ライフサイエンスコーパス: lymphotoxin

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

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

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

4 e local production of the cytokines IL22 and lymphotoxin.

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

6 tromal cells and dendritic cells, partly via lymphotoxin.

7 d increase in CXCL13 was partly mediated via lymphotoxin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 Anti-lymphotoxin alpha has fast nonspecific clearance in cyno

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

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

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

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

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

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

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

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

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

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

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

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

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

39 We identified lymphotoxin-alpha (LTA) as the causative factor for auto

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

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

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

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

44 the injection of lentiviral vectors for the lymphotoxin-alpha (LTalpha) and interferon-gamma (IFNgam

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

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

47 of tumor necrosis factor (TNF) superfamily, lymphotoxin-alpha (LTalpha), also interacts with HVEM.

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

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

50 However, besides TNF, etanercept also blocks lymphotoxin-alpha (LTalpha), which has no clear therapeu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 Lymphotoxin-alpha-deficient mice infected with RSV were

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 Expression of lymphotoxin and homeostatic chemokine receptors was inve

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

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

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

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

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

88 Lymphotoxins are part of a cytokine network well known i

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

90 dy, we provide evidence that TNFSFs, such as lymphotoxins, are likely not a universal mechanism to ma

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

92 The lymphotoxin axis is important for the maintenance of sev

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

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

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

96 immunohistochemistry for levels of RELB and lymphotoxin beta (LTB).

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

98 Lymphotoxin beta (LTbeta) expression in DCs maintained A

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

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

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

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

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

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

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

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

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

108 FAP(+) cells of the LN anlagen express lymphotoxin beta receptor (LTbetaR) and vascular cell ad

109 Lymphotoxin beta receptor (LTbetaR) blockade reduces hom

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

111 Lymphotoxin beta receptor (LTbetaR) deficiency is associ

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

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

114 Lymphotoxin beta receptor (LTbetaR) ligation-induced Air

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

116 Lymphotoxin beta receptor (LTbetaR) signaling is crucial

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

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

119 Lymphotoxin beta receptor (LTbetaR)-driven induction of

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

121 d gastric inflammation via activation of the lymphotoxin beta receptor (LTbetaR).

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

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

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

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

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

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

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

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

130 y member 14 (TNFRSF14, also called HVEM) and lymphotoxin beta receptor are receptors for LIGHT that w

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

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

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

134 Genetic deletion of lymphotoxin beta receptor or lymphotoxin alpha abrogated

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

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

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

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

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

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

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

142 IGHT receptors herpesvirus entry mediator or lymphotoxin beta receptor.

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

144 We found that lymphotoxin beta was overexpressed in tumors containing

145 Lymphotoxin beta-receptor (LTbetaR) signalling promotes

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

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

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

149 the hTNFR2 blocks the biological activity of lymphotoxin beta.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 Here, we show that signaling through the lymphotoxin-beta receptor (LTbetaR) is critical for kidn

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

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

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

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

172 In vitro, tumor necrosis factor (TNF) or lymphotoxin-beta receptor agonist can rescue expression

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

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

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

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

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

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

179 ing by CP- and ILF-resident CCR6(+) ILC3 via lymphotoxin-beta receptor signaling in cDCs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 Cytosolic NIK, stabilized by LIGHT (lymphotoxin-like inducible protein that competes with gl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 orchestrated by lymphoma-provided VEGFC and lymphotoxin (LT).

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

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

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

258 Lymphotoxins (LT) provide essential communication links

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

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

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

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

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

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

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

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

267 The lymphotoxin pathway is critical for the development and

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

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

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

271 systemic inflammation was independent of the lymphotoxin pathway.

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

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

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

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

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

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

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

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

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

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

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

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

284 Lymphotoxin signaling also maintains the expression of a

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

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

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

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

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

290 additional to the recognized requirement for lymphotoxin signals.

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

292 The lymphotoxin system (LT) regulates interactions between l

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

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

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

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

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

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

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

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