ライフサイエンスコーパス: lymphotoxin

1 lear factor-kappaB (RANK) ligand (RANKL) and lymphotoxin.

2 een the sets of genes controlled by Aire and lymphotoxin.

3 tromal cells and dendritic cells, partly via lymphotoxin.

4 d increase in CXCL13 was partly mediated via lymphotoxin.

5 zone (MZ) and requires B cells that express lymphotoxin.

6 derived from lymphocytes (20 kDa), was named lymphotoxin.

7 pendent on the chemokine CXCL13, B cells and lymphotoxin.

8 technique and with tumor necrosis factor-308/lymphotoxin + 250 GG haplotype for prolonged mechanical

9 o 200 ng/ml) and tumor necrosis factor alpha/lymphotoxin (8 to 134 pg/ml).

10 on enhanced mRNA transcripts of flt3 ligand, lymphotoxin A, TNF, and IL-14.

11 Neutralizing Abs against lymphotoxin A, TNF-alpha, and/or flt3 ligand abolished t

12 We report that mice deficient in lymphotoxin, a key molecule in gut immunity, were resist

13 e polymorphism (SNP) haplotype involving the lymphotoxin alpha (LTA) and tumor necrosis factor (TNF)

14 se hypersensitive sites corresponding to the lymphotoxin alpha (LTA) and tumour necrosis factor (TNF)

15 modified by a functional polymorphism in the lymphotoxin alpha (LTA) gene (LTA C+80A, where the CC ge

16 We now demonstrate a critical role for lymphotoxin alpha (LTA) in the pathogenesis of Sjogren's

17 in B cells (lkappaBL), inhibitor-like 1 and lymphotoxin alpha (LTA), in relation to nutritional iron

18 Lymphotoxin alpha (LTalpha) can exist in soluble form an

19 We show that targeted mutation of the lymphotoxin alpha (LTalpha) gene efficiently rescued tum

20 sized the role of type 1 IFN (IFN-alpha) and lymphotoxin alpha (LTalpha) in the pathogenesis of the d

21 tic deletion of lymphotoxin beta receptor or lymphotoxin alpha abrogated development of lymphatic ves

22 ceptor expressed by T lymphocytes (LIGHT) or lymphotoxin alpha and BTLA.

23 model decreased the muscle protein levels of lymphotoxin alpha and Il17a by 32% and 42%, respectively

24 Anti-lymphotoxin alpha has fast nonspecific clearance in cyno

25 ng wild-type control mice and splenectomized lymphotoxin alpha knockout (LT) mice deficient in SLOs a

26 activation on macrophages by T cell-derived lymphotoxin alpha(1)beta(2) controls proinflammatory res

27 ts and effector molecules (interferon gamma, lymphotoxin alpha, and myxovirus resistance 1) were redu

28 onses, the conventional TNF ligand LIGHT and lymphotoxin alpha, as well as herpes simplex virus glyco

29 king either lymphotoxin beta receptor or the lymphotoxin alpha-chain, and there was minimal overlap b

30 s in infection by and immunity to rotavirus, lymphotoxin alpha-deficient (LTalpha(-/-)) mice that lac

31 ne the role of lymph node in CNV, we lasered lymphotoxin alpha-deficient mice (LTalpha-/-) and measur

32 es of transitional B cells in splenectomized lymphotoxin alpha-deficient mice that lack all secondary

33 of two test antibodies, humAb4D5-8 and anti-lymphotoxin alpha.

34 ember, BALM, unique to fish; 3) orthologs of lymphotoxins alpha and beta were not clearly identified

35 ontribute to splenic organization, including lymphotoxins alpha and beta.

36 We identify surface lymphotoxin-alpha (LT-alpha) as common to T(H)0, T(H)1 a

37 olymorphisms in the TNF -308G>A (rs1800629), lymphotoxin-alpha (LTA) 252A>G (rs909253), IL10 -3575T>A

38 The TNF-alpha (TNF) and lymphotoxin-alpha (LTA) genes belong to the TNF gene sup

39 The proinflammatory cytokine lymphotoxin-alpha (LTA) is thought to contribute to the

40 n separated by sex, a variant in intron 1 of lymphotoxin-alpha (LTA), a gene adjacent to TNF, was ass

41 ndertaken, and the pro-inflammatory cytokine lymphotoxin-alpha (LTA), and its key ligand galectin-2 (

42 association between genetic variants in the lymphotoxin-alpha (LTalpha) gene and leprosy.

43 udy, we show in vitro that HRS cells secrete lymphotoxin-alpha (LTalpha) which acts on endothelial ce

44 Lymphotoxin-alpha (LTalpha), lymphotoxin-beta (LTbeta),

45 enes, including interferon-gamma (IFNgamma), lymphotoxin-alpha (LTalpha), tumor necrosis factor-alpha

46 phoid organs, NALT develops independently of lymphotoxin-alpha (LTalpha).

47 t al report that Reed-Sternberg cell-derived lymphotoxin-alpha activates endothelial cells to enhance

48 nct from regions where the ligands LIGHT and lymphotoxin-alpha bound HVEM.

49 recruitment was independent of L-selectin or lymphotoxin-alpha but required CCR7 expression.

50 The tumor necrosis factor gene (TNF) and lymphotoxin-alpha gene (LTA) have long attracted attenti

51 TNF-beta that is encoded by lymphotoxin-alpha gene (LTA) regulates adhesion molecule

52 induced by CD4(+) thymocytes via CD80/86 and lymphotoxin-alpha signals.

53 rdiaI infarction with the LTA gene (encoding lymphotoxin-alpha), and a follow-up study found that an

54 files with differential production of CD40L, lymphotoxin-alpha, and interferon-gamma.

55 e canonical TNF-related cytokines, LIGHT and Lymphotoxin-alpha, and the Ig-related membrane proteins,

56 uired for development of the MZ, i.e., muMT, lymphotoxin-alpha, and TNFR1.

57 c variation at the human LTA locus, encoding lymphotoxin-alpha, is associated with susceptibility to

58 receptors that share the HVEM ligands LIGHT, Lymphotoxin-alpha, or BTLA.

59 ocument a novel link between IL-12Rbeta2 and lymphotoxin-alpha, TNF-alpha, and IFN-gamma expression,

60 vated T cells and impaired overexpression of lymphotoxin-alpha, TNF-alpha, and IFN-gamma in the brain

61 Neutralization of IL-17 in CCR7(-/-) or in lymphotoxin-alpha-deficient animals specifically inhibit

62 Lymphotoxin-alpha-deficient mice infected with RSV were

63 CD8(+) RTEs efficiently populated the gut of lymphotoxin-alpha-deficient mice, which lack lymphoid or

64 egins, ftILCPs accumulate at PP anlagen in a lymphotoxin-alpha-dependent manner.

65 IL-17 acted by promoting lymphotoxin-alpha-independent expression of the chemokin

66 affinity of poxvirus TNFRs for TNFalpha over lymphotoxin-alpha.

67 s the lymphorganogenic cytokines/chemokines, lymphotoxin-alpha/-beta, CCL19, CCL20, CCL21, and CXCL13

68 selectively binds and inhibits TNF/TNFR1 and lymphotoxin-alpha/TNFR1 signaling with good affinity and

69 f SLO microarchitecture; their expression of lymphotoxin alpha1beta2 (LTalpha1beta2) is required for

70 by MZ B cells through expression of membrane lymphotoxin-alpha1beta2 (mLT).

71 show SCS macrophage development depended on lymphotoxin-alpha1beta2, and the cells had low lysosomal

72 tic anti-LTbR antibody or the natural ligand lymphotoxin-alpha1beta2, increased Ccl5 mRNA expression.

73 port that IL-17 signals synergistically with lymphotoxin-alpha3, using the same signaling motifs with

74 Within the CNS, interactions between lymphotoxin alphabeta (LTalphabeta) on Th17 cells and LT

75 cells to the TNF family molecules LIGHT and lymphotoxin alphabeta (LTalphabeta).

76 display IL-7-dependent induction of surface lymphotoxin-alphabeta, demonstrating their potential to

77 th COPD were important sources of CXCL13 and lymphotoxin and also expressed their receptors.

78 tionally significant: mice deficient in both lymphotoxin and CD30 (dKO) signals had significantly sma

79 Expression of lymphotoxin and homeostatic chemokine receptors was inve

80 Using mice deficient in lymphotoxin and Hox11, we report that approximately 25%

81 Cluster formation was dependent on lymphotoxin and the lymphotoxin beta receptor and indepe

82 uantitative RT-PCR, and smaller increases in lymphotoxins and TNF receptors that preceded vessel remo

83 lays a vital role downstream of BAFF, CD40L, lymphotoxin, and other inflammatory mediators.

84 by providing tumor-necrosis factor (TNF) and lymphotoxin, and they stimulated MZ B cells via B cell-a

85 Lymphotoxins are part of a cytokine network well known i

86 Cytokines, including TNF, IFN-gamma, and lymphotoxin, are thought to contribute to its pathogenes

87 fects characteristic of TNF ablation but not lymphotoxin-associated defects characterized by lack of

88 are expressed independently of TNFalpha and lymphotoxin at sites of iBALT formation.

89 The lymphotoxin axis is important for the maintenance of sev

90 ates liver regeneration via a T cell-derived lymphotoxin axis, and pharmacological stimulation of lym

91 munoreactive for TNF receptor 1 (TNF-R1) and lymphotoxin B receptors.

92 promoter regions, a CpG island in exon 4 of lymphotoxin beta (LTB), the 3' end of nuclear factor of

93 phage colony-stimulating factor (GM-CSF) but lymphotoxin beta (LTbeta) does not.

94 Lymphotoxin beta (LTbeta) expression in DCs maintained A

95 Endothelial cell (EC)-specific lymphotoxin beta (LTbeta) receptor signaling is critical

96 Lymphotoxin beta (LTbeta), a cytokine produced by T cell

97 anistically, we show that CD8(+) T cells and lymphotoxin beta are central mediators of HCC formation.

98 DCs were the main producers of lymphotoxin beta in freshly resected HEV(high) breast tu

99 eatment with interferon-gamma, which induced lymphotoxin beta receptor (LT beta R) expression, was re

100 implex virus entry mediator (HVEM) and LIGHT/lymphotoxin beta receptor (LT beta R) interactions decre

101 is study demonstrates enhanced expression of lymphotoxin beta receptor (Lt betaR) during the demyelin

102 We found that a soluble decoy lymphotoxin beta receptor (LT-betaR)-Fc, which can block

103 Our previous studies indicated that lymphotoxin beta receptor (LTbetaR) activation controls

104 ediated by at least two receptors, including lymphotoxin beta receptor (LTbetaR) and herpes simplex v

105 Lymphotoxin beta receptor (LTbetaR) blockade reduces hom

106 eady-state and after bone marrow transplant, lymphotoxin beta receptor (LTbetaR) controls entry of T

107 Lymphotoxin beta receptor (LTbetaR) deficiency is associ

108 onditional gene-deficient mice, we find that lymphotoxin beta receptor (LTbetaR) directly controls th

109 DC-derived lymphotoxin beta receptor (LTbetaR) ligands were critica

110 Lymphotoxin beta receptor (LTbetaR) ligation-induced Air

111 (LT)alpha(1)beta(2) on inducer cells and the lymphotoxin beta receptor (LTbetaR) on stromal cells ini

112 fusion protein between the IgG Fc domain and lymphotoxin beta receptor (LTbetaR) reduces lung fibrosi

113 inflammation mediated by LIGHT, a ligand for lymphotoxin beta receptor (LTbetaR), not only stimulates

114 fic deletion of the thymus medulla regulator lymphotoxin beta receptor (LTbetaR), we show that thymic

115 a substantial reduction in the expression of lymphotoxin beta receptor (LTbetaR)-controlled migration

116 Lymphotoxin beta receptor (LTbetaR)-driven induction of

117 Administration of lymphotoxin beta receptor (LTbetaR)-Ig to wild-type mice

118 these genes in response to engagement of the lymphotoxin beta receptor (LTbetaR).

119 nt region of IgG and extracellular domain of lymphotoxin beta receptor (LTbetaRIg) interrupted clonal

120 Components of lymphotoxin beta receptor (LTBR)-associated signaling co

121 Induction of PNAd in mutant PPs requires lymphotoxin beta receptor activity, and its upregulation

122 f lymphotoxin was confirmed, as the use of a lymphotoxin beta receptor agonist results in partial res

123 both of its identified signaling receptors, lymphotoxin beta receptor and herpes virus entry mediato

124 rmation was dependent on lymphotoxin and the lymphotoxin beta receptor and independent of lymphocytes

125 LIGHT protected mice from colitis via the lymphotoxin beta receptor and was expressed mainly by my

126 ion of LT and LIGHT signaling with a soluble lymphotoxin beta receptor decoy protein attenuated the d

127 LIGHT signals through the lymphotoxin beta receptor in the colon to regulate the i

128 xin axis, and pharmacological stimulation of lymphotoxin beta receptor might represent a novel therap

129 Genetic deletion of lymphotoxin beta receptor or lymphotoxin alpha abrogated

130 lary epithelial cells of mice lacking either lymphotoxin beta receptor or the lymphotoxin alpha-chain

131 mphangiogenesis in the thyroid and implicate lymphotoxin beta receptor signaling in this process.

132 Notch-dependent Esam(hi) DC subset required lymphotoxin beta receptor signaling, proliferated in sit

133 found that an agonistic antibody against the lymphotoxin beta receptor was able to facilitate liver r

134 tinal inflammation when transferred into the lymphotoxin beta receptor-deficient mice, and herpes vir

135 ands, including those that bind CD30 and the lymphotoxin beta receptor.

136 that CD30 signals predated those through the lymphotoxin beta receptor.

137 IGHT receptors herpesvirus entry mediator or lymphotoxin beta receptor.

138 Meanwhile, vascular smooth muscle cell lymphotoxin beta receptors (VSMC-LTbetaRs) protected aga

139 estingly, both the tumor necrosis factor and lymphotoxin beta receptors were down-regulated by NS5A.

140 We found that lymphotoxin beta was overexpressed in tumors containing

141 is factor superfamily member LIGHT activates lymphotoxin beta-receptor signaling, leading to the prod

142 activated, LTalphabeta(+), lymphocytes with lymphotoxin beta-receptor-expressing fibrosarcoma tumor

143 Coexpression of a soluble lymphotoxin beta-receptor:Ig fusion protein, an inhibito

144 the hTNFR2 blocks the biological activity of lymphotoxin beta.

145 t CrmB and CrmD also inhibit the activity of lymphotoxin beta.

146 Lymphotoxin-beta (LTbeta) is a key regulator of immune s

147 A lymphotoxin-beta (LTbeta) receptor-Ig fusion protein (LT

148 Lymphotoxin-alpha (LTalpha), lymphotoxin-beta (LTbeta), and tumor necrosis factor-alp

149 variant NF-kappaB-signaling cascade based on lymphotoxin-beta (LTbeta)/RelB.

150 find that grb2(-/-) B cells are defective in lymphotoxin-beta expression.

151 s and that this loss was caused by decreased lymphotoxin-beta mainly produced by the CD4 T cells.

152 osis factor-alpha (TNF-alpha), whereas decoy lymphotoxin-beta receptor (LT-betaR) fusion protein had

153 ult mice was reduced by systemic blockade of lymphotoxin-beta receptor (LTbeta R) signaling with a so

154 re NIK for activation of NF-kappaB, only the lymphotoxin-beta receptor (LTbeta-R) is expressed in mel

155 The lymphotoxin-beta receptor (LTbetaR) activates the NF-kap

156 K) and TNF receptor family members including lymphotoxin-beta receptor (LTbetaR) and CD40.

157 ammatory mechanism, including membrane-bound lymphotoxin-beta receptor (LTbetaR) and CXC chemokine re

158 LIGHT engages the lymphotoxin-beta receptor (LTbetaR) and HVEM (TNFRSF14),

159 this effect through the interaction with the lymphotoxin-beta receptor (LTbetaR) but not herpes virus

160 Ligation of the lymphotoxin-beta receptor (LTbetaR) by LIGHT (lymphotoxi

161 Moreover, we show that signals through the lymphotoxin-beta receptor (LTbetaR) in DC are also requi

162 R4-activated canonical NF-kappaB pathway and lymphotoxin-beta receptor (LTbetaR) induced non-canonica

163 romal cell microenvironments is dependent on lymphotoxin-beta receptor (LTbetaR) signaling.

164 equires innate lymphoid cells, which promote lymphotoxin-beta receptor (LTbetaR)-dependent maintenanc

165 ors, herpes virus entry mediator (HVEM), and lymphotoxin-beta receptor (LTbetaR).

166 high), is dependent on signaling through the lymphotoxin-beta receptor (LTbetaR).

167 SF-14) is a ligand of stromal cell-expressed lymphotoxin-beta receptor and T cell-expressed herpes vi

168 of six single chain-Fv fragments of the anti-lymphotoxin-beta receptor antibody, statistically signif

169 Signaling through the lymphotoxin-beta receptor controlled the fate of adipocy

170 de development during embryogenesis involves lymphotoxin-beta receptor engagement and subsequent diff

171 al-associated lymphoid tissue by LTbetaR-Ig (lymphotoxin-beta receptor human Ig fusion protein) treat

172 nobese diabetic (NOD) mice were treated with lymphotoxin-beta receptor immunoglobulin fusion protein

173 CICD was strongly activated by both TNF and lymphotoxin-beta receptor ligation in IKKbeta-/- MEFs an

174 as well as pharmacological inhibition of the lymphotoxin-beta receptor markedly delays tumor developm

175 LIGHT, a ligand for the lymphotoxin-beta receptor, establishes lymphoid-like tis

176 on in the thymi of lymphotoxin-deficient and lymphotoxin-beta receptor-deficient mice contributes to

177 ions including BO, and that treatment with a lymphotoxin-beta receptor-immunoglobulin fusion protein

178 analyzed death after ligation of the TNF and lymphotoxin-beta receptors, respectively.

179 (tumor necrosis factor alpha, IL-1beta, and lymphotoxin-beta), and leukocyte genes (S100A9, Aif1/Iba

180 ive CD4 and CD8 T-cell subsets and decreased lymphotoxin-beta, a key factor for maintenance of FRC ne

181 s, which, in turn, removed a major source of lymphotoxin-beta, a survival factor for FRCs during SIV

182 on of lymphoid chemokines CXCL13, CCL19, and lymphotoxin-beta, and is associated with development of

183 tumor necrosis factor (TNF)-alpha, TNF-beta, lymphotoxin-beta, or TNFR1, TNFR2, Fas, or death recepto

184 resembling that observed in B-cell-specific lymphotoxin-beta-deficient mice, including disruption of

185 ated by intragraft TLOs and whether blocking lymphotoxin-beta-receptor (LTbetaR) signaling, a pathway

186 Rather, cell-specific deletion and in vivo lymphotoxin blockade link these systemic autoimmune resp

187 Thus, etanercept-induced TNF/lymphotoxin blockade may break the potentially self-sust

188 cessible to repeat biopsy, the effect of TNF/lymphotoxin blockade with etanercept (soluble TNFR) was

189 Although lymphotoxin can be up-regulated by chemokine CXCL13 and

190 r of the TNF family (BAFF), ICOS ligand, and lymphotoxin, correlated with more well-developed iBALT.

191 he failure of Aire induction in the thymi of lymphotoxin-deficient and lymphotoxin-beta receptor-defi

192 ansfer of splenocytes from wild-type but not lymphotoxin-deficient mice improved liver regeneration i

193 architecture of milky spots was disrupted in lymphotoxin-deficient mice, normal architecture was rest

194 We showed here that, in early postnatal lymphotoxin-deficient mice, the developing Flk-1+ white

195 in dKO mice compared with both wild-type or lymphotoxin-deficient mice.

196 lymphocyte-deficient mice and in conditional lymphotoxin-deficient mice.

197 one in the evolution of the highly organized lymphotoxin dependent B and T white pulp areas within wh

198 al tolerance to CII are AIRE independent but lymphotoxin dependent.

199 ta containing SFB occurred in the absence of lymphotoxin-dependent lymphoid structures and the spleen

200 Previous studies showed that homologous to lymphotoxin, exhibits inducible expression, competes wit

201 at a T cell-restricted ligand, homologous to lymphotoxin, exhibits inducible expression, competes wit

202 The TNF superfamily member homologous to lymphotoxins, exhibits inducible expression, and compete

203 The TNF-related ligand, LIGHT (homologous to lymphotoxins, exhibits inducible expression, and compete

204 ber 14 [TNFSF14; also known as homologous to lymphotoxins, exhibits inducible expression, and compete

205 (TNFSF14, also known as LIGHT [homologous to lymphotoxins, exhibits inducible expression, and compete

206 Notably, lymphotoxin-expressing B cells, CXCR5-expressing DCs and

207 In turn, lymphotoxin-expressing hematopoietic cells trigger the d

208 by connecting the CXCR5 signaling pathway to lymphotoxin expression but not to chemotaxis.

209 imulation in wild-type B cells, elevation of lymphotoxin expression in grb2(-/-) B cells is only indu

210 Peripheral lung homeostatic chemokine and lymphotoxin expression were visualized by immunostaining

211 Baffr(-) (/) (-) animals resulted in limited lymphotoxin expression, which is critical for maintenanc

212 Autopsy tissues were studied for the lymphotoxin granzyme and the apoptosis marker caspase 3.

213 Mice specifically deficient in T-cell lymphotoxin had increased liver damage and a reduced cap

214 +CD11c+ haematopoietic population expressing lymphotoxin has an important role in the formation of Pe

215 on required the cytokines interleukin-22 and lymphotoxin in a commensal bacteria-dependent and -indep

216 ts support a key role for DCs and DC-derived lymphotoxin in the formation of tumor HEVs.

217 al responses to the parasite and the role of lymphotoxin in these events.

218 In this study, we have dissected a lymphotoxin-independent CD30-dependent signal for the in

219 hey also expressed high levels of CXCL13 and lymphotoxins known to support lymphoid organogenesis.

220 is process is dependent on the expression of lymphotoxin ligands by host cells, but not by the transf

221 ) was used to evaluate the importance of the lymphotoxin/LIGHT axis in the development and perpetuati

222 gnatures, and differential dependency on the lymphotoxin/LIGHT signaling axis that help to interpret

223 g CD4(+) T cells and their regulation by the lymphotoxin/LIGHT signaling axis.

224 LIGHT (lymphotoxin-like inducible protein that competes with gl

225 The TNF superfamily cytokine, lymphotoxin-like inducible protein that competes with gl

226 Sustained expression of lymphotoxin-like inducible protein that competes with gl

227 during infection with C. rodentium, but the lymphotoxin-like protein LIGHT did not.

228 The TNF superfamily ligand LIGHT (lymphotoxin-like, exhibits inducible expression and comp

229 cells, derived from either FasL or TNF-alpha/lymphotoxin (LT) alpha double knockout mice, showed that

230 Lymphocytes from lymphotoxin (LT) alpha-deficient mice, which lack segreg

231 B cells were absolutely required to provide lymphotoxin (LT) alpha1beta2, which maintained a protect

232 investigating Ly49e promoter activities and lymphotoxin (LT) alphabeta dependency in resting versus

233 We identified lymphotoxin (LT) and LIGHT, tumor necrosis factor cytoki

234 d the roles of different cellular sources of lymphotoxin (LT) and the adaptive immune response in lym

235 At the same time, lymphotoxin (LT) and TNF are known to be critical for th

236 t on the transcription factor RORgt, and the lymphotoxin (LT) beta receptor (LTbetaR).

237 The lymphotoxin (LT) beta receptor plays a critical role in

238 d require constitutive signaling through the lymphotoxin (LT) beta receptor to be maintained in a ful

239 The importance of lymphotoxin (LT) betaR (LTbetaR) as a regulator of lymph

240 show that Tregs but not non-Treg T cells use lymphotoxin (LT) during migration from allograft to drai

241 The members of the lymphotoxin (LT) family of molecules play a critical rol

242 conditional gene deficiencies, we found that lymphotoxin (LT) from innate cells expressing transcript

243 In this study we blocked lymphotoxin (LT) signaling in a murine model of minor hi

244 ilar to PP formation, ILF formation requires lymphotoxin (LT)- and LT beta receptor-dependent events.

245 Lymphotoxin (LT)-alpha regulates many biologic activitie

246 into T- and B-cell zones, and expression of lymphotoxin (LT)-alpha, LT-beta, and lymphoid chemokines

247 Here, we demonstrate that DCs express the lymphotoxin (LT)-beta receptor (LT beta R) and that in m

248 onical NF-kappaB pathways by ligation of the lymphotoxin (LT)-beta receptor (LTbetaR) plays a crucial

249 lated by positive growth signals through the lymphotoxin (LT)-beta receptor; however, the countering

250 Accumulating evidence indicates that Lymphotoxin (LT)-beta related cytokines directly contrib

251 Lymphotoxin (LT)-deficient mice which have various defec

252 We found that the Lymphotoxin (LT)/TNF alleles, which encode TNF-alpha, we

253 a mouse model of human AIP by overexpressing lymphotoxin (LT)alpha and beta specifically in acinar ce

254 Interactions between lymphotoxin (LT)alpha(1)beta(2) on inducer cells and the

255 KT1(a) subset are selectively dependent upon lymphotoxin (LT)alpha1beta2-LTbeta receptor-dependent di

256 Activated NK cells expressed lymphotoxin (LT)alphabeta on their cell surface, and sec

257 h strong defects in the expression of IL-12, lymphotoxin (LT)beta, and IFN-gamma.

258 kocyte exit from the glands, is regulated by lymphotoxin (LT)betaR signaling.

259 Lymphotoxins (LT) provide essential communication links

260 As a biologically active heterotrimer, Lymphotoxin(LT)alpha1beta2 is unique in the TNF superfam

261 The lymphotoxin LTalpha(1)beta(2) supports the development a

262 Lymphotoxin (LTalpha(1)beta(2)) regulated the production

263 Recent studies revealed that the lymphotoxin/lymphotoxin beta receptor (LT)/LTbetaR syste

264 a, IL-4, IL-5, and TGF-beta(1), but not TNF, lymphotoxin, or IL-17.

265 we report that IL-22 acted downstream of the lymphotoxin pathway and regulated the organization and m

266 In short, the lymphotoxin pathway drives the developmental rather than

267 herefore, input from both Th17 cells and the lymphotoxin pathway induce the formation of an immune-co

268 The lymphotoxin pathway is critical for the development and

269 tiple organs, provoking speculation that the lymphotoxin pathway may play a role in central tolerance

270 nals, which suggests that IL-22 connects the lymphotoxin pathway to mucosal epithelial defense mechan

271 Whereas the lymphotoxin pathway was critical for the induction of th

272 systemic inflammation was independent of the lymphotoxin pathway.

273 Furthermore, surface lymphotoxin, provided by T cells, is critical for liver

274 or on T cells (LIGHT), signaling through the lymphotoxin receptor (LTbetaR) expressed on mature hepat

275 chanism that involves toll-like receptor and lymphotoxin receptor signaling.

276 r ligand for herpes virus entry mediator and lymphotoxin receptor)/herpes simplex virus entry mediato

277 Blockade of germinal center formation with a lymphotoxin-receptor-immunoglobulin fusion protein suppr

278 ymphotoxin-beta receptor (LTbetaR) by LIGHT (lymphotoxin-related inducible ligand that competes for g

279 Overexpression of lymphotoxin-related inducible ligand that competes for g

280 complex with its known ligands homologous to lymphotoxin, showing inducible expression, and competing

281 wn ligands include Fas ligand, homologous to lymphotoxin, showing inducible expression, and competing

282 nation of Fas.Fc, LT-betaR.Fc (homologous to lymphotoxin, showing inducible expression, and competing

283 SF14 [LIGHT (name derived from homologous to lymphotoxins, shows inducible expression, and competes w

284 Finally, Nfkb2 connected lymphotoxin signal within the intestinal niche in reinfo

285 Lymphotoxin signaling also maintains the expression of a

286 We previously showed that lymphotoxin signaling in the fibroblastic reticular cell

287 nes are members of the tumor necrosis factor/lymphotoxin signaling pathway.

288 Indeed, a series of reports has claimed that lymphotoxin signals control the expression of Aire, a tr

289 However, one report argued that lymphotoxin signals regulate the composition and organiz

290 infection with C. rodentium in mice lacking lymphotoxin signals, which suggests that IL-22 connects

291 additional to the recognized requirement for lymphotoxin signals.

292 itecture was restored by reconstitution with lymphotoxin-sufficient hematopoietic cells.

293 The lymphotoxin system (LT) regulates interactions between l

294 system that involves proinflammatory ligand, lymphotoxin that exhibits inducible expression and compe

295 tory factor (MIF), and tumor necrosis factor/lymphotoxin (TNF/LT), each of which significantly contri

296 dtype as well as hepatitis B virus (HBV) and lymphotoxin transgenic mice with and without HCC.

297 re model of M cell differentiation, we found lymphotoxin/tumor necrosis factor alpha induction of CD1

298 The importance of lymphotoxin was confirmed, as the use of a lymphotoxin b

299 trate-resistant prostate cancer by producing lymphotoxin, which activates an IkappaB kinase alpha (IK

300 ates and induced lung B cells to up-regulate lymphotoxin, which further promoted CXCL13 production, e

301 This indicates that neither TNF nor lymphotoxin, which uses the same receptor, was required