ライフサイエンスコーパス: IFN-gamma

1 IFN-gamma binds to its receptor on Leishmania-infected m

2 IFN-gamma is important in mediating the protection, as I

3 IFN-gamma production and expansion of islet-specific glu

4 IFN-gamma released from activated ILC1s promoted the sur

5 IFN-gamma was primarily produced by CD8(+) T cells in th

6 ukin-6 (IL-6) and decreased levels of IL-12, IFN-gamma, and the JAK1, STAT1, NF-kappaB, and extracell

7 The DNA hypermethylation of the IL-12/IFN-gamma pathway was associated with decreased IFN-gamm

8 nd observed that multiple genes of the IL-12/IFN-gamma signaling pathway (IL12B, IL12RB2, TYK2, IFNGR

9 ntially increased numbers of CD44(hi)IL-17(+)IFN-gamma(-) memory T-helper 17 (Th17) cells in the reti

10 f2(-/-) mice showed an increase in IL-1beta, IFN-gamma, MHC II, and Ctss mRNA transcripts compared wi

11 cells were evaluated by intracellular IL-2, IFN-gamma, and TNF-alpha production with IL-21 in CD4 or

12 ability to produce effector cytokines (IL-2, IFN-gamma, IL-17), regardless of differentiation stage.

13 we show that, a network of C19MC miRNA-520G, IFN-gamma, CEBPB and p53 transcriptional-defects promote

14 of cytokines reflecting inflammation (IL-6, IFN-gamma, IP-10, IL-1RA, IL-10), chemotaxis (IL-8), sys

15 minescence-based assay was developed against IFN-gamma and provided an optimized, physiologically rel

16 rentiation and expression (IL-12, TNF-alpha, IFN-gamma) were enhanced in the neutrophilic cohorts.

17 ed the pro-inflammatory cytokines TNF-alpha, IFN-gamma, and IL-2 more than the anti-inflammatory cyto

18 5, IL-6, IL-8, IL-10, IL-12, CRP, TNF-alpha, IFN-gamma, GM-CSF, MIP-1alpha, and Eotaxin-1 in patients

19 rated and significantly induced IFN-alpha2a, IFN-gamma, proinflammatory cytokines (TNF-alpha, IL-2, I

20 Although IFN-gamma typically helps microbial clearance, we found

21 cantly to endometrial innate immunity via an IFN-gamma-dependent effector mechanism.

22 eased splenic Tregs producing both IL-10 and IFN-gamma 8-fold (p < 0.005) compared to LL-vehicle trea

23 IL-10 and IFN-gamma signaling were disrupted by using blocking ant

24 ion in lungs including TNF, IL-6, IL-10, and IFN-gamma.

25 nd T cells, respectively, restored IL-12 and IFN-gamma cytokine levels and BMM -T cell interaction.

26 However, unlike IL-12p40(-/-) and IFN-gamma(-/-) mice, MyD88(-/-) mice survived N. caninum

27 s could suppress proliferation and IL-17 and IFN-gamma production by T cells.

28 d SLAMF6 expression distinguished IL-17- and IFN-gamma-producing gammadelta T cells, respectively.

29 arkers simultaneously (CD154, TNF, IL-2, and IFN-gamma).

30 gulate T-bet and coexpress IL-17, IL-22, and IFN-gamma in a STAT3- and retinoic acid-dependent manner

31 ted with decreased articular IL-12/23p40 and IFN-gamma levels.

32 A significant increase in IL-7, IL-7R, and IFN-gamma protein expression was found in developed gran

33 cell cytokines (IL-17, TNF-alpha, IL-9, and IFN-gamma) and chemokine receptors (CCR1, CCR2, CCR4, CC

34 T cell accumulation and IFN-gamma production, an essential component of virus co

35 was required for the optimal activation and IFN-gamma production of liver ILC1s.

36 TNF-alpha and IFN-gamma caused a lethal cytokine shock in mice that mi

37 Mechanistically, TNF-alpha and IFN-gamma co-treatment activated the JAK/STAT1/IRF1 axis

38 d that only the combination of TNF-alpha and IFN-gamma induced inflammatory cell death characterized

39 eutralizing antibodies against TNF-alpha and IFN-gamma protected mice from mortality during SARS-CoV-

40 inflammatory T-bet, IL-1beta, TNF-alpha, and IFN-gamma as assessed on day 3 posttransplantation.

41 s circulating IL-1beta, IL-6, TNF-alpha, and IFN-gamma levels in response to Mtb infection.

42 played enhanced expression of granzyme B and IFN-gamma by both virus-specific and total CD8(+) T cell

43 HSV DNA copies, and surges in granzyme B and IFN-gamma occurred within the early hours after reactiva

44 interactions between the IFN-alpha/beta and IFN-gamma pathways in achieving optimal antiviral respon

45 communication between the IFN-alpha/beta and IFN-gamma signaling pathways to optimize antiviral IFN-g

46 iferation and cytotoxic response (CD107a and IFN-gamma-producing CD3+ CD8+ T cells) to the tumour-loa

47 racterized by increased T-bet(+) T cells and IFN-gamma production in mesenteric lymph nodes, increase

48 MAIT, and Vdelta2(+) gammadelta T cells) and IFN-gamma production by them, with mycobacterium-specifi

49 cognition receptors, MHC class II genes, and IFN-gamma-induced GTPases, with antimicrobial function.

50 IRF5(13,14), and are controlled by IFN-I and IFN-gamma in vivo(15-17).

51 oid cells through CD40L-CD40 interaction and IFN-gamma release.

52 el of PCa by blocking both the intrinsic and IFN-gamma-induced PD-L1 expression.

53 lation of the IL-2/STAT5, TNF/NF-kappaB, and IFN-gamma signaling pathways.

54 model of AML, dual treatment with MTP-PE and IFN-gamma led to a significant increase in mature CD27(-

55 Furthermore, the combination of MTP-PE and IFN-gamma on AML blasts generated an inflammatory cytoki

56 estored mitochondrial membrane potential and IFN-gamma production.

57 al T cells showed elevated proliferation and IFN-gamma secretion as well as an enhanced capacity to d

58 upregulating cytotoxic effector proteins and IFN-gamma.

59 acy (antigen-specific antibody responses and IFN-gamma production) and biodistribution (antigen and a

60 IFN (T1IFN) signaling, the role of T1IFN and IFN-gamma signaling in differential regulation of TLR7-m

61 Anti-IFN-gamma autoantibody levels decreased over time in Tha

62 Anti-IFN-gamma autoantibody levels were measured in plasma sa

63 ffects that might have been afforded by anti-IFN-gamma treatment.

64 protein, as evidenced by an observed hd-anti-IFN-gamma-induced increase in the specific binding of IF

65 e titers generally decreased with time, anti-IFN-gamma autoantibody disease had a chronic clinical co

66 Data of 74 patients with anti-IFN-gamma autoantibodies at Srinagarind Hospital, Thaila

67 ts and initial data for 4 patients with anti-IFN-gamma autoantibodies at the US National Institutes o

68 mma signaling pathways to optimize antiviral IFN-gamma activity.

69 is important in mediating the protection, as IFN-gamma knockout (KO) mice failed to acquire protectio

70 ediated condition, non-T2 cytokines, such as IFN-gamma and IL-17A, have been implicated in asthma pat

71 Augmented IFN-gamma responses in the HDM allergic airway disease m

72 vation to generate IFN-gamma, with autocrine IFN-gamma then signaling through STAT1.

73 L1 signaling also induced an anergic T-bet(-)IFN-gamma(-) phenotype in CD8(+) T cells and was equally

74 h topical and systemic treatments that block IFN-gamma signaling can effectively reverse vitiligo in

75 IFN signature genes were upregulated by both IFN-gamma and IFN-beta.

76 Here, we show that both IFN-gamma stimulation and murine norovirus (MNV) infecti

77 ed two main agglomerations, characterized by IFN-gamma and IL-10 phenotypes, respectively.

78 high cellular responses, as characterized by IFN-gamma production, upon re-stimulation with SARS-CoV-

79 om latently infected humans, as evidenced by IFN-gamma release upon peptide stimulation.

80 not inhibit STAT1 phosphorylation induced by IFN-gamma.

81 T cell epitopes, we validated the method by IFN-gamma ELISPOT assay and found three novel peptides t

82 Epitope mapping was performed by IFN-gamma ELISpot screening, confirmed by in vitro MHC b

83 ults suggest that NOD2 activation, primed by IFN-gamma, may provide a novel therapeutic option for AM

84 nd neutrophils in response to stimulation by IFN-gamma, IFN-beta, IFN-lambda, IL-4, IL-13, and IL-10

85 ion of the mouse macrophage transcriptome by IFN-gamma and by TDM or its synthetic analogue trehalose

86 DSG3 autoantibodies stimulated DSG3-CAART IFN-gamma secretion and homotypic clustering, consistent

87 change in expression levels of GzmB, CD107a, IFN-gamma, and TNF was examined.

88 However, the control of NK cell IFN-gamma production was not cell intrinsic, revealing a

89 ression inhibited neoantigen specific T cell IFN-gamma production.

90 r and ten analogues stimulated CD8(+) T-cell IFN-gamma release.

91 that when mixed with wild-type tumor cells, IFN-gamma-insensitive tumor cells indeed grow out, which

92 This conserved IFN-gamma transcriptome response in melanoma cells serve

93 In contrast, IFN-gamma response via TCR and plasma IgG specific for B

94 s that discriminated high responders (G-CSF, IFN-gamma, TNF-alpha) correlated with both egress of cir

95 the release of the proinflammatory cytokine, IFN-gamma.

96 and producing the proinflammatory cytokines IFN-gamma and IL-17 in situ.

97 Five cytokines (IFN-gamma, IL-10, IL-6, IL-8, and TNF-alpha) contributed

98 -gamma pathway was associated with decreased IFN-gamma-induced gene expression and decreased IL-12-in

99 Rag deficiency, IFN-gamma deficiency, or depletion of either CD4(+) or C

100 ern recognition receptors and T cell-derived IFN-gamma production.

101 oportion of infants who mounted a detectable IFN-gamma response.

102 e addition of PG (PGE(2)) further diminished IFN-gamma levels in PBMCs, and supplementation of cells

103 profilin in T. gondii had no impact on early IFN-gamma production or parasite proliferation.

104 Accordingly, effector IFN-gamma-producing CD4 and CD8 T cells are significantl

105 own that this depends on PLP-CD8 elaborating IFN-gamma and perforin in a coordinated suppression prog

106 The expression levels of eotaxin, IFN-gamma, IL-6, IL-8, IL-16, MCP-1, MIF and MIP-1 beta

107 lasting colonization in the colon by evading IFN-gamma from group 3-like ILCs.

108 ulatory inflammatory cytokines, for example, IFN-gamma and IL-12, in CCR2i- versus vehicle-treated mi

109 th this observation, we found that exogenous IFN-gamma suppressed macrophage phagocytosis of zymosan

110 As expected, IFN-gamma induced genes involved in Ag presentation and

111 s producing inflammatory mediators following IFN-gamma plus LPS stimulation.

112 5-fold (CI, 2.3- to 9.8-fold; P < 0.001) for IFN-gamma-producing CD4+ T cells, 4.9-fold (CI, 1.3- to

113 1-fold (CI, 0.0- to 6.0-fold; P = 0.030) for IFN-gamma and 5.7-fold (CI, 2.0- to 15.0-fold; P < 0.001

114 Supernatants and cells were analyzed for IFN-gamma and chemokine production and lymphocyte migrat

115 assays indicated that GBP2 is important for IFN-gamma-dependent anti-MNV activity in murine macropha

116 ta provide insight into the requirements for IFN-gamma production and how IFN-gamma enhances local im

117 together, we uncover a nonredundant role for IFN-gamma and its downstream signaling molecules STAT1 a

118 ad increased production of interferon gamma (IFN-gamma) and monokine induced by gamma interferon (MIG

119 interleukin-12 (IL-12) and interferon gamma (IFN-gamma) by as early as 4 hpi, but the level of IFN-ga

120 ng interleukin-4 (IL-4) or interferon gamma (IFN-gamma) did not.

121 -T cell activation through interferon gamma (IFN-gamma) production and CD107a membrane accumulation b

122 e quantified the number of interferon gamma (IFN-gamma)-producing CD4 T cells specific for VZV glycop

123 actor beta (TGF-beta), and interferon gamma (IFN-gamma).

124 s produced proinflammatory interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha).

125 he natural history of anti-interferon-gamma (IFN-gamma) autoantibody-associated immunodeficiency synd

126 Interferon-gamma (IFN-gamma) plays an important role in the control of Lei

127 r ligand TRAIL, as well as interferon-gamma (IFN-gamma) secretion, was more pronounced during C. glab

128 at T cell infiltration and interferon-gamma (IFN-gamma) signaling signatures correspond most highly w

129 nt increase in gB-elicited interferon-gamma (IFN-gamma), granzyme B, and CD107a and a reduction in ly

130 ot the T helper 1 cytokine interferon-gamma (IFN-gamma).

131 lammatory cytokines (e.g., interferon gamma [IFN-gamma] and tumor necrosis factor alpha [TNF-alpha])

132 e IL-12-induced STAT4 activation to generate IFN-gamma, with autocrine IFN-gamma then signaling throu

133 deficient PLP-CD8 exhibited altered granzyme/IFN-gamma profiles, altered migration in recipients, and

134 ved transcriptome response unless cells have IFN-gamma receptor alterations.

135 e of TLR3, we showed the involvement of high IFN-gamma and lower type I IFN response in the early cle

136 equirements for IFN-gamma production and how IFN-gamma enhances local immune responses to prevent Bp-

137 1-3 wk posttransplant and had elevated human IFN-gamma in plasma that correlated negatively with the

138 Specific recovery of human IgG, IFN-gamma, and HIV-1 RNA indicate the diagnostic utility

139 cytic infiltration, higher levels of MHC II, IFN-gamma, IL-1beta, TNF-alpha, and cathepsin S (Ctss) m

140 Immediate IFN-gamma was partially dependent on the T. gondii mouse

141 isk factors, but these cells showed impaired IFN-gamma production.

142 In IFN-gamma(-/-) mice, there is deficient granuloma format

143 A decrease in IFN-gamma production was observed within 24 h after infe

144 mitochondrial metabolism is a key factor in IFN-gamma control of intracellular bacteria, the develop

145 We saw a significant increase in IFN-gamma production by peripheral blood mononuclear cel

146 Consequently, HBV was completely rescued in IFN-gamma-deficient or in TH2 phase coinfected mice demo

147 ly, there is a reduction in cytosolic Trp in IFN-gamma-activated host cells.

148 ated with significantly (p < 0.05) increased IFN-gamma production by CD4(+) T cells.

149 derived dendritic cell numbers and increased IFN-gamma-dependent expression of CXCR3 ligands by airwa

150 -A2 on day 13 of life demonstrated increased IFN-gamma expression (which is a mature antiviral respon

151 The nonmethylated peptide did not induce IFN-gamma, arguing that the methyl lysines are part of t

152 The soluble antigens failed to induce IFN-gamma production, whereas inactivated Bp induced IFN

153 a production, whereas inactivated Bp induced IFN-gamma production.

154 Thus, schistosome-induced IFN-gamma had a prominent antiviral effect that outcompe

155 t for IFN-gammaR indicates that TLR7-induced IFN-gamma activates multiple signaling pathways to regul

156 ecognized indispensable role of TLR7-induced IFN-gamma signaling in promoting AFC and GC responses, l

157 on in the spleens and livers of STm-infected IFN-gamma(-/-) and T-bet(-/-) mice.

158 GRASLND acts to inhibit IFN-gamma by binding to EIF2AK2, and we further demonstr

159 h recalcitrant GA with tofacitinib inhibited IFN-gamma and oncostatin M, as well as IL-15 and IL-21,

160 nflammatory genes, such as gamma interferon (IFN-gamma) and CCL2.

161 at included high levels of gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha),

162 rmore, genetic deletion of gamma interferon (IFN-gamma) but not IL-22 or antibody-mediated depletion

163 ction of granzyme B(+) and gamma interferon (IFN-gamma)(+) MAIT cells relative to that in uninfected

164 e in the levels of CD107a, gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha)

165 intracellular detection of gamma interferon (IFN-gamma), CD107(a/b) degranulation, and CD4(+) T cell

166 naive OVA-TCR transgenic CD4(+) T cells into IFN-gamma-secreting cells.

167 Human CD8(+) T cells can be divided into IFN-gamma- and IL-2-producing cells.

168 lls, and ultimately requires tumor-intrinsic IFN-gamma signaling, via a mechanism that is distinct fr

169 RNA sequencing, we found that in GA lesions IFN-gamma production by CD4(+) T cells is upregulated an

170 Furthermore, we found that EPS limits IFN-gamma production by modulating host immunity in a To

171 cells, T9 CAR-T cells secrete IL9 but little IFN-gamma, express central memory phenotype and lower le

172 together with CD154 upregulation and a lower IFN-gamma response compared with TBE patients.

173 ions: RV-C induced memory cells with a lower IFN-gamma-type response than RV-A without T-helper cell

174 lysine methylation/demethylation of M(LPS + IFN-gamma)/M(IL-10) genes is one of the factors that dir

175 couplers that promote mitophagy reversed LPS/IFN-gamma-mediated activation of macrophages and led to

176 lls decreases, while the CD68(+) macrophage, IFN-gamma(+), TNF-alpha(+), and iNOS(+) immunolabeling f

177 necessary but not sufficient for maintaining IFN-gamma production by Th1 cells.

178 Flow cytometry was used to measure IFN-gamma, IL-9, IL-13, IL-17, and IL-22 cytokine levels

179 12 induction in macrophages & STAT4-mediated IFN-gamma synthesis in T cells.

180 -immune disease-associated variants modulate IFN-gamma- and IL-12-associated outcomes, and in turn, P

181 These results implicated an NKT cell/mTOR/IFN-gamma axis in immunosuppression following endotoxemi

182 well as TNF-alpha, IL-6, or IL-17A, but not IFN-gamma, similarly induced sHLH in SIRPalpha(-/-) mice

183 lded IL-4-producing NKT2 cell subset but not IFN-gamma-producing NKT1 cell subset.

184 neutralized interferon (IFN)-alpha, but not IFN-gamma.

185 mor eradication related to the activation of IFN-gamma-producing CD8 T cells.

186 s also producing abnormally small amounts of IFN-gamma.

187 -induced increase in the specific binding of IFN-gamma to its receptor in U937 cells, enhanced induce

188 of zymosan in vivo, and antibody blockade of IFN-gamma after endotoxemia improved survival of seconda

189 Blockade of IFN-gamma signaling in mice increases lesion size and pa

190 hich was reversed by therapeutic blockade of IFN-gamma.

191 le, aberrant morphology, and, in the case of IFN-gamma-induced persistence, Trp codon-dependent chang

192 not IL-22 or antibody-mediated depletion of IFN-gamma from adaptive immunity-deficient mice signific

193 Nevertheless, antibody depletion of IFN-gamma or genetic deletion of interleukin 2 (IL-2) re

194 was associated with strong downregulation of IFN-gamma and IFN-alpha gene signatures that were revers

195 e statistically significant dysregulation of IFN-gamma, IL-1RA, IL-6, IL-10, IL-19, monocyte chemoatt

196 anti-PD-1 resistance linked to emergence of IFN-gamma signaling mutants, we show that when mixed wit

197 nfiltrating CD4(+) cells had an expansion of IFN-gamma(-) and TNF-alpha(-) double-negative cells comp

198 pression of IL-13 mRNA but not expression of IFN-gamma mRNA (which is indicative of a type 2 immune r

199 pression and a decrease in the expression of IFN-gamma.

200 hat VPA treatment decreased the frequency of IFN-gamma-producing NK cells within L.m infected splenoc

201 that correlated with significant increase of IFN-gamma.

202 mimic the persistent state independently of IFN-gamma.

203 trast, TDM/TDB exerted delayed inhibition of IFN-gamma-induced genes, including pattern recognition r

204 amma) by as early as 4 hpi, but the level of IFN-gamma was significantly lower or undetectable in T.

205 atory drugs was able to restore the level of IFN-gamma.

206 cells, showed (i) decreases in the levels of IFN-gamma and IL-12, (ii) an increase in the level of th

207 Concurrently, decreased levels of IFN-gamma in serum and lower splenic indexes were observ

208 ient CD4(+) T cells express higher levels of IFN-gamma mRNA compared with WT CD4(+) T cells.

209 found a correlation between higher levels of IFN-gamma production by liver natural killer (NK) cells

210 T-bet(-/-) mice induce significant levels of IFN-gamma(-) after challenge.

211 s develop normally but produce low levels of IFN-gamma, with the exception of CD8(+) alphabeta T and

212 s were associated with a higher magnitude of IFN-gamma response when compared to non-conserved epitop

213 Neutralization of IFN-gamma during infection abrogated Ido1 expression and

214 However, the percentage of IFN-gamma(+) ILCs in infected colons was 5- to 10-fold h

215 ons of IL-2-secreting, but lower portions of IFN-gamma-secreting, cells.

216 s but also by limiting NK cell production of IFN-gamma after S. aureus infection in a TLR4-dependent

217 is study, we observed impaired production of IFN-gamma and IL-10 by whole blood from beta-thalassaemi

218 hemin or CoPP in vitro reduced production of IFN-gamma and IL-10 from healthy human PBMCs and decreas

219 n U937 cells, enhanced induced production of IFN-gamma in human PBMC culture, and increased survival

220 rial stimulation and decreased production of IFN-gamma in response to heterologous stimulation and TL

221 The production of IFN-gamma, a type II IFN, was decreased in patients in r

222 er interface and at the C-terminal region of IFN-gamma.

223 ocytic host cell reservoir via regulation of IFN-gamma and IL-10.

224 significant degree of negative regulation of IFN-gamma-induced Ag presentation and antimicrobial gene

225 The release of IFN-gamma, TNF-alpha, IL-2, IL-4, IL-6, IL-10 and IL-17A

226 NK cells were the main source of IFN-gamma production, which was enhanced by IL-15.

227 The provision of a source of IFN-gamma reverses this, coincident with subsequent gran

228 NK cells are likely key sources of IFN-gamma in this model.

229 mpared with mice deficient in all sources of IFN-gamma.

230 ycolipids enhanced expression of a subset of IFN-gamma-induced genes associated with inflammation.

231 th decreased mitogen-induced upregulation of IFN-gamma, TNF, IL-6, CXCL9, CXCL10, and IL-1beta produc

232 nd decreased IL-12-inducible upregulation of IFN-gamma.

233 naling, TLR9-driven fatality is dependent on IFN-gamma receptor signaling.

234 sponses and SLE development are dependent on IFN-gamma signaling in B cells.

235 s of autoimmunity that are less dependent on IFN-gamma, ampicillin but not neomycin treatment correla

236 However, the impact of TDM on IFN-gamma-induced macrophage activation is not known.

237 Of those tested, only IFN-gamma priming prior to MEK inhibitor treatment resul

238 pective of CEBPB, miR-520G overexpression or IFN-gamma treatment.

239 cells to suppress an atypical and pathogenic IFN-gamma response to inhaled HDM.

240 (FH1) cell help was delivered in two phases: IFN-gamma signals were provided early in infection, wher

241 Circulating plasma IFN-gamma levels were also assayed in 400 patients with

242 al clearance, we found that increased plasma IFN-gamma in early clinical sepsis was associated with t

243 pitopes, induced HSV-specific polyfunctional IFN-gamma-producing CD107(ab+) CD4(+) T cells associated

244 in test (TST); 3) enroll based on a positive IFN-gamma release assay (IGRA); 4) enroll based on eithe

245 tivated Bp, but not antigens, induced potent IFN-gamma production by NK cells, resulting in chemo-att

246 with "older" NK cells exhibiting more potent IFN-gamma production to activating stimuli and more robu

247 transplant group, reverting to predominantly IFN-gamma-oriented response in the >24 m group.

248 ) cells in Rag-deficient mice both prevented IFN-gamma production and rescued mutant colonization.

249 ctivity, defined by their ability to produce IFN-gamma and to drive the maturation of high IL-12-prod

250 pha, extended beyond an inability to produce IFN-gamma, as FcRgamma(-) NK cells showed limited potent

251 ells activated mTORC1 in NK cells to produce IFN-gamma, which worsened macrophage phagocytosis, clear

252 lphabeta T(H)1(*) lymphocytes, which produce IFN-gamma normally in response to mycobacterial antigens

253 RS-CoV-2-convalescent subjects also produced IFN-gamma in response to seasonal OC43 S protein.

254 mphoblast expansion and cytokine production (IFN-gamma, IL-2, and TNF), with the highest median magni

255 human skin DCs to express IL-12 and promote IFN-gamma secretion by CD4(+) T cells.

256 anistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the S

257 hed frequencies of membrane protein-reactive IFN-gamma+ T cells were particularly associated with hig

258 Reduced IFN-gamma responses were attributable to a decrease in t

259 ty-deficient mice both significantly reduced IFN-gamma and increased C. trachomatis burden in the end

260 in neurons to control virus spread, regulate IFN-gamma signaling, and prevent acute mortality.

261 (IL-17A/F and IL-36A/IL-36G), T(H)1-related (IFN-gamma and CXCL9/CXCL10), and innate immunity-related

262 sed by Salmonella Typhimurium (STm) requires IFN-gamma and the Th1-associated transcription factor T-

263 and puncture, induced a transient but robust IFN-gamma burst within a proinflammatory cytokine/chemok

264 Epithelial-PBMC co-cultures showed robust IFN-gamma-dependent CXCL9 and CXCL10 production by the e

265 igh levels of IL-1R1 and IL-23R and secreted IFN-gamma, IL-17, and GM-CSF in response to canonically

266 ite burdens correlated with a pulse of serum IFN-gamma at 3 to 4 days postinfection in the absence of

267 antly, while the frequency of tumor-specific IFN-gamma producing CD8(+) T-cells was significantly inc

268 The frequency of VZV-specific IFN-gamma-producing CD4 T cells was significantly higher

269 uction by them, with mycobacterium-specific, IFN-gamma-producing, purely adaptive CD8(+) alphabeta T,

270 bilization of its putative protein substrate IFN-gamma receptor 1 (IFNGR1) at the protein level in TN

271 from follicular T helper (Tfh)-IL-17 to Tfh-IFN-gamma.

272 (+) cells produce helper cytokines, and that IFN-gamma(+) cells produce cytotoxic molecules.

273 oid leukemia (AML) cells, demonstrating that IFN-gamma treatment upregulated the expression of NOD2 s

274 Our findings suggest that IFN-gamma-producing PLZF(lo)RORgammat(lo) iNKT1 cells pl

275 Collectively, this work suggests that IFN-gamma responsiveness allows myelin-specific CD8 T ce

276 =0.009) but we saw no difference between the IFN-gamma production in the vaccine only group compared

277 -mediated inflammatory process driven by the IFN-gamma pathway.

278 lation of T cell-derived IL-10 increased the IFN-gamma and IL-17A response to HDM, reducing IL-13 lev

279 13 polarization included IL-5 in addition to IFN-gamma and IL-13.

280 rient when the human host cell is exposed to IFN-gamma.

281 estricted Th1 responses and in particular to IFN-gamma- and TNF-alpha-expressing CD4(+) T cells.

282 t become highly activated when responding to IFN-gamma.

283 tive disease, whereas the shared response to IFN-gamma and IFN-beta in neutrophils was increased.

284 osed to IL-4/IL-13 and monocyte responses to IFN-gamma or IFN-beta emerged as opposing predictors of

285 In turn, IFN-gamma released by Vdelta2(+) cells upregulates IL-12

286 significantly higher levels of IL-12p70 upon IFN-gamma and LPS stimulation than those from individual

287 sive CD8(+) T-cell clones was measured using IFN-gamma ELIspot.

288 t of chronic Chagas' disease patients, using IFN-gamma secretion as a readout.

289 lar responses were assessed using an ex-vivo IFN-gamma enzyme-linked immunospot assay.

290 he interaction in 58 human cell lines, where IFN-gamma in vitro exposure leads to a conserved transcr

291 s were dependent on IL-18 and IL-12, whereas IFN-gamma secretion was restricted by high concentration

292 posure to both IFN-alpha and -gamma, whereas IFN-gamma appeared to inhibit invasion of S. aureus.

293 Nevertheless, whereas IFN-gamma(-/-) mice succumb rapidly to STm infections, T

294 It will be worth investigating whether IFN-gamma-producing ILCs also improve endometrial resist

295 suggested that T1 CRSsNP was associated with IFN-gamma signaling and antiviral immunity controlled by

296 lipopolysaccharide (LPS) in combination with IFN-gamma inhibited PINK1-dependent mitophagy in macroph

297 wever, phenotype shifted significantly, with IFN-gamma-dominated response in the pretransplant group

298 epithelial cells following stimulation with IFN-gamma and Bp.

299 ranscription when the cells are treated with IFN-gamma.

300 e, Th1 cells act to restrict bacteria within IFN-gamma-dependent iNOS(+) granulomas and prevent disse