PD-L1(-/-)), PD-L2 (PD-L2(-/-)), or both (PD-L1/L2(-/-)) to wild-type (WT) C

235 stitutive levels of PD-L1 and PD-L2 and that PD-L2 overexpression inhibited neoantigen specific T cel

236 Immunologic effects of PD-L2 overexpression were evaluated by IFN-gamma ELISPOT

237 egulates respiratory immunity, targeting the PD-L2 pathway has therapeutic potential for asthma, canc

238 In addition, the PD-1:PD-L1/PD-L2 pathway plays a critical role in regulating T cell

239 lerance, we generated mice lacking PD-L1 and PD-L2 (PD-L1/PD-L2(-/-) mice) and compared them to mice

240 is (NSN) in mice lacking PD-L1 (PD-L1(-/-)), PD-L2 (PD-L2(-/-)), or both (PD-L1/L2(-/-)) to wild-type

241 In the current study, we analyzed PD-L1, PD-L2, PD-1, and cytolytic activity (CYT) expression, as

242 PD-L1, PD-L2, PD-1, CYT expression, and mutational density are

243 Mice deficient in PD-L2 (Pdcd1lg2(-/-)), PD-L1 and PD-L2 (Cd274(-/-)Pdcd1l

244 ed death 1 (PD-1) and its ligands, PD-L1 and PD-L2, play an important role in the maintenance of peri

245 Our findings suggest that PD-L2 plays a pivotal role in the regulation of TH9 cell

246 ute to a substantial proportion of PD-L1 and PD-L2 positivity, and a conspicuous CD8-positive T-lymph

247 mab prevents PD-1 ligation by both PD-L1 and PD-L2, preventing the immune dysregulation that otherwis

248 s ICOS-L (inducible costimulator ligand) and PD-L2 (programmed death ligand 2).

249 In contrast, PD-L2 promoted IFN-gamma production, irrespective of con

250 d PDCD1LG2, respectively) loci and PD-L1 and PD-L2 protein expression.

251 gether, our findings indicate that PD-L1 and PD-L2 provide distinct negative regulatory checkpoints p

252 at the programmed death 1 ligands (PD-L1 and PD-L2), provide a protective barrier during T cell- and

253 a fatal inflammatory phenotype in PD-L1(-/-)PD-L2(-/-) Rag(-/-) recipients of naive CD4 T cells.

254 trate that programmed cell death 1 ligand 2 (PD-L2) regulates the production of natural Abs against p

255 ssion of the PD-1 pathway ligands, PD-L1 and PD-L2, remain poorly understood.

256 eactivate" T cell functions, but the role of PD-L2 remains unclear.

257 ntibodies specific to its ligands (PD-L1 and PD-L2) results in restoration of functional competence (

258 the complete ectodomains of murine PD-1 and PD-L2 revealed a 1:1 receptor:ligand stoichiometry and d

259 Anti-PD-1 and anti-PD-L1, but not anti-PD-L2, reversed tolerance weeks after tolerogenic therap

260 lper 1 cell immunity against malaria through PD-L2's competition with PD-L1.

261 Moreover, blocking PD-L2 selectively activated CD8 T cells at secondary sit

262 Soluble serum PD-L2 showed suggestive positive association with improv

263 tic cells (DC) activated with a human B7-DC (PD-L2)-specific IgM Ab can induce strong antitumor respo

264 This human PD-1/PD-L2 structure provide critical insights for the design

265 harbors a striking pocket in the murine PD-1/PD-L2 structure.

266 fected mice, demonstrating that the PD-L1(+)/PD-L2(+) subpopulation of AAMvarphis originates from blo

267 dritic cell function on cross-linking B7-DC (PD-L2), supporting robust T-cell responses in vitro.

268 Expression of PD-1, PD-L1, PD-L2, TGF-beta, IL-5, and IL-10 mRNA was measured by re

269 cy has been attributed to a tryptophan (W110(PD-L2)) that is unique to PD-L2 and has been assumed to

270 nducer of the human genes encoding PD-L1 and PD-L2 through the vitamin D receptor, a ligand-regulated

271 infections to understand the contribution of PD-L2 to immunity.

272 tantly, administration of soluble multimeric PD-L2 to mice with lethal malaria was sufficient to dram

273 gest an unexpectedly limited contribution of PD-L2 to PD-1 ligation during interactions of activated

274 S >=1 was present in 60%, while only 20% had PD-L2 TPS >=1.

275 opsies from immune infiltration(LO) (ie, low PD-L2) tumors.

276 The 3-4-fold greater affinity of PD-L2 versus PD-L1 for human PD-1 is principally due to

277 Lack of PD-L2 was associated with significantly increased TGF-be

278 determined, and the expression of PD-L1 and PD-L2 was evaluated by immunohistochemistry.

279 Interestingly, PD-L1 but not PD-L2 was found to be expressed on inflamed islets of NO

280 Mechanistic studies in mice showed that PD-L2 was indispensable for establishing effective CD4(+

281 Tumor expression of PD-L1 and PD-L2 was present on the cell membranes.

282 the gene encoding the more tissue-restricted PD-L2 was regulated only in myeloid cells.

283 ia programmed death 1 ligand (PD-L1) but not PD-L2 was required for conversion.

284 L1 and ICOS-L were moderately expressed, and PD-L2 was weakly expressed on unstimulated tracheal, bro

285 the ex vivo expression of PD-1 and a ligand (PD-L2) was assessed in 38 cSCC biopsy specimens from 24

286 onversely, programmed cell death 1 ligand 2 (PD-L2) was higher in rVVG-primed mice throughout.

287 Low programmed death-ligand 2 (PD-L2) was the most sensitive/specific marker to segrega

288 ne PD-1 adopt new conformations upon binding PD-L2, we hypothesized that mutations in these two loops

289 PD-L1 and PD-L2 were expressed at very low levels on iLCs.

290 a marker of T-cell exhaustion, and PD-L1 and PD-L2 were expressed by a subset of tumor dendritic cell

291 PD-L1 and PD-L2 were expressed on tumor cells to varying degrees,

292 The immunomodulatory functions of PD-L1 and PD-L2 were tested by coculturing untreated or IFN-gamma-

293 We found that the PD-1 ligands PD-L1 and PD-L2 were upregulated on GC B cells.

294 CD86, ICOS-L, and programmed death ligand 2 [PD-L2]) were not expressed on class II(+) cells.

295 ssion of programmed death ligand (PD-L)1 and PD-L2 - which were partially dependent on IDO.

296 These studies show immuno-regulation by PD-L2, which has the potential to be translated into an

297 cells, including pancreatic islet cells; and PD-L2, which is restricted to macrophages and dendritic

298 PD-1 variant with three substitutions binds PD-L2 with an affinity two orders of magnitude higher th

299 was 12.2 (range 0-95.8); mean expression of PD-L2 with CPS was 7.9 (range 0-37.3) and with TPS was 1

300 ression of PD-1 and its ligand PD-L1 but not PD-L2 within the central nervous system (CNS) of mice wi