ライフサイエンスコーパス: SFB

1 SFB adhere tightly to the surface of epithelial cells in

2 SFB cause an increase in serum amyloid A (SAA), suggesti

3 SFB cytotoxicity was evaluated by multiple assays in the

4 SFB induce autoantibodies in lung during the pre-arthrit

5 SFB induced PP Tfh cell differentiation by limiting the

6 SFB primed and induced Th17 cells locally in the LP and

7 SFB-induced gut Th17 cells are preferentially recruited

8 SFB-positive, but not SFB-negative, females had a substa

9 SFBs, standardized by using toxic Pfiesteria (coupled wi

10 ith N-succinimidyl-4-18F-fluorobenzoate (18F-SFB) under slightly basic condition (pH 8.5).

11 ing N-succinimidyl-4-18F-fluorobenzoate (18F-SFB) with glycine at 90 degrees C (pH 8) for 20 min.

12 ing N-succinimidyl 4-18F-fluorobenzoate (18F-SFB) with N-(2-aminoethyl)maleimide.

13 ith N-succinimidyl-4-18F-fluorobenzoate (18F-SFB).

14 35 +/- 5 (mean +/- SD) min starting from 18F-SFB, and the tracer 18F-FB-T84.66 diabody was synthesize

15 [18F]SFB remains an optimal reagent for labeling proteins and

16 f N-succinimidyl 4-[18F]fluorobenzoate ([18F]SFB), an agent widely used for labeling proteins and pep

17 Using this method, [18F]SFB can be synthesized in decay-corrected radiochemical

18 For the [18F]SFB synthesis, the quaternary salt is first converted to

19 uorobenzoic acid, which is converted to [18F]SFB by treatment with N,N-disuccinimidyl carbonate.

20 toward aerobic glycolysis and, accordingly, SFB cytotoxicity was dramatically increased by glucose w

21 nduced in mesenteric lymph nodes early after SFB colonization and distributed across different segmen

22 R)-expressing Th17 cells recognizing both an SFB epitope and self-antigen, thus augmenting autoimmuni

23 We identified an SFB-dependent role of type 3 innate lymphoid cells (ILC3

24 tion, S(13m) -RNase has a 23 bp deletion and SFB(13)' has a 1 bp substitution that lead to premature

25 nalyzed for total immunoglobulin A (IgA) and SFB-specific IgA production.

26 in lung during the pre-arthritic phase, and SFB-dependent lung pathology requires the T helper 17 (T

27 ree alleles, S(6m2)-RNase, S(13m)-RNase, and SFB(13)', however, these transcripts presumably result i

28 ween those of P. tenella SFB(8) and P. avium SFB(1).

29 obes such as segmented filamentous bacteria (SFB) and certain extracellular pathogens.

30 vergrowth of segmented filamentous bacteria (SFB) and increased microbial loads in deep tissues.

31 Segmented filamentous bacteria (SFB) are autochthonous bacteria inhabiting the intestina

32 Segmented filamentous bacteria (SFB) are found in multiple species and play an important

33 Segmented filamentous bacteria (SFB) are sufficient to induce TH17 cells and to promote

34 Segmented filamentous bacteria (SFB) are Th17-inducing commensals that potentiate autoim

35 microbiota, segmented filamentous bacteria (SFB) colonize the guts of a variety of vertebrates and i

36 Segmented filamentous bacteria (SFB) contribute to immune-system maturation.

37 In rodents, segmented filamentous bacteria (SFB) induce intestinal Th17 cells, but analogously funct

38 ization with segmented filamentous bacteria (SFB) is known to promote IL-17 production in the gut; he

39 e with mouse-segmented filamentous bacteria (SFB) partially restored T cell numbers, suggesting that

40 presence of segmented filamentous bacteria (SFB) promotes Th17 differentiation and the development o

41 Intestinal segmented filamentous bacteria (SFB) protect from ameba infection, and protection is tra

42 of mice with segmented filamentous bacteria (SFB), a commensal that induces IL-17A production, exacer

43 , especially segmented filamentous bacteria (SFB), are a crucial factor that drives T helper 17 (Th17

44 ies, such as segmented filamentous bacteria (SFB), are sufficient to induce the expansion of Th17 cel

45 cillales and segmented filamentous bacteria (SFB), as well as an increase of interleukin 17 (IL-17) p

46 microbiota, segmented filamentous bacteria (SFB), distantly provoke lung pathology.

47 ial species, segmented filamentous bacteria (SFB), in inducing a robust T-helper cell type 17 (Th17)

48 of commensal segmented filamentous bacteria (SFB), known to promote Th17 cells.

49 ota, such as segmented filamentous bacteria (SFB), promote their differentiation.

50 ut commensal segmented filamentous bacteria (SFB)-induced systemic arthritis despite the production o

51 dysbiosis by segmented filamentous bacteria (SFB)-positive fecal transfer significantly suppressed th

52 by commensal segmented filamentous bacteria (SFB).

53 vergrowth of segmented filamentous bacteria (SFB).

54 pecific for segmented filamentous bacterium (SFB) after cecal ligation and puncture (CLP)-induced sep

55 al microbe, segmented filamentous bacterium (SFB), is sufficient to induce the appearance of CD4(+) T

56 us lithium-iodine (Li-I) solar flow battery (SFB) by incorporation of a built-in dye-sensitized TiO2

57 ollected in a transect of San Francisco Bay (SFB) and their temporal variations within the Bay over t

58 logic evidence of direct interaction between SFB and intraepithelial mononuclear cells.

59 omenon resulted from the interaction between SFB and the passively acquired maternal mucosal immunity

60 Two assays, standardized fish bioassays (SFBs) with juvenile fish and fish microassays (FMAs) wit

61 se beads into a novel swirl flow bioreactor (SFB), of low capital and running costs and of simple con

62 other T cells, recognize antigens encoded by SFB.

63 tence of colonization of the neonatal gut by SFB depends on the immune status of both mothers and pup

64 Previous stimulation of mucosal immunity by SFB did not prevent the translocation of M. morganii in

65 ondrial damage and ROS drive cell killing by SFB, while glycolytic cell reprogramming may represent a

66 After the climax, SFB quickly declined to very low levels in the small int

67 Consequently, SFB can promote IL-17-dependent immune and autoimmune re

68 findings suggest that microbiota containing SFB create an intestinal milieu that may induce Ag-speci

69 7 cells in response to microbiota containing SFB occurred in the absence of lymphotoxin-dependent lym

70 tiation as well as how microbiota containing SFB regulate Ag-specific intestinal Th17 cells remain po

71 lls in the presence of microbiota containing SFB was dependent on MHC class II expression by CD11c+ c

72 ence of cognate Ag and microbiota containing SFB.

73 In contrast, SFB depletion protected from obesity-induced hepatocellu

74 y, we demonstrate that Th17 cells controlled SFB burden.

75 r, protein sequences of the pollen-expressed SFB alleles were not identical, harbouring 12 amino-acid

76 Conjugation of (18)F-SFB to IL2 yielded (18)F-FB-IL2 as the major product.

77 (18)F-SFB was efficiently prepared using a 3-step radiochemica

78 Purified (18)F-SFB was incubated with IL2 in borate buffer (pH 8.5) and

79 (18)F-SFB was produced with a 34%-38% radiochemical yield.

80 N-succinimidyl 4-(18)F-fluorobenzoate ((18)F-SFB) for the synthesis of N-(4-(18)F-fluorobenzoyl)inter

81 N-succinimidyl-4-(18)F-fluorobenzoate ((18)F-SFB) prosthetic group.

82 N-succinimidyl-4-(18)F-fluorobenzoate ((18)F-SFB) prosthetic group.

83 N-succinimidyl-4-(18)F-fluorobenzoate ((18)F-SFB) under a slightly basic condition.

84 N-succinimidyl-4-(18)F-fluorobenzoate ((18)F-SFB) was conjugated to S-2-((2-(S-4-amino-4-carboxybutan

85 N-succinimidyl-4-(18)F-fluorobenzoate ((18)F-SFB), and its biodistribution, tumor-targeting potential

86 N-succinimidyl-4-(18)F-fluorobenzoate ((18)F-SFB).

87 N-succinimidyl-4-(18)F-fluorobenzoate ((18)F-SFB).

88 N-succinimidyl 3-(18)F-fluorobenzoate ((18)F-SFB).

89 gnificantly higher (P < 0.05) than for (18)F-SFB-5F7 (25.4 +/- 10.3); however, kidney uptake was 28-3

90 ted (125)I-SGMIB-5F7, whereas that for (18)F-SFB-5F7 was lower than coincubated (125)I-SGMIB-5F7 and

91 26%-28% higher (P < 0.05) than that of (18)F-SFB-5F7.

92 aphy purification was 25%-35% based on (18)F-SFB.

93 The binding affinity of (19)F-SFB-conjugated NAPamide, (19)F-FB-NAPamide, was determin

94 RMSH-1 and RMSH-2 and their respective (19)F-SFB-conjugated peptides ((19)F-FB-RMSH-1 and (19)F-FB-RM

95 s about 25-30% ( n = 5) starting from [(18)F]SFB ( n = 5) with an effective specific activity about 4

96 uccinimidyl 4-[ (18)F]fluorobenzoate ([(18)F]SFB) with Boc-Dmt-Tic--Lys(Z)-OH under slightly basic co

97 gent N-succinimidyl-4-[(18)F]fluorobenzoate (SFB) to the anti-VEGFR2 antibodies.

98 T cells with antigen receptors specific for SFB-encoded peptides differentiated into RORgammat-expre

99 1c(+) cells was necessary and sufficient for SFB-induced Th17 cell differentiation.

100 tion of the radiolabeled antibodies and free SFB differed from the distribution of the targeted MBs.

101 adiolabeled antibodies alone (n = 3) or free SFB (n = 3).

102 Remarkably, germ-free animals harboring SFBs alone developed EAE, showing that gut bacteria can

103 cuyer et al. (2014) provide evidence for how SFB induce antigen-specific T helper 17 cells and promot

104 The Li-I SFB can be charged at a voltage of 2.90 V under 1 sun AM

105 nto RORgammat-expressing TH17 cells, even if SFB-colonized mice also harboured a strong TH1 cell indu

106 led a temporal increase in the Gd anomaly in SFB from the early 1990s to the present.

107 (TCR) repertoire of intestinal TH17 cells in SFB-colonized mice has minimal overlap with that of othe

108 The dynamic changes in SFB colonization of the small intestines of the differen

109 crease in anthropogenic Gd concentrations in SFB, from 8.27 to 112 pmol kg(-1) over the past two deca

110 hoid cells (ILCs) resulted in an increase in SFB-independent Th17 cell differentiation.

111 further explored the role of bone marrow in SFB-mediated protection.

112 liferation in CLP-treated SFB(+), but not in SFB(-), mice.

113 naling in the enteric epithelium resulted in SFB dysbiosis due to reduced expression of alpha-defensi

114 ony-stimulating factor (GM-CSF) signaling in SFB-colonized mice prevented GMP expansion, decreased gu

115 opsoids caused no juvenile fish mortality in SFBs even at high densities, and low larval fish mortali

116 ce of a small group of commensals, including SFB, and results in an impaired mucosal barrier.

117 prone to spontaneous colitis with increased SFB and Th17 cells.

118 Interestingly, SFB-specific CD4 T cells underwent Ag-driven proliferati

119 s using mice that either contained or lacked SFB as a normal gut-resident microbe.

120 ature transcripts dominated the very limited SFB-induced molecular changes detected in SI-LP CD4(+) T

121 mice or rats with SFB indigenous to mice (M-SFB) or rats (R-SFB), M-SFB and R-SFB showed host-specif

122 ndigenous to mice (M-SFB) or rats (R-SFB), M-SFB and R-SFB showed host-specific adhesion to small int

123 d A (SAA), suggesting that SAA might mediate SFB's effects on BMDCs.

124 Most SFB-induced Th17 cells recognized SFB in an MHCII-depend

125 SFB-positive, but not SFB-negative, females had a substantial population of Th

126 thway dynamically regulates the abundance of SFB as well as mucosal barrier function in the adult ani

127 by reciprocal crossings and backcrossings of SFB-monoassociated, formerly germ-free, immunocompetent

128 onses, and immunoglobulin A (IgA) coating of SFB in the gut.

129 There was a strong cosegregation of SFB positivity and diabetes protection in females, but n

130 We studied the effect of SFB on the mucosal immune system by monoassociating form

131 A second group of SFB-monoassociated mice was colonized with a gram-negati

132 ated to the dynamic changes in the levels of SFB coated with secretory IgA (sIgA), which resulted fro

133 found that low concentrations (2.5-5 muM) of SFB had a relatively modest effect on LCSC-2 or 293 T ce

134 We monitored the number of SFB on the mucosa of the small intestine in the four dif

135 ere, we exploit the incomplete penetrance of SFB colonization of NOD mice in our animal facility to e

136 that MHCII-dependent antigen presentation of SFB antigens by intestinal dendritic cells (DCs) is cruc

137 Gene expression profiling of SFB-treated cells was consistent with a shift toward aer

138 alies were observed in the southern reach of SFB, which is surrounded by several hospitals and resear

139 tional program clearly distinct from that of SFB, suggesting an alternative mechanism of promoting Th

140 In contrast, insulitis did not depend on SFB colonization.

141 omponent S-haplotype-specific F-box protein (SFB).

142 to mice (M-SFB) or rats (R-SFB), M-SFB and R-SFB showed host-specific adhesion to small intestinal EC

143 th SFB indigenous to mice (M-SFB) or rats (R-SFB), M-SFB and R-SFB showed host-specific adhesion to s

144 Most SFB-induced Th17 cells recognized SFB in an MHCII-dependent manner.

145 secondary lethal infection with recombinant SFB Ag-expressing virulent Listeria (but not wild-type v

146 kin 23 (IL-23) and IL-22, which can regulate SFB.

147 wever, the corresponding introns and S-RNase-SFB intergenic regions showed considerable differences.

148 f whether the pups were scid/scid or scid/+, SFB could be found earlier on the mucosa of the small in

149 Since SFB targets mitochondria, cell metabolic reprogramming m

150 cinoma, the multikinase inhibitor Sorafenib (SFB) usually fails to eradicate liver cancer.

151 cid replacements between those of P. tenella SFB(8) and P. avium SFB(1).

152 that of conventionally reared mice, and that SFB-specific IgA was produced but accounted for less tha

153 We determined that SFB, by driving differentiation and egress of PP Tfh cel

154 We found that SFB stimulated GCRs in PP from day 6 after monoassociati

155 Our findings generally indicate that SFB are one of the single most potent microbial stimuli

156 of mice and rats, it has been observed that SFB are absent during the suckling period and appear in

157 lly restored T cell numbers, suggesting that SFB and other MMb organisms are required for full immune

158 17 production in the gut; here, we show that SFBs also induced IL-17A-producing CD4(+) T cells (Th17)

159 psis primed for a protective response by the SFB-specific CD4 T cells.

160 ed relatively disease-free regardless of the SFB status.

161 onally, we found that in peripheral tissues, SFB selectively expand dual T cell receptor (TCR)-expres

162 aracterize cancer cell metabolic response to SFB, we measured oxygen consumption, generation of react

163 Similar to SFB, B. adolescentis was closely associated with the gut

164 Moreover, CLP-treated SFB(+) mice showed resistance to secondary lethal infect

165 rwent Ag-driven proliferation in CLP-treated SFB(+), but not in SFB(-), mice.

166 The protocols for the synthesis of unlabeled SFB and the quaternary salt precursor 4-formyl-N,N,N-tri

167 roduction was restricted to the ileum, where SFB makes direct contact with the epithelium and induces

168 aluate the effect of prior colonization with SFB on the ability of M. morganii to translocate to the

169 Transient gut colonization with SFB or SAA administration alone transiently increased th

170 Colonization with SFB was correlated with increased expression of genes as

171 aboratory mice, which are not colonized with SFB.

172 ociating formerly germfree C3H/HeN mice with SFB.

173 ocolonization of germ-free mice or rats with SFB indigenous to mice (M-SFB) or rats (R-SFB), M-SFB an