ライフサイエンスコーパス: IFN-gammaR

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

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

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

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

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

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

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

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

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

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

11 046, while only a subset of mice lacking the IFN-gammaR alone and virtually no mice lacking the IFN-a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 1 and 28 postchallenge, whereas infection in IFN-gammaR(-) mice was evident in 100% of animals from d

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

126 developed a mouse model in which interferon (IFN)gammaR(-/-) mice infected intranasally with murine g

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

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

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

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

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

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

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

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

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

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

137 % (wild-type mice) to 90% (IFN-gamma(-/-) or IFN-gammaR(-/-) mice) and a decrease in the average surv

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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