ライフサイエンスコーパス: IL-21

1 IL-21 also influenced responsiveness to IL-4 because exp

2 IL-21 and IFN-gamma are coexpressed by Tfh cells during

3 IL-21 can induce both plasma cells and regulatory B cell

4 IL-21 differentially promoted the expression of the chem

5 IL-21 does not induce Il1b expression in CD4(+) T cells,

6 IL-21 drastically increased the number of IL-10(+) Bregs

7 IL-21 enhanced GrB expression in control CD19(+) B cells

8 IL-21 induced STAT1 phosphorylation, and this was augmen

9 IL-21 is a type I cytokine essential for immune cell dif

10 IL-21 is in clinical use to promote tumor rejection and

11 IL-21 promotes B cell and CTL responses in vivo, conferr

12 IL-21 promotes transcription of all miR-29 species throu

13 IL-21 was also induced by IL-6 and promoted Th17 differe

14 IL-21 was produced at high levels by human CD4(+) centra

15 IL-21, a Tfh cell-derived cytokine, provides instruction

16 IL-21-deficient mice have smaller infarcts, improved neu

17 IL-21-induced IL-1beta processing in cDCs does not requi

18 IL-21-mediated cMyc upregulation is only observed in IL-

19 IL-21-stimulated T follicular helper cells are considere

20 IL-21/IL-21R interactions were also important for the ex

21 Histamine, IL-6, IL-17, IL-21 and IL-22 induced the expression of H4R in monocyt

22 onocytes were treated with histamine, IL-17, IL-21 and IL-22, and a H4R antagonist (JNJ7777120), the

23 iotic regimens significantly reduced IL-17A, IL-21, IL-22 and IFN-gamma mRNA levels in the terminal i

24 IL-17A, IL-21, IL-22, TNF-alpha and IL-6 are also produced in ex

25 Inflammatory cells and IL-17A(+), IL-17F(+), IL-21(+), IL-22(+), and IL-23(+) cells were examined by

26 (that is, interleukin-17A (IL-17A), IL-17F, IL-21 and IL-22), tumor necrosis factor-alpha (TNF-alpha

27 Because the Th17 cytokines IL-17F, IL-21 and TNF-alpha, and TGF-beta induce differentiation

28 rated that IFN-beta inhibits IL-17A, IL-17F, IL-21, IL-22, and IFN-gamma secretion in CD4(+) lymphocy

29 Individual neutralization of IL-17A, IL-17F, IL-21, IL-22, TNF-alpha or IL-6 does not change TIL-deri

30 IL-1beta, IL-21, and PTX3 concentrations were similar in the study

31 ed by high baseline serum interleukin IL-21 (IL-21), as measured using a now 'redundant' enzyme linke

32 o mutating B cells, secreted interleukin 21 (IL-21), induced expression of the transcription factor B

33 0-targeted therapy, we fused interleukin 21 (IL-21), which induces direct lymphoma cytotoxicity and a

34 tly and negatively regulated interleukin 21 (IL-21); Foxp1 also dampened expression of the costimulat

35 implicated in regulation of interleukin-21 (IL-21) and IL-17 secretion in mice and humans.

36 by eliminating production of interleukin-21 (IL-21) by donor T cells or IL-21 receptor (IL-21R) signa

37 Interleukin-21 (IL-21) can be produced by CD8 T cells from HIV-1-infecte

38 rol, it is not known whether interleukin-21 (IL-21) contributes to early HIV-1 immunity.

39 Interleukin-21 (IL-21) has been implicated in the development of Th2-med

40 une cell-mediated effects of interleukin-21 (IL-21) in mantle cell lymphoma (MCL), providing a precli

41 maintained by T-cell-derived interleukin-21 (IL-21), and promoted repeated rounds of divisions of sel

42 all subset of gp120-specific interleukin-21 (IL-21)-secreting CXCR5(+) CD4(+) T cells were significan

43 l a relationship among TLR engagement, IL-4, IL-21, and IFN-gamma that regulates T-bet expression in

44 expression of IL-17, TNF-alpha, IL-6, IL-4, IL-21, TGF-beta1 and IFN-gamma were significantly increa

45 thermore, IL-6-stimulated production of IL-4/IL-21 through c-Maf induction is responsible for impaire

46 TAT3 and STAT1 activation profiles for IL-6, IL-21, and IL-27, as well as for cytokine pairs over tim

47 ivated by several cytokines, including IL-6, IL-21, and IL-27, each of these cytokines has a very dif

48 e the salivary interleukin (IL)-1beta, IL-6, IL-21, IL-33, and pentraxin-3 (PTX3) concentrations in p

49 B-cell lymphoma 6, IL-21, inducible costimulator, CXCR5, and programmed cel

50 ent in the presence of interleukin-7 (IL-7), IL-21, and the glycogen synthase-3beta inhibitor TWS119,

51 Conversely, abrogating IL-21 receptor signaling in donor T cells and inhibiting

52 Additionally, IL-21, in combination with ART, was associated with redu

53 two potent differentiation-promoting agents, IL-21 and cytosine guanine dinucleotide-enriched oligo-d

54 cells, to the anti-CD20 antibody (alphaCD20-IL-21 fusokine).

55 Further, the alphaCD20-IL-21 fusokine stabilizes IL-21 and prolongs its half-li

56 the dual functional ability of the alphaCD20-IL-21 fusokine to induce direct apoptosis and activate i

57 In vivo alphaCD20-IL-21 therapy resulted in a significant tumor control in

58 Expression of IL-17, but also IL-21 and IL-22, was observed in all eczema subtypes.

59 Although IL-21 can activate several STAT family transcription fac

60 Although IL-21 was efficiently induced by IL-12 in naive CD4(+) T

61 Our work highlights the diversity among IL-21 producing CD4(+) Tfh cells, and the interrelations

62 e NKG2D gene, which is enhanced by IL-10 and IL-21 and decreased by STAT3 inhibition.

63 xpression and blunted responses to IL-10 and IL-21.

64 xpression of FOXP3, Bcl-6, PRDM1, IL-10, and IL-21.

65 licited acquired responsiveness to IL-12 and IL-21 for IL-10 production.

66 ally stimulated in the presence of IL-12 and IL-21 to generate TFH cells.

67 ure of CD8 T cells to IL-2, IL-7, IL-15, and IL-21 increased granzyme B production.

68 ptors for IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21.

69 AT3 phosphorylation and binding to IL-17 and IL-21 promoters and reduced IFN regulatory factor 4 and

70 release of IL-5, IFNgamma, IL-10, IL-17 and IL-21.

71 r cytokines, including IFN-gamma, IL-17, and IL-21.

72 nd higher numbers (P < .01) of IL-17F(+) and IL-21(+) cells in nasal biopsies were observed in SAs co

73 5) of neutrophils, IL-17A(+), IL-17F(+), and IL-21(+) cells in bronchial biopsies and higher numbers

74 , soluble CD40L in combination with IL-2 and IL-21 induces these activities in both memory and naive

75 at soluble BAFF in combination with IL-2 and IL-21 is a T cell contact-independent inducer of human B

76 gene, but also opposing actions of IL-2 and IL-21 on BCL6 expression, with increased BCL6 expression

77 ciprocal influence of interleukin (IL)-2 and IL-21.

78 and extending these findings, TNF, IL-2, and IL-21 also synergistically triggered the proliferation o

79 Furthermore, we identify TNF, IL-2, and IL-21 as CD4(+) T-cell cytokines that synergistically me

80 ion that the soluble factors BAFF, IL-2, and IL-21 induce memory and DN B cell activation and differe

81 the important collaboration between IL-4 and IL-21 in shaping T-dependent Ab responses.

82 urther show that the combination of IL-4 and IL-21 skews naive CD8(+) T cells to produce IL-21, which

83 n Ag that induced type 1 immunity), IL-4 and IL-21 were coproduced by individual Tfh cells, revealing

84 These cells produced IL-4 and IL-21, and they more robustly promoted peanut-specific I

85 NKT cell-derived interferon-gamma, IL-4, and IL-21 cytokines and perforin and granzyme B cytotoxins,

86 ed interferon-gamma, interleukin (IL)-4, and IL-21 cytokines; and NKT cell-derived perforin and granz

87 cells when stimulated with CD40L, IL-4, and IL-21 was also determined.

88 Moreover, rfhSP-D inhibited CD40L/IL-4- and IL-21-mediated IgE production (77.12%; P = 0.02) by B ce

89 hibited the production of autocrine IL-6 and IL-21 in 2D2 T cells, which in turn reduced their Th17 d

90 IL-6 and IL-21 induced p-STAT3/p-STAT1 ratios > 1, leading to the

91 on was decreased in the presence of IL-6 and IL-21, and to a lesser extent by IL-4 and TNF-alpha.

92 Tfh cells following interleukin-6 (IL-6) and IL-21 stimulation, and viral DNA is detectable in fully

93 ar brake that blocks the autocrine IL-6- and IL-21-induced Th17 differentiation pathways in autoreact

94 analysis revealed enhancements in IL-6- and IL-21-induced Th17 differentiation pathways in these T c

95 ven ART, SIV-infected RMs given both ART and IL-21 showed improved restoration of intestinal Th17 and

96 between clinical attachment level (CAL) and IL-21 (P = 0.02).

97 monstrated increased production of CD40L and IL-21 in vitro.

98 Tfh cells and IL-21 are involved in infectious and autoimmune diseases

99 e role of follicular and blood Tfh cells and IL-21 in human and experimental allergic disease.

100 ated both the number of IL-21(+) T cells and IL-21 production, suggesting a feedback loop in tolerant

101 gnate interaction between Tfh , B cells, and IL-21 drives B cells to proliferate and differentiate in

102 e in Tfr cells, inhibits CD25 expression and IL-21-mediated inhibition of CD25 is Bcl-6 dependent.

103 TH1 and TFH effector cytokines IFN-gamma and IL-21 and the TFH marker CXCR5, demonstrating that the c

104 sion of T-bet and Bcl6 and for IFN-gamma and IL-21.

105 ntributes to the development of IL17A(+) and IL-21(+) populations.

106 tokines, a proliferation-inducing ligand and IL-21, and attenuated LPS-induced iBALT formation.

107 eduction in circulating Tfh cell numbers and IL-21 production, which was correlated with reduced plas

108 r elements bound by IL-2-activated STAT5 and IL-21-activated STAT3 in T cells and identified Il2ra as

109 Anti-IL-21 treatment also led to a reduction in GC B cells, C

110 of lupus-prone B6.Sle1.Yaa mice with an anti-IL-21 blocking Ab reduced titers of autoantibodies, dela

111 her, these findings reveal a novel antiviral IL-21-miR-29 axis that promotes CD4 T-cell-intrinsic res

112 es, cytokines produced by Tfh cells, such as IL-21 and IL-4, provide B cell helper signals.

113 Currently available IL-21 ELISA kits should not be used to counsel individua

114 STAT3, activated by IL-21, controls the epigenetic status of the il22 promot

115 , and this can be synergistically boosted by IL-21.

116 regions within the MIR29 gene is enriched by IL-21 signalling.

117 9 (miR-29) as an antiviral factor induced by IL-21 in CD4 T cells.

118 and IgHJ usage, clustering apart from CD40L/IL-21 and control conditions.

119 o bind HEp-2 cells, whereas those from CD40L/IL-21-stimulated cells did not.

120 TLR activators, but not CD40L/IL-21, similarly promoted increased sharing of CDR3 sequ

121 , and favored secretion of IgM, unlike CD40L/IL-21, which drove IgM and IgG more evenly.

122 proliferation similarly differed, with CD40L/IL-21 inducing proliferation of most memory and naive B

123 uired alongside STAT4 to coordinate Tfh cell IL-21 and IFN-gamma production and for promotion of the

124 Moreover, in Th17 memory cells, IL-21 selectively inhibited T-bet upregulation and GM-CS

125 r to CD4(+) T follicular helper (Tfh) cells, IL-21-producing CD8(+) T cells generated in the presence

126 chultz et al. (2016) report that circulating IL-21-producing CD4(+) T cells are phenotypically, trans

127 ssive accumulation of Tfh cells coexpressing IL-21 and IFN-gamma, and suppressed their production of

128 Induction of a T-cell subset coexpressing IL-21 and IFN-gamma might combine IL-21-mediated T-cell

129 expressing IL-21 and IFN-gamma might combine IL-21-mediated T-cell aid for antibody production while

130 under homeostatic or lymphopenic conditions IL-21 acts directly on CD8 T cells to favor the accumula

131 B cell and CTL responses in vivo, conferring IL-21 with a role in both humoral and cellular responses

132 In contrast, IL-21 induced BCL6 and diminished IL-9 expression in wil

133 The cytokine IL-21 has been shown to influence immune responses throu

134 The cytokine IL-21 was able to overcome TFR cell-mediated suppression

135 transcription factor Bcl6, and the cytokine IL-21, and that these cells localize to germinal centers

136 gp140 fused to the species-matched cytokines IL-21 or GM-CSF in rabbits and mice.

137 Mice treated with decoy IL-21 receptor Fc fusion protein are protected from repe

138 CD8(+) T cell-derived IL-21 contributes to the production of protective virus-

139 antibodies, indicating that Tfh cell-derived IL-21 is critical for pathological B cell cues in lupus.

140 te infection, is associated with an elevated IL-21(+) CD4 T subset, and these cells bear a phenotypic

141 We postulated that a bolus of enhanced IL-21-primed polyclonal antigen-specific CTL combined wi

142 atients display CD4(+) T cells with enhanced IL-21 expression and high in vivo frequencies of regulat

143 omponents of the chimeric Env-GM-CSF and Env-IL-21 molecules were functional in vitro, but none of th

144 Notably, exogenous IL-21 limits early HIV-1 infection in humanized mice, an

145 GC response evolved, TFH cells extinguished IL-21 production and switched to IL-4 production, showed

146 Finally, IL-21, but not IFN-gamma, promotes CD11c expression inde

147 Finally, IL-21-mediated induction of STAT1 phosphorylation, as we

148 acts the magnitude of the response following IL-21 costimulation.

149 d that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation.

150 ese results demonstrate a novel function for IL-21 in tuning NK and CD4(+) T cell interactions promot

151 Blocking mAbs for IL-21/IL-21R, inducible T-cell costimulator (ICOS)/ICOS

152 (MCL), providing a preclinical rationale for IL-21 therapy in this aggressive disease.

153 The requirement for IL-21 to establish CD8 TE/TEM and TRM subsets was overco

154 In this study, we identify a novel role for IL-21 as an inducer of the costimulatory ligand CD86 on

155 identify a previously unappreciated role for IL-21 in EAE and reveal that IL-21-mediated signaling su

156 e to HIV-1 infection, and suggest a role for IL-21 in initial HIV-1 control in vivo.

157 s study reveals a context-dependent role for IL-21 in sustaining effector phenotype CD8 T cells and i

158 this report demonstrates a critical role for IL-21 in the generation of a primary effector CD8 T cell

159 and follicular Th cell paradigms to generate IL-21 and IL-17A, which drive pathogenic germinal center

160 e identified a subpopulation of GFP(+), high IL-21 producing Tfh cells present only in Peyer's Patche

161 Human IL-21 and IL-21R deficiencies cause severe, primary immu

162 like CD4 T cell-driven B cell hyperactivity, IL-21 signaling on Ag-specific donor CD8 T cells is crit

163 Thus, we have identified IL-21 as an inducer of IL-22 production in CD4+ T cells

164 Together, we identify IL-21(+)CD4(+) T cells as pTfh cells, implicating them a

165 healthy donor B cells with CD40L, anti-IgM, IL-21, CpG, IFN-alpha, IL-6 or BAFF induces miR-155 and

166 More importantly, IL-21-propagated HLA-DR(+) NK cells produce macrophage m

167 athways and increased neuronal cell death in IL-21 receptor-deficient (IL-21R-deficient) mice compare

168 ly lower than those before ART initiation in IL-21-treated animals but not in controls.

169 diated cMyc upregulation is only observed in IL-21-sensitive cells.

170 T3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells.

171 udies focused mainly on the role of STAT3 in IL-21 signaling.

172 ation and production of cytokines, including IL-21, and inhibited class switch recombination and B ce

173 act-dependent and soluble factors, including IL-21, IL-4, IL-9, and IFN-gamma.

174 ress factors enabling B-cell help, including IL-21, CXCL13, ICOS, and MAF.

175 rail-deficient CD8(+) T cells have increased IL-21 receptor (IL-21R) expression and hyperresponsivene

176 naive and CMV-infected mice shows increased IL-21 mRNA in infected mice, whereas in vitro NK assays

177 t, during per-oral microsporidial infection, IL-21 was critical for the generation of an optimal effe

178 Instead, IL-21 production by CD8 T cells was associated with high

179 predicted by high baseline serum interleukin IL-21 (IL-21), as measured using a now 'redundant' enzym

180 haracterized by Bcl-6 expression but lacking IL-21 secretion.

181 study in detail the kinetics of CD40 ligand/IL-21-induced B-cell differentiation to define new bioma

182 Here the authors show Grail also limits IL-21 receptor expression and function in CD8(+) T cells

183 exhibited an involution of GCs without local IL-21 production in GCs.

184 ar helper cells had lower expression of Maf, IL-21, and ICOS, and this was accompanied by a reduction

185 In mice, IL-21:IL-21R interactions influence the phenotype of T f

186 Breg cells modulated IL-21 receptor expressions on TFH cells and B cells, and

187 Moreover, IL-21 and AhR signalling in T cells control IL-22 produc

188 In vitro assays demonstrated that mutant IL-21(Leu49Pro) did not induce signal transducer and act

189 mors that otherwise were resistant to native IL-21 treatment.

190 gnaling by the fusokine compared with native IL-21 at equimolar concentrations.

191 Because neither IL-12 nor IL-21 was required in vivo, however, additional pathways

192 or Tfh cell production of IFN-gamma, but not IL-21, and for a robust GC reaction.

193 In a context of diet-induced obesity, IL-21 KO mice, compared with WT animals, exhibited lower

194 findings demonstrate that in the absence of IL-21/IL-21R signaling, Il2(-/-) mice retained a deficie

195 linical potential, the biological actions of IL-21 are not yet fully understood and the full range of

196 lecular mediators that impact the actions of IL-21.

197 Finally, although blockade of IL-21 did not affect GCB cells in Sfpi1(lck-/-) mice, an

198 We used blockade of IL-21 to dissect the mechanisms by which this cytokine p

199 The combination of IL-21 and IFN-gamma baseline expression closely predicte

200 mechanistic insight into the contribution of IL-21 to the pathogenesis of murine lupus, while reveali

201 ating that CD40L determines the direction of IL-21-dependent B cell differentiation.

202 for GC B cell maturation, with disruption of IL-21 signaling representing a potential therapeutic str

203 The negative effect of IL-21 on Tfr cells in mice is cell intrinsic and associa

204 To distinguish the effect of IL-21 on the immune system from that of its effect on Tr

205 ments were performed to assess the effect of IL-21 on the immune system.

206 Here, we investigated the effects of IL-21 administration on both inflammation and virus pers

207 Intriguingly, the effects of IL-21 on T cells can be complex and vary depending on th

208 This correlated with increased expression of IL-21 and CD40L in Tfh cells from Sfpi1(lck-/-) mice com

209 nd IL-12 controlled respective expression of IL-21 and IFN-gamma, with IL-21 being key for humoral im

210 athophysiology and the potential interest of IL-21 and CD40 as therapeutic targets in ITP.

211 omyelitis (EAE); however, the involvement of IL-21 in these processes has remained controversial.

212 cterized by the production of high levels of IL-21 and low levels of IFN-gamma.

213 17 cytokines but did reveal higher levels of IL-21, the main cytokine secreted by CD4 T follicular he

214 r differentiation of Th17 cells, the loss of IL-21 or IL-21 receptor (IL-21R) does not protect mice f

215 ents positively regulated both the number of IL-21(+) T cells and IL-21 production, suggesting a feed

216 The peak of IL-21 expression, observed during the acute infection, i

217 s were Th9-differentiated in the presence of IL-21.

218 The production of IL-21 by T follicular helper (Tfh) cells is vital in dri

219 B cell-T cell interaction and production of IL-21.

220 ntiYIL-6R treatment resulted in reduction of IL-21+CD4+ (Th17) cells (P = 0.006 vs. control) and CXCR

221 e, we identify IL-6 as a master regulator of IL-21 in effector CD8(+) T cells.

222 In view of the critical role of IL-21 in controlling immune homeostasis, early hematopoi

223 The role of IL-21 in the generation of CD8 effectors was cell intrin

224 its effect on Tregs, we analyzed the role of IL-21/IL-21R signaling in mice made genetically deficien

225 ew our current understanding of the roles of IL-21 in the generation of phenotypically distinct CD4 a

226 strating the KD025 inhibits the secretion of IL-21, IL-17, and interferon gamma along with decreasing

227 ized by expression of Bcl-6 and secretion of IL-21.

228 Treg cells was seen in the adipose tissue of IL-21 knockout (KO) mice compared with WT animals fed bo

229 Aberrant upregulation of IL-21 in CD4(+) T cells expressing mutant Ikaros was res

230 s-specific CD8 T cells remained dependent on IL-21 for optimal accumulation in lymphopenic environmen

231 ally, GzmB(+) B-cell number was dependent on IL-21 production, and B cells from tolerant recipients b

232 equire caspase-1 or caspase-8 but depends on IL-21-mediated death and activation of serine protease(s

233 ntiation of Th17 cells, the loss of IL-21 or IL-21 receptor (IL-21R) does not protect mice from activ

234 f interleukin-21 (IL-21) by donor T cells or IL-21 receptor (IL-21R) signaling of donor B cells.

235 ells deficient in IL-4, interferon-gamma, or IL-21 augmented atherosclerosis in ApoE(-/-)Jalpha18(-/-

236 The inability to perceive IL-21 signals under competitive conditions also resulted

237 pha, and compared with activators CD40L plus IL-21, to identify differentially responsive cell popula

238 iltrating CD4(+) T cells are the predominant IL-21 source.

239 IL-21 skews naive CD8(+) T cells to produce IL-21, which, in turn, acts in an autocrine manner to su

240 creased C. albicans colonization and reduced IL-21 expression.

241 bit elevated BAFF and DN B cells and reduced IL-21.

242 tion of these Tc2 cells in the lung requires IL-21, and bleomycin treated IL-21- and IL-21R-deficient

243 These results demonstrate lineage-restricted IL-21-induced IL-1beta via a non-canonical pathway and p

244 Although Th cells from HIV patients secrete IL-21 in a Nef-dependent manner, they barely express CD4

245 -regulates the ability of T cells to secrete IL-21 and IL-17 by 90% and 60%, respectively, but not IF

246 current kit, confirmed higher baseline serum IL-21 in patients with autoimmunity (542 pg/mL vs. 222 p

247 the frequency of total and SIV Env-specific IL-21(+) TFH cells and total germinal center B cells, th

248 n this study, we quantified SIV Env-specific IL-21-producing TFH cells for the first time, to our kno

249 We assessed circulating HIV-specific IL-21(+)CD4(+) T cells and showed transcriptional and ph

250 her, the alphaCD20-IL-21 fusokine stabilizes IL-21 and prolongs its half-life.

251 When culturing such IL-21(+)CD40L(-) Th cells with B cells, the former direc

252 In summary, IL-21 is a central memory T cell-associated cytokine tha

253 These findings demonstrate that IL-21 is a major target of immune system regulation.

254 Further, we demonstrate that IL-21 leads to natural killer (NK)-cell-dependent lysis

255 Accumulating studies demonstrate that IL-21 modulates the differentiation of various CD4 and C

256 Herein, we demonstrate that IL-21 possesses potent cytotoxicity against MCL cell lin

257 Here we demonstrate that IL-21-producing CD8 T cells are not associated with CD4

258 ed to as 2D2xTH mice), and demonstrated that IL-21 is critical for the development of a variant form

259 Previously, we established that IL-21 exerts direct cytotoxicity on IL-21R-expressing di

260 In this study, we provide evidence that IL-21, a cytokine produced during chronic inflammation o

261 We find that IL-21 or IFN-gamma directly promote T-bet expression in

262 We identify that IL-21-induced direct cytotoxicity is mediated through si

263 Together, these data indicate that IL-21 has potent antitumor activity against MCL cells vi

264 We propose that IL-21 acts in a context-dependent manner to accentuate T

265 ansient focal brain ischemia, we report that IL-21 is highly up-regulated in the injured mouse brain

266 ciated role for IL-21 in EAE and reveal that IL-21-mediated signaling supports generation and stabili

267 mphoid organ aggregate cultures to show that IL-21 directly suppresses HIV-1 replication, and identif

268 Here we show that IL-21 triggers IL-22, but not IL-17 production by CD4+ T

269 Here we show that IL-21 unexpectedly induces IL-1beta production in conven

270 Moreover, our results suggest that IL-21 may contribute to AHR through its ability to both

271 These results suggest that IL-21 plays an important role in the allergic diathesis

272 Together, these data suggest that IL-21 supplementation of ART reduces residual inflammati

273 unding acute stroke lesions, suggesting that IL-21-mediated brain injury may be relevant to human str

274 The gene encoding the IL-21 receptor (Il21r) showed a marked difference in str

275 sion in cDCs at least partially explains the IL-21-mediated pathologic response occurring during infe

276 inst a variety of cancers not expressing the IL-21 receptor (IL-21R) through immune activation.

277 ients with loss-of-function mutations in the IL-21 receptor (IL-21R).

278 ic, as stronger defects were observed in the IL-21-deficient compartment from the bone marrow chimeri

279 th follicular and blood Tfh cells and of the IL-21/IL-21R system in the context of allergic disorders

280 These IL-21-expanded NK cells also have increased NKG2D expres

281 plasma cell differentiation in vitro through IL-21 secretion and SLAMF5 interaction.

282 In postmortem human brain tissue, IL-21 localized to perivascular CD4(+) T cells in the ar

283 L-21R) expression and hyperresponsiveness to IL-21 signalling as Grail promotes IL-21R ubiquitination

284 e lung requires IL-21, and bleomycin treated IL-21- and IL-21R-deficient mice develop inflammation bu

285 rplay between STAT1 and STAT3 in fine-tuning IL-21 actions.

286 Our study uncovers IL-21 deficiency as a novel cause of early-onset IBD in

287 we demonstrate that CD4 help is provided via IL-21 production, a common gamma-chain cytokine closely

288 In vitro, IL-21 stimulation combined with an anti-CD40 agonist ant

289 gulation as an additional mechanism by which IL-21 can elicit immunomodulatory effects.

290 These findings identify a mechanism by which IL-21 reinforces humoral immunity by restricting Tfr cel

291 those reported for viral infections in which IL-21 has been primarily associated with the generation

292 While IL-21 is an essential autocrine amplification factor for

293 induced by CpG or CD40L in combination with IL-21, but not BCR stimulation, suggesting the importanc

294 ent cell-mediated cytotoxicity compared with IL-21 and/or anti-CD20 antibody treatments.

295 y secretion, whereas CD40 costimulation with IL-21 or IFN-gamma promotes a T-bet+ B cell phenotype.

296 express granzyme B (GrB) when cultured with IL-21, a cytokine overproduced in CD and UC mucosa.

297 tive expression of IL-21 and IFN-gamma, with IL-21 being key for humoral immunity.

298 y immunodeficiency, as illustrated here with IL-21 deficiency.

299 atment of DBA/2J-->F1 chronic GVHD mice with IL-21 strongly promoted donor CD8 T cell expansion and r

300 In vivo treatment with IL-21 results in complete FC-muMCL1 tumor regression in