ライフサイエンスコーパス: PD-L2

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

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

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

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

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

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

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

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

9 are the function and expression of PD-L1 and PD-L2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 dies show overlapping functions of PD-L1 and PD-L2 and indicate a key role for the PD-L-PD-1 pathway

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

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

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

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

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

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

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

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

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

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

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

38 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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 1 (PD-1) receptor and its ligands, PD-L1 and PD-L2, are a co-inhibitory pathway that contributes to t

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

54 We identify here PD-1 ligand 2 (PD-L2) as a second ligand for PD-1 and compare the funct

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 ts had minimal expression of PD-1, PD-L1, or PD-L2, but intragraft induction of all three molecules o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 Engagement of PD-1 by PD-L2 dramatically inhibits T cell receptor (TCR)-mediat

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

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

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

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

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

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

106 .4 [12.2] years) detected increased PD-1 and PD-L2 expression in high-risk cSCC.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 ed T cell activation, showing that PD-L1 and PD-L2 function to inhibit T cell activation.

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

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

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

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

130 We prepared PD-L1.Ig and PD-L2.Ig fusion proteins and showed that each bound to a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 In contrast, PD-L2 is expressed on placental endothelium and medullar

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 These results suggest that PD-L1 and PD-L2 might have different functions in regulating type

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

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

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

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

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

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

178 Using mAbs, we show that blockade of PD-L2 on dendritic cells results in enhanced T cell prol

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 At low antigen concentrations, PD-L2-PD-1 interactions inhibit strong B7-CD28 signals.

196 In contrast, at high antigen concentrations, PD-L2-PD-1 interactions reduce cytokine production but d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 Blockade of both PD-L1 and PD-L2 showed an additive effect.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 ed death-1 (PD-1) and its ligands, PD-L1 and PD-L2, which are homologs of B7, constitute an inhibitor

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

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

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