ライフサイエンスコーパス: TLR5

1 imal husbandry practices rather than loss of TLR5.

2 h concomitant TLR6 mutation), 1 IRAK1, and 1 TLR5.

3 erated C57BL/6 mice with LoxP sites flanking Tlr5.

4 ary responses or recognition of flagellin by TLR5.

5 main with the convex surface of the opposing TLR5.

6 V sequence and increased association of MUC1/TLR5.

7 ost immunity, in part via its recognition by TLR5.

8 ing the dependence of IL-1beta production on TLR5.

9 cells lining the renal vasculature expressed TLR5.

10 ng was assessed with HEK293 cells expressing TLR5.

11 onses by inducing proteolytic degradation of TLR5.

12 ells but does not affect activation of human TLR5.

13 nd most CD172alpha(+)LPDCs also co-expressed TLR5.

14 r of which is incapable of signaling through TLR5.

15 red monocyte-derived dendritic cells through TLR5.

16 flagellin or heat-killed B. pseudomallei by TLR5(1174C)>T genotype in healthy subjects.

17 lude that the hypofunctional genetic variant TLR5(1174C)>T is associated with reduced organ failure a

18 In a dominant model, TLR5(1174C)>T was associated with protection against in-

19 We tested the association of TLR5(1174C)>T with outcome in 600 Thai subjects with mel

20 riant that encodes a defective TLR5 protein, TLR5(1174C)>T, to elucidate the role of TLR5 in melioido

21 TLR5 and found that B. pseudomallei induced TLR5(1174C)- but not TLR5(1174T)-dependent activation of

22 ers of TLR5(1174T) compared with carriers of TLR5(1174C).

23 e those in TLR1 (1805GG), TLR2 (2258GA), and TLR5 (1174CT).

24 , IL-1ra, G-CSF, and IL-1beta in carriers of TLR5(1174T) compared with carriers of TLR5(1174C).

25 B. pseudomallei induced TLR5(1174C)- but not TLR5(1174T)-dependent activation of NF-kappaB.

26 te-normalized levels of IL-10 in carriers of TLR5(1174T).

27 entrations further decreased (p < 0.05) in a TLR5(392Stop) SNP rUTI subgroup.

28 beta mRNA in human primary immune cells from TLR5 616LL homozygote carriers, as compared with 616FF c

29 netically deficient in Toll-like receptor 5 (TLR5), a component of the innate immune system that is e

30 ortance of TLR5 function in RA, we used anti-TLR5 Ab therapy in CIA mice.

31 s that neutralized the Toll-like receptor 5 (TLR5)-activating activity of flagellin, an important par

32 These findings indicate that TLR5 activation by flagellin mediates innate immune resp

33 TLR5 activation by flagellin permits the physical intera

34 TLR5 activation in MCF7 cells induced a single and susta

35 aeruginosa or different mutants defective in TLR5 activation were resistant to AM phagocytosis and ki

36 is functional, we compared human and bovine TLR5 activity and signalling in cognate cell lines.

37 he ability of flagellated isolates to induce TLR5 activity.

38 count: TLR4 (aGMR, 1.22; 95% CI, 1.03-1.45), TLR5 (aGMR, 1.19; 95% CI, 1.01-1.41), and TLR6 (aGMR, 1.

39 s also stimulated hepcidin, most notably the TLR5 agonist flagellin in an IL-6-dependent manner.

40 Here, we demonstrate that the TLR5 agonist flagellin restores antibiotic-impaired inna

41 harmacologically optimized derivative of the TLR5 agonist flagellin.

42 In this study, we used flagellin, a TLR5 agonist protein ( approximately 50 kDa) extracted f

43 sive activity of entolimod, a clinical stage TLR5 agonist that activates NF-kappaB-, AP-1-, and STAT3

44 n structurally analogous to a clinical stage TLR5 agonist, entolimod.

45 enicity of recombinant proteins containing a TLR5 agonist, flagellin, and either full-length or selec

46 We show that TLR5 agonist, flagellin, can promote monocyte infiltrati

47 protective effects of pretreatment with the TLR5 agonist, indicating a window following reperfusion

48 guing observation as C. jejuni FlaA is not a TLR5 agonist.

49 a-derived flagellin, a Toll-like receptor 5 (TLR5) agonist, protects mice from C. difficile colitis b

50 bility of flagellin, a Toll-like receptor 5 (TLR5) agonist, to serve as an effective adjuvant in this

51 n vivo and suggest clinical applications for TLR5 agonists as hepatoprotective and antimetastatic age

52 Overall, these results indicate the use of TLR5 agonists as mitigators and protectants of acute ren

53 ese results define systemically administered TLR5 agonists as organ-specific immunoadjuvants, enablin

54 Anticancer efficacy of TLR5 agonists stems from TLR5-dependent activation of nu

55 TLR5 agonists, bacterial flagellin and engineered flagel

56 no effect on stimulation by TLR2, TLR3, and TLR5 agonists.

57 Toll-like receptor 5 (TLR5) agonists are favorably positioned as potential sys

58 MyD88-dependent stimulation of TLR1/2 and TLR5 also upregulated PD-L1 expression on CMFs in cultur

59 th PAK mutants or in WT PAK-infected primary TLR5(-/-) AMs, demonstrating the dependence of IL-1beta

60 TLR5 signaling cassette comprising of human TLR5 and a secreted derivative of Salmonella flagellin s

61 Although both TLR5 and CD172alpha(+) lamina propria dendritic cells (L

62 ammalian species, lack surface expression of TLR5 and do not respond to flagellin.

63 eversibly inhibiting recruitment of MyD88 to TLR5 and downstream signaling events.

64 embryonic kidney-293 cells transfected with TLR5 and found that B. pseudomallei induced TLR5(1174C)-

65 IgG1 was the dominant isotype and partially TLR5 and inflammasome dependent.

66 strate IgG2c responses toward flagellin were TLR5 and inflammasome dependent; IgG1 was the dominant i

67 ed immunofluorescence colocalization of Muc1/TLR5 and Muc1/phosphotyrosine staining patterns in mouse

68 IgA anti-FliC responses were TLR5 and MyD88 dependent and caspase-1 independent.

69 al signals provided by the gut flora through TLR5 and MyD88 signaling.

70 ng and not through stimulatory signaling via TLR5 and MyD88.

71 that activates the innate immune system via TLR5 and Naip5/6, and generates strong T and B cell resp

72 eptors (PRRs) are (i) flagellin, detected by TLR5 and NLRC4 (Ipaf); and (ii) T3S rod proteins (PrgJ a

73 ed a correlation between early expression of TLR5 and the magnitude of the antibody response.

74 olymorphisms (SNP) in the flagellin receptor TLR5 and the TLR downstream effector molecules MyD88 and

75 TLR3, TLR7 and TLR9, but not to TLR2, TLR4, TLR5 and TLR8 ligands.

76 We found that TLR5 and TNF-alpha pathways are interconnected, because

77 synovial fluid and the strong correlation of TLR5 and TNF-alpha with each other and with disease acti

78 lin permits the physical interaction between TLR5 and TRIF in human colonic epithelial cells (NCM460)

79 ve effects of flagellin on survival required TLR5 and were observed even in the absence of neutrophil

80 e, we report that immunization of wild-type, TLR5(-/-), and MyD88(-/-) adoptive transfer recipient mi

81 ed flagellin receptors Toll-like receptor 5 (TLR5) and NOD-like receptor C4 (NLRC4).

82 nsynonymous variant in Toll-like receptor 5 (TLR5) and show that it leads to altered NF-kappaB signal

83 TLR signaling, including elevation of TLR4, TLR5, and IL-1R1, with decreases in IL-1R-associated kin

84 LPDCs expressed high levels of TLR5, and most CD172alpha(+)LPDCs also co-expressed TLR5

85 Using two tumor models that do not express TLR5, and thereby do not directly respond to CBLB502, we

86 wnregulation of Toll-like receptor 3 (TLR3), TLR5, and TLR7.

87 in pDCs in response to TLR1/2, TLR2/6, TLR3, TLR5, and TLR8 engagement in mDCs and TLR7 and TLR9 in p

88 ck of CTSK inhibited the expression of TLR4, TLR5, and TLR9 and their downstream cytokine signaling i

89 Human TLR2, TLR4, TLR5, and TLR9 gene polymorphisms were assessed in 278 H

90 Comparison of MyD88-, TLR2-, TLR4-, TLR5-, and TLR9-deficient mice and their respective wild

91 Wild-type and TLR5(-/-) APCs were able to stimulate high levels of OVA

92 terminus of TRIF and extracellular domain of TLR5 are required for TRIF-induced TLR5 degradation.

93 which multiple TLR pathways (e.g., TLR2/TLR4/TLR5) are blocked are not as compromised in their respon

94 Here, we report that, in contrast to TLR5 as a "carrier of Salmonella," TLR11 works as a "blo

95 etermined the crystal structure of zebrafish TLR5 (as a variable lymphocyte receptor hybrid protein)

96 r protein MyD88 is critical for signaling by TLR5, as well as IL-1Rs and IL-18Rs, major downstream me

97 Toll-like receptor 5 (TLR5) binding to bacterial flagellin activates signaling

98 that exploit pathogen recognition elements, TLR5 biosensors have the potential to carry out broad-sp

99 uilding on our previous research that bovine TLR5 (bTLR5) is functional, we compared human and bovine

100 , to generate mice that lacked expression of TLR5 by IECs (TLR5(DeltaIEC)) or DCs (TLR5(DeltaDC)), re

101 Scarified corneas of adult B6, TLR5(-/-), Camp(-/-) (cathelicidin-related antimicrobial

102 n of flagellin via the Toll-like receptor 5 (TLR5) contributes to exacerbate B. cenocepacia-induced l

103 2alpha(-), LPDCs induced Th17 cells, whereas TLR5-deficient LPDC did not induce Th17 cells.

104 Flagellin receptor TLR5-deficient mice (T5KO) display elevated intestinal p

105 ory phenotype is not a consistent feature of TLR5-deficient mice and document a novel role for TLR5 i

106 It has been shown that TLR5-deficient mice develop metabolic syndrome and have

107 However, we report that TLR5-deficient mice from two different animal colonies d

108 TLR5-deficient mice have been reported to develop sponta

109 europathy, but this blockade is abrogated in Tlr5-deficient mice.

110 domain of TLR5 are required for TRIF-induced TLR5 degradation.

111 ion of TLR5 by IECs (TLR5(DeltaIEC)) or DCs (TLR5(DeltaDC)), respectively.

112 ar to previous findings from TLR5-null mice, TLR5(DeltaIEC) mice had low-grade inflammation (mild spl

113 Development of this inflammation in the TLR5(DeltaIEC) mice was eliminated by administration of

114 mice that lacked expression of TLR5 by IECs (TLR5(DeltaIEC)) or DCs (TLR5(DeltaDC)), respectively.

115 icancer efficacy of TLR5 agonists stems from TLR5-dependent activation of nuclear factor-kappaB (NF-k

116 able lidocaine derivative QX-314, leading to TLR5-dependent blockade of sodium currents, predominantl

117 We report that TLR5-dependent commensal bacteria drive malignant progre

118 y, depletion of commensal bacteria abrogates TLR5-dependent differences in tumor growth.

119 ults define the liver as the key mediator of TLR5-dependent effects in vivo and suggest clinical appl

120 icrobe, Tyler et al. (2013) demonstrate that TLR5-dependent induction of anti-flagellin antibodies pr

121 nd protection against Candida keratitis in a TLR5-dependent manner.

122 omotes the development of allergic asthma by TLR5-dependent priming of allergic responses to indoor a

123 the MLN, but not the spleen, sFliC drives a TLR5-dependent recruitment of CD103(+) dendritic cells (

124 ude that in addition to MyD88, TRIF mediates TLR5-dependent responses and, thereby regulates inflamma

125 CBLB502 is a novel agonist for TLR5 derived from Salmonella flagellin.

126 expression dramatically suppresses flagellin/TLR5-deriven NFkappaB activation in NCM460 cells.

127 n colonic epithelial cells (NCM460), whereas TLR5 does not interact with TRAM upon flagellin stimulat

128 In vitro, the level of TLR5 downstream genes, IL-6 and IL-8, was highly induced

129 t unlike the Salmonella Typhimurium flagella-TLR5 driven pro-inflammatory axis, C. jejuni flagella in

130 ct and an indirect mechanism are involved in TLR5-driven RA inflammation and bone destruction.

131 gnaling of TLR4, plays an inhibitory role in TLR5-elicited responses by inducing proteolytic degradat

132 cular mechanism that PTEN deletion inhibited TLR5-elicited responses, we hypothesized that PTEN regul

133 Here, we report that TLR5 engagement is crucial for bacterial clearance by AM

134 Altogether, these findings demonstrate that TLR5 engagement plays a major role in P. aeruginosa inte

135 ses by controlling the involvement of Mal in TLR5 engagement.

136 inflammatory responses elicited by flagellin/TLR5 engagement.

137 the flagellin receptor Toll-like receptor 5 (TLR5) exhibit a profound loss of flagellin-specific immu

138 Significant sequence variation in TLR5 exists between animal species but its impact on act

139 owed that interactions between flagellin and TLR5 expressed on both donor hematopoietic and host nonh

140 tion of TLR5 signaling can inhibit growth of TLR5-expressing tumors and protect normal tissues from r

141 ation with neither LPS nor IFN-gamma altered TLR5 expression by the monocytes.

142 Induction of RegIIIgamma requires TLR5 expression in hematopoietic cells and is dependent

143 ly, TNF-alpha has a feedback regulation with TLR5 expression in RA monocytes, whereas expression of t

144 anti-TNF-alpha therapy can markedly suppress TLR5 expression in RA monocytes.

145 aeruginosa bacteria, and 3) corresponded to TLR5 expression on MDSCs in vitro and in vivo.

146 r of TNF-alpha in RA synovial fluid and that TLR5 expression on these cells strongly correlates with

147 Tlr5(fl/fl) siblings were used as controls.

148 Indeed, by activating the TLR5, flagella can elicit activation of the MAPK and NF-

149 ctural basis and mechanistic implications of TLR5-flagellin recognition, we determined the crystal st

150 Two TLR5-FliC 1:1 heterodimers assemble into a 2:2 tail-to-t

151 Loss of TLR5 from DCs did not associate with development of infl

152 Last, to evaluate the importance of TLR5 function in RA, we used anti-TLR5 Ab therapy in CIA

153 mmation and bone erosion are alleviated when TLR5 function is blocked.

154 hus, in contrast to T5KO mice, loss of human TLR5 function protects from weight gain, but in analogy

155 (R392X, rs5744168), a portion of humans lack TLR5 function.

156 These two identified TLR5 functions are potentiated by TNF-alpha, because inh

157 In the context that TLR5 functions to recognize pathogens and activate innat

158 The TLR5 gene encodes an innate immunity receptor.

159 Increased TLR4 and TLR5 gene expression in whole blood was demonstrated in

160 In the TLR5 gene, rs5744174/F616L was associated with increased

161 ctal cancer progression might be mediated by TLR5 genotype-dependent flagellin sensing.

162 oteobacteria evading antibody coating in the TLR5(-/-) gut.

163 Loss of TLR5 has more impact on MLN than splenic Ab responses, r

164 el biosensor utilizing toll-like receptor 5 (TLR5) has been conducted.

165 and IL-8, was highly induced by flagellin in TLR5 high-expressing cells compared with TLR5 low-expres

166 In contrast, the absence of TLR5 hindered the initial activation and clonal expansio

167 members overexpressed flagellar genes in the TLR5(-/-) host.

168 and reciprocal results were found for human TLR5 (hTLR5) in human cells, indicative of host cell spe

169 atory effects were dramatically inhibited in TLR5(-/-);IL-10(-/-) mice.

170 These data show complex roles for TLR4, TLR5, IL-1R and CD11c+ cells in constitutive epithelial

171 of the modified bare gold surface following TLR5 immobilization were characterized.

172 The MUC1 cytoplasmic tail associated with TLR5 in all cells tested, including HEK293T cells, human

173 regulating host-microbial communication via TLR5 in colonic epithelial cells.

174 e generated mice with specific disruption of Tlr5 in IECs or DCs by using a breeding scheme that allo

175 es of plasma cells, demonstrating a role for TLR5 in immunity to TIV.

176 epithelial cell (IEC) vs dendritic cell (DC) TLR5 in mediating these phenotypes are not clear; modifi

177 ein, TLR5(1174C)>T, to elucidate the role of TLR5 in melioidosis.

178 ght to establish the role of TLR2, TLR4, and TLR5 in postseptic mice with Pseudomonas aeruginosa pneu

179 regulating host-microbial communication via TLR5 in the gut epithelium.

180 deficient mice and document a novel role for TLR5 in the rapid targeting of flagellin by intestinal p

181 TCL1A, TMEM176B, FOXP3, TOAG-1, MAN1A1, and TLR5) in the peripheral blood of 67 kidney transplant re

182 controlling Mal recruitment, PTEN regulates TLR5-induced inflammatory responses.

183 sponses, we hypothesized that PTEN regulated TLR5-induced responses by controlling the involvement of

184 al-TLR5 interaction, resulting in diminished TLR5-induced responses.

185 in, the sole ligand of Toll-like receptor-5 (TLR5), induces an innate defense that is sufficient to p

186 rotein that stimulates Toll-like receptor 5 (TLR5), induces epithelial expression of RegIIIgamma and

187 specific IgG1 response was induced through a TLR5-, inflammasome-, and MyD88-independent pathway.

188 Furthermore, PTEN deletion disrupted Mal-TLR5 interaction, resulting in diminished TLR5-induced r

189 on at the plasma membrane and suppressed Mal-TLR5 interaction.

190 TLR5 interacts primarily with the three helices of the F

191 TLR5 is a pathogen recognition receptor activated by bac

192 In this study, we show that TLR5 is elevated in RA and osteoarthritis ST lining and

193 Furthermore, expression of TLR5 is elevated in RA synovial fluid macrophages and RA

194 ver, the regulation and pathogenic effect of TLR5 is undefined in RA.

195 We found that Toll-like receptor 5 (TLR5) is co-expressed with neurofilament-200 in large-di

196 Toll-like receptor 5 (TLR5) is considered an attractive target for anticancer

197 neutrophils and monocytes expressed mRNA for TLR5, it appeared to be translated into protein only by

198 radiation chimeras previously engrafted with TLR5 knockout hematopoietic cells showed that interactio

199 engineered to secrete bacterial flagellin, a TLR5 ligand (TLR5L), can engender a costimulatory signal

200 Cross-tolerance was observed by TLR5 ligand flagellin and heat-killed or live bacteria r

201 ed T-84 cells treated basolaterally with the TLR5 ligand flagellin was prevented when the polarized c

202 id affect IL-12 or IL-1beta induction by the TLR5 ligand flagellin.

203 lunted cytokine responses to TLR4 ligand and TLR5 ligand stimulation relative to PB DCs, yet similarl

204 ide (LPS, both TLR4 ligands), and flagellin (TLR5 ligand).

205 HCMV infection also potentiated TLR5 ligand-stimulated cytokine production.

206 Fas in IECs reduced the ability of TLR4 and TLR5 ligands and the intestinal pathogens Salmonella typ

207 on with Toll-like receptor (TLR) 2, TLR4, or TLR5 ligands than blood from APOepsilon3/APOepsilon3 pat

208 Treatment with TLR4 and TLR5 ligands, but not TLR2 and 9 ligands, increased expr

209 teoclast maturation directly through myeloid TLR5 ligation and indirectly via TNF-alpha production fr

210 cytes and macrophages are more responsive to TLR5 ligation compared with fibroblasts despite the proi

211 onclusion, we document the potential role of TLR5 ligation in modulating transcription of TNF-alpha f

212 rconnected, because TNF-alpha is produced by TLR5 ligation in RA myeloid cells, and anti-TNF-alpha th

213 Our aim was to examine the impact of TLR5 ligation in rheumatoid arthritis (RA) and experimen

214 agellin postonset treatment in CIA and local TLR5 ligation in vivo provoke homing and osteoclastic de

215 TLR2 and TLR5 ligation increased beta2-integrin affinity, as asse

216 agen-induced arthritis (CIA) and local joint TLR5 ligation models.

217 es were conducted to investigate the role of TLR5 ligation on RA and mouse myeloid cell chemotaxis or

218 TLR2 or TLR5 ligation rapidly activated integrin-dependent leuko

219 in TLR5 high-expressing cells compared with TLR5 low-expressing cells.

220 Our results suggest that expression of TLR5 may be a predictor for RA disease progression and t

221 onses, the smoking-induced downregulation of TLR5 may contribute to smoking-related susceptibility to

222 or RA disease progression and that targeting TLR5 may suppress RA.

223 TLR5-mediated Abeta-fiber blockade, but not capsaicin-me

224 aB transcriptional activity while increasing TLR5-mediated AP-1 transcription.

225 eficial effect of CBLB502, and suggests that TLR5-mediated immune modulation may be a promising appro

226 tool for antitumor vaccination that directs TLR5-mediated immune response toward cancer cells and do

227 On the basis of TLR5-mediated immunomodulatory function, we examined the

228 er the significance of TNF-alpha function in TLR5-mediated pathogenesis.

229 agellin and a cell reporter system to assess TLR5-mediated responses, we also show that the presence

230 TLR5-mediated sensing of flagellin promoted plasma cell

231 Finally, TLR5-mediated sensing of the microbiota also impacted an

232 using agonistic anti-Fas augmented TLR4- and TLR5-mediated TNF-alpha and IL-8 production by IECs.

233 Our data thereby demonstrated that TLR5 mediates CD172alpha(+)LPDC induction of Th17 cells

234 ell development, it is still unclear whether TLR5 mediates the CD172alpha(+)LPDC induction of Th17 ce

235 ia adherent to the corneas of IL-1R (-/-) or TLR5 (-/-) mice penetrated beyond the epithelial surface

236 Postseptic wild-type and tlr4(-/-) and tlr5(-/-) mice displayed high susceptibility to P. aerug

237 mice but not Toll-like receptor 5-deficient (TLR5(-/-)) mice, indicating that they resulted from infl

238 ein level of TLR5, whereas it does not alter TLR5 mRNA level.

239 n inhibited flagellin-induced association of TLR5/MyD88 compared with controls.

240 Flagellin functioning via the TLR5/NFkappaB pathway was identified as the key UPEC vir

241 e lacking the receptor Toll-like receptor 5 (TLR5-null mice), which recognizes flagellin, have an alt

242 Similar to previous findings from TLR5-null mice, TLR5(DeltaIEC) mice had low-grade inflam

243 In mice, flagellin activation of TLR5 on DCs leads to production of interleukin-22.

244 Flagellin-induced activation of TLR5 on dendritic cells elicited production of the cytok

245 Mal interacted with TLR5 on flagellin, and Mal deficiency inhibited flagelli

246 Expression of TLR5 on IECs regulates the composition and localization

247 We also found that TLR5 on RA monocytes is an important modulator of TNF-al

248 c CD8(+) T cell proliferation independent of TLR5 or MyD88 expression by the recipient animal.

249 ent on TLR9 signaling and was not induced by TLR5 or other NF-kappaB activators, such as TNF-alpha.

250 Mice deficient solely in TLR2, TLR4, TLR5, or TLR9 did not show enhanced parasite expulsion,

251 se 8 during stimulation of TLR2, TLR3, TLR4, TLR5, or TLR9 results in receptor interacting protein (R

252 By recognizing flagellin, TLR5 plays a quintessential role in microbial recognitio

253 f cancer patients are influenced by a common TLR5 polymorphism.

254 In contrast, the TLR2 and TLR5 polymorphisms did not vary in frequency or function

255 TRIF-induced TLR5 protein degradation is completely inhibited in the

256 te that TRIF-induced caspase activity causes TLR5 protein degradation.

257 lysis and flow cytometry were used to detect TLR5 protein in both cell types.

258 d a genetic variant that encodes a defective TLR5 protein, TLR5(1174C)>T, to elucidate the role of TL

259 ion reduces recognition of flagellin by host TLR5, providing an evasive strategy to infecting bacteri

260 The dominant TLR5(R392X) polymorphism abrogates flagellin responses i

261 Co-expression of TLR5 receptor and agonist in Mobilan-infected cells esta

262 Toll-like receptor 5 (TLR5) recognition of flagellin instigates inflammatory s

263 Vertebrate Toll-like receptor 5 (TLR5) recognizes bacterial flagellin proteins and activa

264 of bacteria that are recognized by TLR4 and TLR5, respectively.

265 ocytic MDSCs cause gammadelta lymphocytes in TLR5-responsive tumors to secrete galectin-1, dampening

266 and malignant evolution are recapitulated in TLR5-responsive/unresponsive ovarian and breast cancer p

267 The T allele at TLR5 rs5744174 (p.Phe616Leu) and the C allele at TLR9 rs

268 The TLR5 rs5744174 T allele carriers have higher PBMCs IFN-g

269 In addition, activation of TLR5 signaling can inhibit growth of TLR5-expressing tum

270 an that drives expression of self-activating TLR5 signaling cassette comprising of human TLR5 and a s

271 Cell, Rutkowski and colleagues indicate that TLR5 signaling deficiency, which occurs in approximately

272 Interestingly, flagellin/TLR5 signaling in breast cancer cells inhibits cell prol

273 s2072493/N592S and rs5744174/F616L modulated TLR5 signaling in response to flagellin or to different

274 ted cells established an autocrine/paracrine TLR5 signaling loop resulting in constitutive activation

275 ghly expressed in breast carcinomas and that TLR5 signaling pathway is overly responsive in breast ca

276 This unique ability of MUC1 to control TLR5 signaling suggests its potential role in the pathog

277 appa B (NF-kappaB) activation (indicative of TLR5 signaling) in tissues and cells of mice treated wit

278 ucidate the mechanism by which MUC1 inhibits TLR5 signaling.

279 trast to most other species, suggesting that TLR5 signalling has evolved differently in ruminants.

280 Here, we characterized the dynamics of TLR5 signalling, responsible for the recognition of flag

281 tases of multiple tumors regardless of their TLR5 status.

282 TLR5 stimulation significantly improves pathological cha

283 Mice lacking Tlr5 (T5KO) develop insulin resistance and increased adi

284 To extend application of TLR5-targeted anticancer immunotherapy to tumors that do

285 sts a deleterious immunoregulatory effect of TLR5 that may be mediated by IL-10 and identifies this r

286 Moreover, Toll-like receptor 5 (TLR5), the mammalian receptor for FLA, was required for

287 ading to an increase in its association with TLR5, thereby competitively and reversibly inhibiting re

288 Wild-type, tlr2(-/-), tlr4(-/-), tlr5(-/-), tlr2 4(-/-) mice that underwent CLP were seco

289 ) or TLR4 (-/-) corneas, but not TLR2 (-/-), TLR5 (-/-), TLR7 (-/-), or TLR9 (-/-), were more suscept

290 with specific ligands for TLR2, TLR3, TLR4, TLR5, TLR7, TLR8 and TLR9 in the presence or absence of

291 l-like receptor 2/6 (TLR2/6), TLR2-CD14, and TLR5 to similar extents in a model cell line.

292 TLR2- and TLR5-triggered integrin activation in leukocytes require

293 ntrast, IL-17 is consistently upregulated in TLR5-unresponsive tumor-bearing mice but only accelerate

294 utionary divergence between bovine and human TLR5 was also apparent in relation to responses measured

295 iopsy immunofluorescence studies showed that TLR5 was expressed mainly on the apical side of the epit

296 We found that TLR5 was highly expressed in breast carcinomas and that

297 rapy to tumors that do not naturally express TLR5, we created an adenovirus-based vector for intratum

298 ells abolishes the cellular protein level of TLR5, whereas it does not alter TLR5 mRNA level.

299 the maintenance of surface CD14 and TLR4 and TLR5, which declined over time in mock-infected macropha

300 nonsmokers, the most striking change was for TLR5, which was downregulated in healthy smokers (1.4-fo

301 Activation of TLR5 with its ligand flagellin results in neuronal entry