ライフサイエンスコーパス: IFN-gammaR

1 IFN-gammaR signaling induced Blimp1 expression in B cell

2 IFN-gammaR(-/-) and parental 129/SvEv mice developed mil

3 IFN-gammaR-/- recipients of WT cells developed severe TE

4 phil function, influenza infection activates IFN-gammaR signaling and abrogates AM-dependent bacteria

5 the secretion of IFN-gamma is not affected, IFN-gammaR-/- mice do not have the ability to resolve th

6 Gamma interferon receptor alpha (IFN-gammaR alpha) is stable but posttranslationally modi

7 Although IFN-gammaR/STAT1 signaling promotes a Th1 response via t

8 Both 129 and IFN-gammaR(-) mice became infected, although the extent

9 mice that were deficient in both IL-17R and IFN-gammaR compared with wild-type animals.

10 sed the Abeta-induced expression of CD40 and IFN-gammaR.

11 This survival pattern in IFN-gamma(-/-) and IFN-gammaR(-/-) mice correlated with higher viremia and

12 Moreover, 45D-immunized IFN-gamma(-/-) and IFN-gammaR(-/-) mice demonstrate MOG tetramer-positive C

13 the lungs, whereas MHC class II (MHCII) and IFN-gammaR deficiency impairs late control in the lungs,

14 Experiments with IFN-gamma knockout mice and IFN-gammaR knockout mice demonstrated that IFN-gamma was

15 re stimulated with Mtb antigen and SLPI, and IFN-gammaR expression levels were measured.

16 stis clearance in anti-IFN-gamma-treated and IFN-gammaR-deficient mice was associated with significan

17 r knockout mice based on the 129 background (IFN-gammaR(-)) were challenged orally with approximately

18 ng B effector 1 (Be1) cells is controlled by IFN-gammaR-mediated signals, STAT1-deficient B cells up-

19 homatis and that in the absence of host cell IFN-gammaR expression, both Th1 and Th2 cells lead to in

20 Compared with WT counterparts, IFN-gammaR-deficient PLP-CD8 were defective in suppressi

21 lent in gamma interferon receptor-deficient (IFN-gammaR(-/-)) mice, demonstrating that IFN-gamma-medi

22 ungs were also observed in the mice of donor IFN-gammaR(-/-) T cells.

23 es in lung GVHD did occur in mice with donor IFN-gammaR(-/-) T cells when treated in vivo with anti-I

24 nd the transfer of donor T cells from either IFN-gammaR(-/-) or IFN-gamma knockout (IFN-gamma(-/-)) m

25 ar injections of plasmids with cDNA encoding IFN-gammaR/Fc can retard lupus development and progressi

26 blood T cells, which constitutively express IFN-gammaR beta-chain mRNA, resulted in a loss of expres

27 Although the newly expressed IFN-gammaR in Chlamydia-infected cells were capable of b

28 Using a newly generated mouse that expresses IFN-gammaR only on airway epithelial cells, we show that

29 FN-gammaR expression and chimeras expressing IFN-gammaR only on hematopoietic cells.

30 Few IFN-gammaR-/- lymphocytes infiltrated thyroids even in t

31 Finally, IFN-gammaR expression was lower in TB compared with HD p

32 e B6.Sle1b mice sufficient and deficient for IFN-gammaR indicates that TLR7-induced IFN-gamma activat

33 Even IFN-gamma-producing cells from IFN-gammaR(-/-) mice could acquire IL-4-producing capaci

34 VHD was also observed using donor cells from IFN-gammaR(-/-) T cells compared with control donors.

35 Proliferation of bone marrow Mphi from IFN-gammaR-intact MRL-Fas(lpr) costimulated with CSF-1 o

36 ependent of STAT1 but requiring a functional IFN-gammaR, take over.

37 he use of the receptor for interferon-gamma (IFN-gammaR) and the ITAM adaptor Fcgamma as an example,

38 via an intricate interplay between IFN-gamma/IFN-gammaR and IL-7/IL-7R pathways.

39 tumour-infiltrating T cells in an IFN-gamma/IFN-gammaR signalling-dependent manner, which may serve

40 However, a cell type-specific IFN-gamma/IFN-gammaR-dependent mechanism regulates CD8(+) T suppre

41 se and suggests that targeting the IFN-gamma/IFN-gammaR/JAK/STAT/T-bet/CD38 pathway could play a role

42 -bet by B cells is dependent on an IFN-gamma/IFN-gammaR/T-bet autocrine feedback loop.

43 betaR (IFN-alphabetaR(-/-)), the IFN-gammaR (IFN-gammaR(-/-)), or both receptors (IFN-alphabetagammaR

44 to mice lacking the IFN-gamma receptor gene (IFN-gammaR-/-) and into control mice (IFN-gammaR+/+).

45 (i) IFN-gammaR-/- mice are markedly more susceptible to C. n

46 type I IFNs (IFN-alpha/betaR), type II IFN (IFN-gammaR), and both type I and type II IFNs (IFN-alpha

47 Importantly, IFN-gammaR-deficient BC-CML and AML were completely resi

48 Moreover, neutralization of IL-17 in IFN-gammaR(-/-) or IFN-gamma in IL-17R(-/-) mice further

49 Additionally, in IFN-gammaR(-) mice the infection was so extensive that f

50 antly reduced whereas it is less affected in IFN-gammaR(-/-) recipients although CD8(+) T cell infilt

51 resulted in the elimination of Th1 cells in IFN-gammaR-/- mice.

52 A defect in IFN-gammaR increased tumor growth, whereas tumor growth

53 tigens to donor lymphocytes was defective in IFN-gammaR/STAT1-deficient, donor-derived APCs in fully

54 zing Abs or in mice with targeted defects in IFN-gammaR each eliminated the PDL-1-mediated stimulator

55 gnificantly delayed in chimeras deficient in IFN-gammaR expression and chimeras expressing IFN-gammaR

56 e in Mphi elicited by Mphi growth factors in IFN-gammaR-deficient MRL-Fas(lpr) mice is a result of en

57 in uninfected cells, despite the increase in IFN-gammaR expression.

58 1 and 28 postchallenge, whereas infection in IFN-gammaR(-) mice was evident in 100% of animals from d

59 dative species is significantly inhibited in IFN-gammaR(-/-) but is less affected in IL-17R(-/-) reci

60 er apoptotic Mphi within the interstitium in IFN-gammaR-deficient MRL-Fas(lpr) mice.

61 ion rates by B. burgdorferi N40 are lower in IFN-gammaR-deficient mice than in control animals.

62 nism responsible for the increase in Mphi in IFN-gammaR-deficient MRL-Fas(lpr) mice, we evaluated Mph

63 ncited more severe interstitial nephritis in IFN-gammaR-deficient than in IFN-gammaR-intact MRL-Fas(l

64 wild-type (WT) CD8(+) T cells is reduced in IFN-gammaR(-/-) or IL-17R(-/-) mice compared with WT con

65 pe (WT) PLP-CD8 were robustly suppressive in IFN-gammaR-deficient mice, IFN-gammaR-deficient PLP-CD8

66 was substantially lower in 129 mice than in IFN-gammaR(-) mice.

67 al nephritis in IFN-gammaR-deficient than in IFN-gammaR-intact MRL-Fas(lpr) mice, consisting of an in

68 of HEK 293 cells with C. psittaci increased IFN-gammaR expression only in cells expressing either TL

69 bsets, we demonstrate that influenza-induced IFN-gammaR signaling in AMs impairs their antibacterial

70 E. falciformis-infected IFN-gammaR(-/-) and IFN-gamma(-/-) mice developed dramat

71 IL-17A and IL-22 in E. falciformis-infected IFN-gammaR(-/-) mice resulted in a reduction in infectio

72 induction of arteritis in gammaHV68-infected IFN-gammaR-deficient mice can occur in the absence of sp

73 MCMV-infected IFN-gammaR-/- mice shed preformed infectious MCMV in spl

74 Furthermore, E. muris-infected IFN-gammaR-deficient mice did not exhibit anemia or an i

75 By 4 days after infection, IFN-gammaR signaling was found to restrict DENV replicat

76 tective Th1 cells during L. major infection, IFN-gammaR and STAT1 are dispensable.

77 s, the fusion protein with 791delG inhibited IFN-gammaR function by 48.7 +/- 5%, whereas fusion prote

78 Furthermore, transfer of such cells into IFN-gammaR-deficient mice limited their death following

79 en IL-4(-/-) Th2 cells were transferred into IFN-gammaR(-/-) mice, indicating that IFN-gamma was resp

80 rbate bacterial burden when transferred into IFN-gammaR(-/-) mice.

81 knockout mouse aortas were transplanted into IFN-gammaR-deficient recipients and in which neointima f

82 y, T cells from IFN-gamma receptor knockout (IFN-gammaR(-/-)) mice, capable of producing IFN-gamma bu

83 ormally in both IFN-gamma receptor knockout (IFN-gammaR-/-) and IL-12 p40 knockout (IL-12-/-) mice.

84 N-gamma-/-) and IFN-gamma receptor knockout (IFN-gammaR-/-) animals lost up-regulation of surface B7-

85 FN-gamma-/-) or IFN-gamma receptor knockout (IFN-gammaR-/-) mice as compared with WT animals.

86 ortant for the development of these lesions, IFN-gammaR-/- mice, which develop TEC H/P similar to IFN

87 e also found that in peritoneal macrophages, IFN-gammaR itself required tonic signaling from Fcgamma

88 gene (IFN-gammaR-/-) and into control mice (IFN-gammaR+/+).

89 ly suppressive in IFN-gammaR-deficient mice, IFN-gammaR-deficient PLP-CD8 exhibited suboptimal suppre

90 xenograft and syngeneic solid tumor models, IFN-gammaR knockout CAR T cells displayed more potent tu

91 amma mice express a dominant-negative mutant IFN-gammaR in mononuclear phagocytes.

92 Although the patients showed no IFN-gammaR activity, their healthy heterozygous parents

93 w-derived macrophages from wild-type but not IFN-gammaR(-/-) mice.

94 d inhibited TEC H/P in IFN-gamma-/-, but not IFN-gammaR-/- recipients.

95 in vivo can occur in the apparent absence of IFN-gammaR signaling in T cells.

96 cific IgM B cell responses in the absence of IFN-gammaR signaling indicated that this cytokine plays

97 n the other hand, occurred in the absence of IFN-gammaR, except in the central nervous system (CNS) (

98 hermore, we demonstrated that the absence of IFN-gammaR/STAT1 signaling in hematopoietic APCs impaire

99 e most likely due to the decreased amount of IFN-gammaR-alpha protein after infection.

100 they lose expression of the second chain of IFN-gammaR (IFN-gammaR2).

101 The differential effects of IFN-gammaR/STAT1 signaling on endogenous and exogenous a

102 in vitro and in vivo and that engagement of IFN-gammaR expressed by DCs leads to suppression of IL-1

103 d in a transient induction or enhancement of IFN-gammaR beta-chain mRNA expression in Th1 clones and

104 e showed that B cell intrinsic expression of IFN-gammaR and the IFN-gamma-induced TF T-bet were requi

105 tective immunity required host expression of IFN-gammaR but was independent of induced NO synthase ex

106 studies, showed that mast cell expression of IFN-gammaR contributed to the development of many Fcepsi

107 B, probably because of the low expression of IFN-gammaR detected in these individuals.

108 cytokine production and/or the expression of IFN-gammaR.

109 Viral titers in eyes and ganglia of IFN-gammaR-/- mice were not significantly different from

110 ted mast cells and occurred independently of IFN-gammaR expression.

111 logy observed with wt gammaHV68 infection of IFN-gammaR-deficient mice.

112 In hematologic malignancies, knockout of IFN-gammaR (IFN-gammaRKO) in CAR T cells increased their

113 In this article, we show that the lack of IFN-gammaR signaling in CD8(+) T cells promotes TM forma

114 both IL-4 and IFN-gamma, expressed levels of IFN-gammaR beta-chain transcripts similar to those produ

115 of IL-4, continued to express high levels of IFN-gammaR beta-chain transcripts.

116 ect was associated with changes in levels of IFN-gammaR, we investigated the effects of Bryo-1 on the

117 on using novel mice with conditional loss of IFN-gammaR (IFNGR1).

118 The loss of IFN-gammaR beta-chain expression in Th1 populations was

119 This might limit the migration of IFN-gammaR-/- lymphocytes to thyroids.

120 resistance was dependent on the presence of IFN-gammaR(+) ILC2s.

121 Real-time PCR indicated that recipients of IFN-gammaR-/- bone marrow expressed less mRNA for IFN-ga

122 f Bryo-1 on the expression and regulation of IFN-gammaR chains in monocytic cells.

123 In addition, up-regulation of IFN-gammaR expression in Chlamydia-infected HeLa cells c

124 These results demonstrate the roles of IFN-gammaR signaling in protection from initial systemic

125 y regulated in the hapten-challenged skin of IFN-gammaR(-/-) or IL-17R(-/-) recipients compared with

126 alpha/betaR action was distinct from that of IFN-gammaR, since IFN-alpha/betaR(-/-) mice did not disp

127 atopoietic organs and GVHD target tissues of IFN-gammaR/STAT1-deficient recipient mice, leading to ra

128 Importantly, deletion of IFN-gamma or IFN-gammaR in several lupus-predisposed mouse strains re

129 genicity of 45D in mice lacking IFN-gamma or IFN-gammaR was not due to deviation toward an enhanced I

130 peptide recall of primed IFN-gamma (-/-) or IFN-gammaR(-/-) CD8 T cells up-regulated pro-TGF-beta pr

131 be reduced through targeting of IFN-gamma or IFN-gammaR.

132 % (wild-type mice) to 90% (IFN-gamma(-/-) or IFN-gammaR(-/-) mice) and a decrease in the average surv

133 brains and spinal cords of IFN-gamma(-/-) or IFN-gammaR(-/-) mice.

134 titution of mammalian target of rapamycin or IFN-gammaR signaling is sufficient to block this process

135 nonuclear cells from HDs, but not from TB or IFN-gammaR patients.

136 thy heterozygous parents showed only partial IFN-gammaR activity.

137 hemopoietic reconstitution, but only partial IFN-gammaR function.

138 (iv) At week 5 postinfection, IFN-gammaR-/- mice have recruited greater numbers of leu

139 RAG/IFN-gammaR(-/-) mice had elevated numbers of lung CD4(+)

140 However, RAG/IFN-gammaR(-/-) mice developed a dysregulated immune res

141 Impaired lung CD8(+) T cell responses in RAG/IFN-gammaR(-/-) mice were associated with elevated lung

142 Neither RAG/IFN-gammaR(-/-) nor RAG/IL-4Ralpha(-/-) mice displayed i

143 Importantly, tumor-bearing mice receiving IFN-gammaR(-/-) T cells versus wild-type donor T cells d

144 Mice deficient for the IFN-gamma receptor (IFN-gammaR(-/-)) maintain higher viral loads during MPyV

145 independent of both the IFN-gamma receptor (IFN-gammaR) and the IFN-alpha/beta receptor IFNAR1.

146 matory cytokine receptor IFN-gamma receptor (IFN-gammaR) as essential signals that synergize to promo

147 so induced expression of IFN-gamma receptor (IFN-gammaR) both in endothelial and smooth muscle cells.

148 eptor (IL-1R), or interferon-gamma receptor (IFN-gammaR) but instead required IL-18R, IL-33R, and ada

149 ors involving the interferon gamma receptor (IFN-gammaR) complex as a model system, we demonstrate th

150 reversed in AIP1/interferon-gamma receptor (IFN-gammaR) doubly-deficient aorta donors.

151 The absence of IFN-gamma receptor (IFN-gammaR) or STAT1 signaling in donor cells has been s

152 We studied interferon-gamma receptor (IFN-gammaR) signaling in fibroblasts from homozygous pat

153 ic tumor models, whereas IFN-gamma receptor (IFN-gammaR) signaling in solid tumor cells facilitates C

154 ot been linked to interferon-gamma receptor (IFN-gammaR) signaling.

155 zation of the two interferon gamma receptor (IFN-gammaR) subunits, receptor chain 1 (IFN-gammaR1, the

156 mutant mice lacking the IFN-gamma receptor (IFN-gammaR) were infected by inoculation with B. burgdor

157 eron (IFN)-gamma(2/-) or IFN-gamma receptor (IFN-gammaR)(-/-) mice resulted in substantial production

158 oth chains of the interferon gamma receptor (IFN-gammaR), whereas Th1 cells do not express the second

159 ipients deficient in the IFN-gamma receptor (IFN-gammaR).

160 ecessive, partial interferon-gamma receptor (IFN-gammaR)2 deficiency (homozygous for mutations R114C

161 Mice lacking the IFN-gamma receptor (IFN-gammaR-/-) developed and maintained striking chronic

162 r the interferon gamma (IFN-gamma) receptor (IFN-gammaR) or interleukin 4 receptor alpha (IL-4Ralpha)

163 nstructed a MRL-Fas(lpr) IFN-gamma-receptor (IFN-gammaR)-deficient strain.

164 rs (R), including gamma interferon receptor (IFN-gammaR), interleukin 1 receptor (IL-1R), and type 8

165 astic arteries in gamma interferon receptor (IFN-gammaR)-deficient mice with a frequency comparable t

166 marked phosphorylation of its own receptor (IFN-gammaR)-alpha chain.

167 se in the expression of IFN-gamma receptors (IFN-gammaR).

168 ism by which Chlamydia psittaci up-regulates IFN-gammaR expression and evaluate this effect on IDO in

169 mydia is susceptible to IDO, it up-regulates IFN-gammaR expression to a greater degree than either IL

170 ic and nonhematopoietic compartment-specific IFN-gammaR signaling exerts additive effects in orchestr

171 susceptible to C. neoformans infection than IFN-gammaR+/+ mice.

172 ateral ureteral ligation we established that IFN-gammaR signaling does not alter Mphi recruitment int

173 Further, we found that IFN-gammaR-deficient PLP-CD8 exhibited altered granzyme/

174 ed to the phosphorylation site indicate that IFN-gammaR alpha is phosphorylated by the U(S)3 kinase.

175 Gene transcription studies revealed that IFN-gammaR-deficient CDllb(lo)Gr1(lo) promyelocytes from

176 idney transplant model, we further show that IFN-gammaR(-/-) donor kidneys harbor higher MPyV levels

177 Hence, our data suggest that IFN-gammaR signaling actively blocks the formation of TM

178 The IFN-gammaR complex is composed of two IFN-gammaR1 and tw

179 he IFN-alphabetaR (IFN-alphabetaR(-/-)), the IFN-gammaR (IFN-gammaR(-/-)), or both receptors (IFN-alp

180 te that the architecture of the EpoR and the IFN-gammaR complexes differ significantly.

181 tation experiments STAT1 did not dock at the IFN-gammaR of FA-C cells, an abnormality corrected by tr

182 Although both the IFN-gammaR(-/-) and the IFN-alphabetagammaR(-/-) animals

183 In contrast, the IFN-gammaR(-/-) mice mounted a Th2 response, with a pred

184 s constitutively express transcripts for the IFN-gammaR beta-chain, whereas mRNA for this signaling c

185 However, the IFN-gammaR was not required for establishment of latency

186 046, while only a subset of mice lacking the IFN-gammaR alone and virtually no mice lacking the IFN-a

187 xpression in MZB precursors, deletion of the IFN-gammaR (C57BL/6J [B6], B6.129S7-Ifngr1tm1Agt/J) or I

188 mice lacking the ligand-binding chain of the IFN-gammaR (IFN-gammaR1-/-) or the signaling chain (IFN-

189 cells do not express the second chain of the IFN-gammaR (IFN-gammaR2) and are therefore unresponsive

190 and by posttranslational modification of the IFN-gammaR alpha protein.

191 is absolutely dependent on expression of the IFN-gammaR and the T-box transcription factor, T-bet.

192 Thus, both chains of the IFN-gammaR are dispensable for the generation of Th1 Ag-

193 results indicate that down-regulation of the IFN-gammaR beta-chain correlates with impaired IFN-gamma

194 distinguished based on the expression of the IFN-gammaR beta-chain.

195 s well as markedly reduced expression of the IFN-gammaR beta-chain.

196 xperiments demonstrate colocalization of the IFN-gammaR chains with the TCR during activation of naiv

197 Inhibition of the IFN-gammaR complex formation correlated with inhibition

198 Formation of the IFN-gammaR complex, as assessed by tyrosine phosphorylat

199 of the signaling IFN-gammaR2 subunit of the IFN-gammaR on mDCs was downregulated upon high-dose IVIg

200 et, a transcription factor downstream of the IFN-gammaR signaling.

201 nhibition of tyrosine phosphorylation of the IFN-gammaR-alpha chain and subsequent signal transductio

202 e NOD mouse resulted in a segregation of the IFN-gammaR-deficient genotype from the diabetes-resistan

203 s expected given their cytokine profile, the IFN-gammaR(-/-) mice produced fewer CD8(+) IFN-gamma(+)

204 al burden in the joints, suggesting that the IFN-gammaR(-/-) mice were not impaired in controlling sp

205 ctions of IFN-gamma are mediated through the IFN-gammaR and STAT1.

206 f the IFN-alpha/betaR, signaling through the IFN-gammaR confers approximately 140-fold greater resist

207 dulated SLPI levels by signaling through the IFN-gammaR in HDs.

208 n many tumor cell lines mediated through the IFN-gammaR.

209 criptional activators must be coupled to the IFN-gammaR in B cells.

210 etes-resistant gene(s) closely linked to the IFN-gammaR loci derived from the 129 mouse strain.

211 and IFN-gamma was reduced twofold, while the IFN-gammaR-deficient MRL-Fas(lpr) bone marrow Mphi remai

212 L-SAT in IFN-gamma-/- or WT mice even though IFN-gammaR-/- lymphocyte donors produced as much IFN-gam

213 IFN-gamma and tumor cell signaling through IFN-gammaR were particularly important for the anticance

214 We propose that synergistic TLR9/IFN-gammaR activation of T-bet(+) B cells is a mechanism

215 ction in the number of infected cells due to IFN-gammaR signaling by 2 days after infection, coincide

216 inistration of B. burgdorferi-immune sera to IFN-gammaR-deficient mice that have been infected with B

217 Unexpectedly, IFN-gammaR-/- splenocytes or bone marrow did not induce

218 Bone marrow-transplant experiments using IFN-gammaR-/- mice implicated IFN-gamma as a crucial nex

219 d at the predisease stage, particularly when IFN-gammaR/Fc expression was enhanced by electroporation

220 Whereas IFN-gammaR signals are dispensable for the T-bet-depende

221 istant to CD4- and CD8-mediated GVL, whereas IFN-gammaR/IFNAR1 double-deficient CP-CML was fully GVL

222 demonstrated in radiation chimeras in which IFN-gammaR expression was limited to parenchymal cells,