ライフサイエンスコーパス: IFN-gamma production

1 ning), this was not the case for others (eg, IFN-gamma production).

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

3 h22 cells displayed marked plasticity toward IFN-gamma production.

4 ighest level of lymphocyte proliferation and IFN-gamma production.

5 tely restored Th cell proliferation, but not IFN-gamma production.

6 aforementioned cellular immune response and IFN-gamma production.

7 2 in NK cells suppressed IL-12/IL-18-induced IFN-gamma production.

8 diabetic intervention approaches modulating IFN-gamma production.

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

10 like receptor G1(+) effector CD8 T cells and IFN-gamma production.

11 n provides sufficient energy for TLR-induced IFN-gamma production.

12 IFN-DC-mediated NK cell activation and early IFN-gamma production.

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

14 G2D-dependent cell-mediated cytotoxicity and IFN-gamma production.

15 coordination of subsequent cytotoxicity and IFN-gamma production.

16 like receptor G1(+) effector CD8 T cells and IFN-gamma production.

17 s and dampened effector T-cell expansion and IFN-gamma production.

18 nction, as measured by CD107a expression and IFN-gamma production.

19 et of SS in NOD mice, in part by suppressing IFN-gamma production.

20 roinflammatory mediators and T cell-mediated IFN-gamma production.

21 nfirmed that 10 of 26 epitopes (38%) induced IFN-gamma production.

22 d counteract the benefits of increased early IFN-gamma production.

23 nvironment, permitting T cell glycolysis and IFN-gamma production.

24 ic effectiveness was critically dependent on IFN-gamma production.

25 T cells but not CD8 T cells were impaired in IFN-gamma production.

26 tion gene 3 (LAG-3) expression and a lack of IFN-gamma production.

27 mor microenvironment act to reduce MAIT cell IFN-gamma production.

28 lls, which promoted T cell proliferation and IFN-gamma production.

29 -stimulatory signal like CD28 that triggered IFN-gamma production.

30 diabetes development, T-cell expansion, and IFN-gamma production.

31 escribed as a Th1-mediated process involving IFN-gamma production.

32 lished the effect of fenofibrate in reducing IFN-gamma production.

33 chemokine, with a negligible effect on IL-10/IFN-gamma production.

34 ed glycolytic reprogramming was required for IFN-gamma production.

35 P1C)-stimulated and IL-12/18 cytokine-primed IFN-gamma production.

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

37 nd spleens of infected mice at times of peak IFN-gamma production.

38 se, DNA-HSP65 and CpG/CFP promoted IL-10 and IFN-gamma production.

39 which neither expressed IL-12 nor stimulated IFN-gamma production.

40 rotein stability are critical in suppressing IFN-gamma production.

41 IL-10Ralpha blockade preferentially restores IFN-gamma production.

42 tially killed by NK cells and trigger potent IFN-gamma production.

43 e of IL-9 or IL-4 enhanced allergen-specific IFN-gamma production.

44 Toll-like receptor ligands further enhanced IFN-gamma production.

45 s to KIR2DL4 and HLA-G did not block NK cell IFN-gamma production.

46 L-12 and stimulated T cell proliferation and IFN-gamma production.

47 ppression of CD4(+) T cell proliferation and IFN-gamma production.

48 -1-like phenotype characterized by IL-10 and IFN-gamma production.

49 Transient knockdown of Ifng-as1 also reduced IFN-gamma production.

50 estored mitochondrial membrane potential and IFN-gamma production.

51 s downregulate allergic inflammation through IFN-gamma production.

52 manner, and this is essential for MAIT cell IFN-gamma production.

53 acutely as a transcription factor to promote IFN-gamma production.

54 ting lymphocyte apoptosis through regulating IFN-gamma production.

55 molecules require additional stimulation for IFN-gamma production.

56 o observed despite overall downregulation of IFN-gamma production.

57 activation receptors alone is sufficient for IFN-gamma production.

58 psis by activating NK cells and facilitating IFN-gamma production.

59 pSTAT4, nuclear translocation, and impaired IFN-gamma production.

60 ll responses were observed in the absence of IFN-gamma-production.

61 nd are associated with low-level interferon (IFN)-gamma production.

62 d with excessive Treg cell interferon-gamma (IFN-gamma) production.

63 that correlated with increased type II IFN (IFN-gamma) production.

64 ing mice displayed reduced interferon-gamma (IFN-gamma) production.

65 unction of CD4(+) T cells, interferon-gamma (IFN-gamma) production.

66 essed greater capacity for interferon-gamma (IFN-gamma) production.

67 or locus on chromosome region 8q controlling IFN-gamma production after stimulation with live BCG (Ba

68 m-specific in vitro recall gamma interferon (IFN-gamma) production after CHMI, and innate IFN-gamma r

69 egulated autologous T-cell proliferation and IFN-gamma production against a peptide pool consisting o

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

71 mice was associated with impaired IL-12 and IFN-gamma production and a concomitant increase in IL-4

72 ing, based on significantly higher levels of IFN-gamma production and a remarkable increase in CD8(+)

73 ty in HLA/antigen-matched tumors and induced IFN-gamma production and activation.

74 leading to NK cells that display diminished IFN-gamma production and at least a transiently impaired

75 in + 2-DG treatment more potently suppressed IFN-gamma production and cell proliferation in activated

76 fically in NK cells, resulted in an enhanced IFN-gamma production and consequently protected mice fro

77 CCR7(+) Dectin-1(-)M1 cells, accompanied by IFN-gamma production and cytolytic function in T cells.

78 f SIY-specific CD8(+) T cells, with enhanced IFN-gamma production and cytotoxic capability.

79 idenced by enhanced proliferation, survival, IFN-gamma production and cytotoxicity toward tumors.

80 opositivity is associated with lower NK cell IFN-gamma production and degranulation after in vitro re

81 l responses, which correlated with decreased IFN-gamma production and degranulation by Tim-3 KO cells

82 lopment of KLF12-deficient NK cells, altered IFN-gamma production and degranulation, and impairment o

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

84 gside STAT4 to coordinate Tfh cell IL-21 and IFN-gamma production and for promotion of the GC respons

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

86 important to understand temporal changes in IFN-gamma production and how these changes relate to the

87 AR-20347 significantly reduced IL-12-induced IFN-gamma production and IL-22-dependent serum amyloid A

88 (SOCS1) protein in T cells, which inhibited IFN-gamma production and killing of CEF-pulsed monocytes

89 population was fully functional as judged by IFN-gamma production and MHC class I-restricted cytotoxi

90 IFN-gamma production and microbicidal activity were impa

91 Tregs in wounded skin attenuated IFN-gamma production and proinflammatory macrophage accu

92 n was shown by a dose-dependent induction of IFN-gamma production and proliferation by the CD4 T-cell

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

94 data highlight T-bet-independent pathways to IFN-gamma production and reveal a novel role for this tr

95 munity against this parasite is dependent on IFN-gamma production and subsequent macrophage activatio

96 T-bet is a master regulator for IFN-gamma production and Th1 differentiation.

97 demonstrated an inverse correlation between IFN-gamma production and the time from clinical presenta

98 er studies have shown that gamma interferon (IFN-gamma) production and activation of Th1 cells charac

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

100 Induced interferon gamma (IFN-gamma) production and NKp46/NKp30 activating recepto

101 -CXCL10 antibodies reduced gamma interferon (IFN-gamma) production and Th17 cell infiltration, as wel

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

103 om CLP hosts showed decreased proliferation, IFN-gamma production, and survival compared with sham co

104 eration, interleukin 2 and interferon gamma (IFN-gamma) production, and phosphorylated STAT1 expressi

105 y GA, the T cell proliferation and their Th1 IFN-gamma production are further inhibited, whereas the

106 eptor signaling, as NK cell cytotoxicity and IFN-gamma production are regulated by signal transducer

107 lar flow cytometry was employed to determine IFN-gamma production as a functional readout.

108 A 2-way MLR, adopting IFN-gamma production as a marker of alloresponse, result

109 active CD4(+) T cells and elevated IL-21 and IFN-gamma production, associated with a higher frequency

110 stimulate iNKT cells in vivo, with increased IFN-gamma production at 24 h compared with alphaGalCer,

111 restored OM-specific PBMC proliferation and IFN-gamma production at 5 wpi.

112 , whereas addition of IL-10 increased T cell IFN-gamma production but decreased monocyte production o

113 This was associated with an increase in IFN-gamma production but not cytotoxicity of NK cells du

114 critical for CD8 T cell activation (promotes IFN-gamma production but not proliferation or granzyme B

115 ogic features was reversed, with no role for IFN-gamma production but substantial correction after re

116 activity also induced spontaneous IL-22 and IFN-gamma production, but these cytokines had also uniqu

117 his was confirmed by in vitro measurement of IFN-gamma production by activated T cells.

118 an essential second signal for induction of IFN-gamma production by activating NK cell receptors tha

119 sin-converting enzyme inhibitors potentiated IFN-gamma production by Ag-specific T cells via C5aR/B2R

120 -) macrophages enhances Th1 polarization and IFN-gamma production by antigen-specific CD4(+) T cells

121 The functional loss of IFN-gamma production by antigen-specific CD4(+) T cells

122 Identification of excessive IFN-gamma production by blood and lymph node-derived T c

123 e high TRAIL expression by SG-resident ILC1, IFN-gamma production by both ILC1 and cNK was minimal at

124 We analyzed the role of IFN-gamma production by brain-resident cells in resistan

125 sing bone marrow chimeric mice revealed that IFN-gamma production by brain-resident cells is essentia

126 However, the physiological role of IFN-gamma production by brain-resident cells, including

127 ns through effects on leukocyte recruitment, IFN-gamma production by CD4 and CD8 T cells, and the act

128 IFN-gamma production by CD4(+) and CD8(+) peripheral blo

129 -helper (Th) cell type 1 inflammation (e.g., IFN-gamma production by CD4(+) effector T cells).

130 e were functionally defective in suppressing IFN-gamma production by CD4(+) T cells in coculture.

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

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

133 ATP synthase alone was sufficient to impair IFN-gamma production by CD4(+) T cells.

134 -2) on NK cells accounted for the diminished IFN-gamma production by CD56(bright) NK cells, whereas M

135 A strong dependency on PI3Kdelta for IFN-gamma production by CD8(+) T cells in vitro was not

136 s principally reflected profoundly defective IFN-gamma production by circulating gammadelta T cells a

137 tion into the intestinal lamina propria, and IFN-gamma production by colitogenic CD4(+) T cells.

138 ce displayed enhanced capacities to suppress IFN-gamma production by effector T cells, suggesting tha

139 However, Eomes is fully dispensable for IFN-gamma production by gammadelta T cells.

140 Cytotoxicity and IFN-gamma production by human gammadelta T cells underli

141 stein and equol decrease IL-12/IL-18-induced IFN-gamma production by human NK cell subsets, but do no

142 xpression at low O2 levels and the unchanged IFN-gamma production by IL-10-deficient Th1 cells stimul

143 0, IL-6, and TNF-alpha production as well as IFN-gamma production by IL-12p70-mediated activation of

144 was accompanied by significant reduction in IFN-gamma production by immune cells in the spleens and

145 Nonetheless, Treg treatment abrogated IFN-gamma production by intraislet CD8(+) and CD4(+) T c

146 iphosphate accelerated interleukin-12-driven IFN-gamma production by liver ILC1s.

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

148 After MCMV infection, Ly49D augmented IFN-gamma production by MCMV-specific Ly49H(+) NK cells

149 r release of alarmins, pyroptosis, and early IFN-gamma production by memory CD8 T cells, all of which

150 -gamma only in CD11b(+) cells suggested that IFN-gamma production by microglia, which is the only CD1

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

152 Here, we have reported that noncognate IFN-gamma production by Mtb antigen-independent memory C

153 from H. polygyrus (HES) was found to dampen IFN-gamma production by mycobacteria-specific CD4(+) T c

154 When activated in vitro, however, IFN-gamma production by naive wild type and tristetrapro

155 ads to production of IFN-alpha, which drives IFN-gamma production by natural killer cells.

156 2-independent and the events associated with IFN-gamma production by neutrophils are not understood.

157 n NK cells we show that TYK2 is required for IFN-gamma production by NK cells in response to IL-12 an

158 g endotoxemia suggested that NKT cells drove IFN-gamma production by NK cells via mTORC1.

159 ulate that SP-D may constitutively stimulate IFN-gamma production by NK cells, possibly via NKp46.

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

161 29 expression were inversely correlated with IFN-gamma production by NK cells, suggesting that TRIM29

162 ry cytokine combinations capable of inducing IFN-gamma production by NK cells.

163 g protein 2 (TAB2), a key adaptor protein in IFN-gamma production by NK cells.

164 IL-18 and are unable to optimally stimulate IFN-gamma production by NK cells.

165 nocytogenes and observed that IS001 enhanced IFN-gamma production by NKT, CD4(+), and CD8(+) T cells

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

167 ting conditions resulted in higher levels of IFN-gamma production by pTreg compared with thymic Treg,

168 ected phenotype was associated with enhanced IFN-gamma production by T cells and decreased accumulati

169 CD19-hBtk B cells promoted IFN-gamma production by T cells and expression of the im

170 ients with sepsis via modulation of IL-10 on IFN-gamma production by T cells and TNF-alpha production

171 quently, CCL2 deficient MSCs did not inhibit IFN-gamma production by T cells and upon transfer no lon

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

173 5 (miR155) promotes CD4(+) Th1 responses and IFN-gamma production by targeting suppressor of cytokine

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

175 he rate of glycolysis significantly impaired IFN-gamma production by the CD56(bright) subset of cells

176 ent with a neutralizing Ab to CX3CL1 reduced IFN-gamma production by the lung NK cells.

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

178 and evaluated the mechanistic regulation of IFN-gamma production by these cells in vivo.

179 , commensurate with increased activation and IFN-gamma production by these immature NK cell subsets.

180 IFN-gamma production by these lymphocytes likely plays a

181 Innate gamma interferon (IFN-gamma) production by CD8(+) T cells following exposu

182 were present in the explant, showing a great IFN-gamma production capacity and expressing granzyme B.

183 ional Tg Th1 effectors demonstrated enhanced IFN-gamma production compared with polyclonal cells, pro

184 ors, and were more activated, with decreased IFN-gamma production, compared to both healthy donors an

185 Functionally, Th1 cells with graded IFN-gamma production competence differentially activated

186 feron (IFN)-gamma in vitro, and this reduced IFN-gamma production could be partially reversed by bloc

187 rogram as well as glycolysis and OXPHOS, but IFN-gamma production could be reinstated by retrovirus-m

188 mmatory lymphocytes in diabetes development, IFN-gamma production could represent an attempted limita

189 cytotoxicity increases and pSTAT4-dependent IFN-gamma production decreases in response to endogenous

190 The mTORC1 and IFN-gamma production defects were partially rescued by s

191 F12 was dispensable for NK cell development, IFN-gamma production, degranulation, and proliferation i

192 the metabolic requirements of murine NK cell IFN-gamma production depending upon the activation signa

193 uced capacity to prime antigen (Ag)-specific IFN-gamma production during co-culture with naive transg

194 lly, Nod1-deficient T cells exhibit impaired IFN-gamma production during dextran sulfate sodium (DSS)

195 Although IL-12 alone is required for NK cell IFN-gamma production during primary T. gondii infection,

196 roducing cells and the signals that regulate IFN-gamma production during T. gondii infection.

197 deficient T cells exhibited markedly reduced IFN-gamma production during the early phase of Mtb infec

198 uced T cell activation and interferon gamma (IFN-gamma) production during infection.

199 ing MCMV infection but did not show enhanced IFN-gamma production following direct ex vivo cytokine s

200 o demonstrated a reduced capacity to sustain IFN-gamma production following in vitro activation.

201 nt with recovery of T cell proliferation and IFN-gamma production following stimulation of CD3/CD28.

202 monstrated substantially diminished IL-2 and IFN-gamma production following TCR stimulation of his "u

203 ed recipients initially retained the stunted IFN-gamma production found prior to transfer, and cells

204 of HSCs to suppress the proliferation of and IFN-gamma production from activated T cells, suggesting

205 t secreted factors from tumor tissue reduced IFN-gamma production from MAIT cells.

206 as demonstrated by early and Ag-independent IFN-gamma production, granzyme B expression, and degranu

207 molecule-1, NKp46, and NKG2D) and decreased IFN-gamma production, had a significantly higher risk of

208 These data suggest that IFN-gamma production has antiviral effects in rabies, la

209 attributed the key distal event to excessive IFN-gamma production; however, the proximal events drivi

210 Ifng locus, leading to elevated interferon (IFN)-gamma production in a nuclear factor (NF)-kappaB-T-

211 factor for Th1 cells, which in turn supports IFN-gamma production in a feed-forward manner.

212 induced intracellular Leishmania killing and IFN-gamma production in a macrophage-T cell coculture sy

213 Remarkably, both BTK inhibitors stimulated IFN-gamma production in a mixed lymphocyte reaction.

214 re required to support both cytotoxicity and IFN-gamma production in all NK cells.

215 e, we examined the effect of IL-10 on T cell IFN-gamma production in an in vivo cecal ligation and pu

216 that, although SOCE is required for NK cell IFN-gamma production in an NFAT-dependent manner, NK cel

217 g by allergen-IgE immune complexes increased IFN-gamma production in B cells of allergic patients dur

218 regulating allergic reactions via modulating IFN-gamma production in B cells.

219 that synergize to induce antigen-independent IFN-gamma production in CD4(+) and CD8(+) TEM cells.

220 s associated with enhanced proliferation and IFN-gamma production in CXCR3(+) cells.

221 d IL-18, which is a crucial system for early IFN-gamma production in listeriosis.

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

223 The developmental mechanism of IFN-gamma production in neutrophils arms the innate immu

224 ur phenotypic findings, we observed a higher IFN-gamma production in peripheral CD4 memory T cells an

225 , STIM1-deficient T cells displayed enhanced IFN-gamma production in response to elevated levels of I

226 e divided cells did not demonstrate enhanced IFN-gamma production in response to innate cytokine stim

227 d a major locus on chromosome 8q controlling IFN-gamma production in response to stimulation with liv

228 IL-7 restored ex vivo IFN-gamma production in septic patients.

229 0-treated septic mice demonstrated increased IFN-gamma production in splenocytes.

230 tion begins at the onset of T cell entry and IFN-gamma production in the CNS prior to the appearance

231 hat NK cells do require multiple signals for IFN-gamma production in the context of target cell recog

232 tionally, combination therapy induced higher IFN-gamma production in the LTB state than in the high t

233 d with decreased gammadelta T cell IL-17 and IFN-gamma production in the thymus as well as in periphe

234 =0.009) but we saw no difference between the IFN-gamma production in the vaccine only group compared

235 ion of cytotoxicity receptors, and extensive IFN-gamma production in the virtual absence of IL-10.

236 ts in a markedly reduced capacity to inhibit IFN-gamma production in tolerized T cells.

237 Importantly, lenalidomide did not trigger IFN-gamma production in unstimulated NK cells.

238 nsferred CTLs enhances T cell activation and IFN-gamma production in vitro, leading to a significant

239 ase, making the ability to monitor and track IFN-gamma production in vivo of a substantial benefit.

240 tions capable of eliciting gamma interferon (IFN-gamma) production in NK cells.

241 liferative response and cytokine (IL-17A and IFN-gamma) production, in addition to upregulation of im

242 gen target (ESAT-6), taking into account the IFN-gamma production induced by BCG (IFNgamma-ESAT6BCG).

243 Monokine induced by IFN-gamma, MCP-1, and IFN-gamma production induced in T. cruzi-infected infant

244 ammation promotes tumor progression, whereas IFN-gamma production is essential for antitumor immunity

245 indicates that activation receptor-dependent IFN-gamma production is regulated on the transcriptional

246 T-bet ablation restricted interferon-gamma (IFN-gamma) production, loss of Blimp-1 prevented GzmB ex

247 IFN-gamma production, mainly by natural killer cells, wa

248 a pulmonary tularaemia model, POP2 enhances IFN-gamma production, modulates neutrophil numbers, impr

249 Protection against CL was associated with IFN-gamma production, negative LST results, impaired abi

250 of Eomes in CD4(+) T cells did not impact on IFN-gamma production nor increase Th2 or Th17 responses.

251 Impaired metabolism underlies the reduced IFN-gamma production observed in activated RTEs.

252 The inhibition of IFN-gamma production occurs through blocking the repress

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

254 -2.4 Gy radiation enhances proliferation and IFN-gamma production of PBMC or purified T cells induced

255 oxicity defect and the impaired actR-induced IFN-gamma production of Tyk2(-/-) NK cells.

256 nature predominantly reflected the impact of IFN-gamma production on a wide range of host immune resp

257 ngitis virus to genetically eliminate either IFN-gamma production or CD25 expression and assess the i

258 nt IL-13 responses, but had little effect on IFN-gamma production or cell proliferation.

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

260 lation and TNF-alpha but not cytotoxicity or IFN-gamma production, potentially favoring the progressi

261 of (64)Cu-PTSM and analyzed cell viability, IFN-gamma production, proliferation, apoptosis, and DNA

262 n of these cells correlated with high T-cell IFN-gamma production (r(s) = 0.573, P = .005) and low se

263 tory antigen target, when accounting for the IFN-gamma production shared with that induced by BCG (LO

264 creased mitogen-stimulated gamma interferon (IFN-gamma) production suggested immunomodulation, which

265 T cells in vitro decreased proliferation and IFN-gamma production, suggesting additional effects of s

266 However, the observation of impaired IFN-gamma production suggests that the efficacy of such

267 It induces a short boost of IFN-gamma production that leads to a significant but lim

268 n in group 1 ILCs is required to limit their IFN-gamma production, thereby allowing the development o

269 ened mTOR activity, glycolytic capacity, and IFN-gamma production, thereby allowing tumor progression

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

271 -gamma reporter transgenic model that allows IFN-gamma production to be visualized and quantified in

272 sion in RTEs, driving aerobic glycolysis and IFN-gamma production to the level of mature T cells.

273 cond locus on chromosome region 3q affecting IFN-gamma production triggered by the 6-kDa early secret

274 cells did not impact NK cell maturation and IFN-gamma production upon NK cell activating receptor (a

275 cose availability does not alter the rate of IFN-gamma production upon TLR-mediated activation.

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

277 be determined by levels of interferon gamma (IFN-gamma) production using an enzyme-linked immunospot

278 ukin (IL)-12/IL-18-induced interferon-gamma (IFN-gamma) production versus controls.

279 Increased IFN-gamma production was accompanied by a poor germinal

280 ession was observed on DenV-infected DC, and IFN-gamma production was enhanced in licensed/educated N

281 IL-13, IL-17A, and TNF-alpha was normal, but IFN-gamma production was increased in lung cells from ai

282 Stimulation of NK cell IFN-gamma production was independent of glycolysis or mi

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

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

285 Moreover, CCL17-induced IFN-gamma production was reduced when Th1-polarized norm

286 Accordingly, NKT cells were less activated, IFN-gamma production was significantly reduced, and leve

287 L-17 compared with the control mice, whereas IFN-gamma production was similar in both groups.

288 T cell recruitment and IFN-gamma production was similar in lungs of infected B6

289 (+)IL-10(+)IFN-gamma(+) frequencies and Treg-IFN-gamma production were found in women with current Pl

290 onuclear cells (PBMCs) and interferon gamma (IFN-gamma) production were significantly suppressed in c

291 displayed enhanced cytolytic capability and IFN-gamma production when co-cultured with GB cells or p

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

293 ment requires additional signals for optimal IFN-gamma production, which could be provided by IFN-bet

294 endogenous ligands to NKT cells, leading to IFN-gamma production, which in turn, stimulated 3T3-L1 a

295 tissue frequencies and a reduction in their IFN-gamma production, which is a critical effector funct

296 y in these cells reduced both viral load and IFN-gamma production, which suggests that targeting CCR4

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

298 oper T cell activation and gamma interferon (IFN-gamma) production, which are critical for infection

299 features of HLH were completely dependent on IFN-gamma production, with complete correction after los

300 tion, with complete correction after loss of IFN-gamma production without any role for CD8(+) T cell-