ライフサイエンスコーパス: LFA

1 LFA based on-site rapid screening devices provide positi

2 LFA performed on 465 undiluted CSF samples had a sensiti

3 LFA-1 cross-linking increased the presence of LAT-GRB2-S

4 LFA-1 function is regulated through conformational chang

5 LFA-1 inhibition blocked IFN-gamma secretion, splenocyte

6 LFA-1 is also needed to polarize the cytotoxic machinery

7 LFA-1 stimulation in PBMCs, CD4(+) T cells, or the T cel

8 LFA-1 was the prevailing ligand for endothelial ICAM-1 i

9 LFA-1, but not alpha4 integrins, contributed to B-cell m

10 LFA-1-activating antibodies and those inhibitory antibod

11 LFA-1-FAK1 decreased T-cell-dendritic cell (DC) dwell ti

12 ns lymphocyte function-associated antigen 1 (LFA-1) (CD11a/CD18) and macrophage-1 antigen (CD11b/CD18

13 to lymphocyte function-associated antigen 1 (LFA-1) activation and leukocyte recruitment.

14 Lymphocyte function-associated antigen 1 (LFA-1) affinity and avidity changes have been assumed to

15 induction of leukocyte functional antigen 1 (LFA-1) affinity maturation, which is consistent with a m

16 rin leukocyte function associated antigen 1 (LFA-1) binds the intercellular adhesion molecule 1 (ICAM

17 in lymphocyte function-associated antigen 1 (LFA-1) during acute inflammation.

18 rmediates of leukocyte functional antigen 1 (LFA-1) form a concentric array at the immunological syna

19 Lymphocyte function-associated antigen 1 (LFA-1) mediated adhesion modulates TCR-pMHC tension by i

20 s, lymphocyte function-associated antigen 1 (LFA-1), and very late antigen 4 (VLA-4).

21 ed lymphocyte function-associated antigen 1 (LFA-1)-mediated PMN adhesion to ICAM-1 under flow condit

22 in lymphocyte function-associated antigen 1 (LFA-1).

23 Lymphocyte function-associated antigen 1 (LFA-1, CD11a/CD18, alphaLbeta2-integrin) and its ligands

24 in lymphocyte function-associated antigen 1 (LFA-1; CD11a/CD18) is a key T cell adhesion receptor tha

25 and leukocyte function-associated antigen-1 (LFA-1) derived peptides was measured by surface plasmon

26 ed lymphocyte function-associated antigen-1 (LFA-1) extension that corresponds to intermediate affini

27 rin leukocyte function associated antigen-1 (LFA-1) is known to induce cross-talk to the alpha4beta1

28 ell leukocyte function-associated antigen-1 (LFA-1) regulation in primary murine effector T cells.

29 of leukocyte function-associated antigen-1 (LFA-1) that was required for their survival within the g

30 in lymphocyte function-associated antigen-1 (LFA-1) to mediate cell arrest and migration.

31 r (lymphocyte function-associated antigen-1 (LFA-1)) results in the clustering of the toxin.receptor

32 died pH regulated binding affinity of ICAM-1/LFA-1 at pH 7.4, 6.5, and 4.0 without and with magnesium

33 eptides retain its ability to inhibit ICAM-1/LFA-1 interaction.

34 In 4 of 10 LFA-positive cases agreeing to LP, the cerebrospinal flu

35 he 3 assays were as follows: LFA-PCR, 92.2%; LFA-RPLA, 94.8%; and PCR-RPLA, 97.4%.

36 ) and expressing adhesion molecules (VLA-4(+)LFA-1(+)) complementary to activated brain endothelium.

37 that with LFA-1 antibodies, we can activate LFA-1 and inhibit alpha4beta1, inhibit both LFA-1 and al

38 as IL-15, IL-12, or IL-18, does not activate LFA-1 but increases the responsiveness of the cells to s

39 nvestigate the signals necessary to activate LFA-1 in human NK cells.

40 ted with rapid colocalization of both active LFA-1 and DNAM-1 at the immune synapse.

41 In addition, LFA-1 promoted expression of Bcl-6, a transcriptional re

42 though increased affinity mediates adhesion, LFA-1 cross-linking induced the association and activati

43 bit LFA-1 but not alpha4beta1, or not affect LFA-1 or alpha4beta1 These findings are important for th

44 icates that kindlin-3-mediated high-affinity LFA-1 controls both the early transient integrin-depende

45 regulating the accumulation of high-affinity LFA-1 in focal zones of adherent cells.

46 y, CXCL1-mediated induction of high-affinity LFA-1 required HPK1, but macrophage antigen 1 (Mac-1) af

47 ndothelial venules, whereas macrophage-1 Ag, LFA-1, and CXCR4 were involved in their trafficking thro

48 (IDAS), the binding site of other allosteric LFA-1 inhibitors.

49 T-cell alpha4beta1 (VLA-4) and alphaLbeta2 (LFA-1) in in vivo and in vitro models of inflammation.

50 -sensing constructs of integrin alphaLbeta2 (LFA-1) to visualize intramolecular tension during cell m

51 n is initiated by activation of alphaLbeta2 (LFA-1), which can be induced by rolling on E-selectin (s

52 lulose membrane and gold nanoparticles on an LFA for quantifying TSH levels.

53 0.31 mIU L(-1) (never achieved before on an LFA format), below the commonly accepted minimum concent

54 cilitated by interactions between ICAM-1 and LFA-1.

55 on of JAM-A regulates leukocyte adhesion and LFA-1 binding.

56 n glycoprotein ligand-1, macrophage-1 Ag and LFA-1 integrins, and CXCR4 to get access across high end

57 re, we compared the involvement of CD103 and LFA-1, and their respective ligands, in the maturation o

58 ein expression, target cell conjugation, and LFA-1-, CD2-, and NKG2D-dependent activation of NK cells

59 the distribution of two antigens (HLA-DR and LFA-1) that HIV-1 acquires from infected cells among ind

60 LFA)-1 (alphaLbeta2) integrin expression and LFA-1-mediated T-lymphocyte functions.

61 phate-mediated intracellular Ca(2+) flux and LFA-1 activation that support chemokine-induced arrest i

62 cell receptors by enhancing calcium flux and LFA-1 integrin activation.

63 AM-1 by T cell-expressed T cell receptor and LFA-1, respectively.

64 ited to immune synapses along with talin and LFA-1, and loss of RIAM profoundly suppresses Ag-depende

65 ng chemomechanical crosstalk between TCR and LFA-1 receptor signaling.

66 le in the binding and trafficking of TCR and LFA-1 to the cell surface.

67 Although the T-cell receptor (TCR) and LFA-1 can generate intracellular signals, the immune cel

68 fewer T-APC conjugates, lower CD69, TCR, and LFA-1 surface expression, as well as lower overall TCR r

69 Anti-LFA-1 monoclonal antibody was used in a multiple minor a

70 .e. fibronectin, anti-CD3 antibody, and anti-LFA-1 antibody) were measured using impedance spectrosco

71 The anti-LFA-1 treatment led to fewer contacts between Tregs and

72 Similar results were obtained when anti-LFA-1 Ab was used to block the clustering of wild-type T

73 CD11c(+) cells, mice were treated with anti-LFA-1 Abs to reduce the number of CD11c(+) cells in this

74 pulse tolerance induction strategy with anti-LFA-1 rather than long-term treatment.

75 bited leukocyte function-associated antigen (LFA)-1 (alphaLbeta2) integrin expression and LFA-1-media

76 cking leukocyte function-associated antigen (LFA)-1 in organ transplant recipients prolongs allograft

77 that lymphocyte function-associated antigen (LFA-1) transferred onto LLV was able to trigger the clus

78 and identified the cell surface receptor as LFA-1 (CD11a/CD18; alphaLbeta2 integrin).

79 eded for the activation of integrins such as LFA-1 is poorly understood.

80 A lateral flow assay (LFA) can provide a rapid and cost-effective means to det

81 ptococcal antigen (CRAG) lateral flow assay (LFA) had 100% sensitivity and specificity on cerebrospin

82 ptococcal antigen (CRAG) lateral flow assay (LFA) has simplified diagnosis as a point-of-care test ap

83 acid hybridization-based lateral flow assay (LFA) holds great potential to address these limitations

84 d the performance of the lateral flow assay (LFA) on cerebrospinal fluid (CSF) samples for the diagno

85 The lateral flow assay (LFA) strip sensor possesses many advantages as a diagnos

86 rapid, semi-quantitative lateral flow assay (LFA) was developed to screen the oxytetracycline (OTC) a

87 lipoarabinomannan (LAM) lateral flow assay (LFA), LAM enzyme-linked immunosorbent assay (ELISA), and

88 eously by ELISA or paper lateral flow assay (LFA).

89 e available, including a lateral flow assay (LFA).

90 ic of the antibody-based lateral flow assay (LFA).

91 Here we present a novel liposome flux assay (LFA) that is applicable to most K(+) channels.

92 CrAg was measured using lateral flow assays (LFA) and latex agglutination (LA) tests in 645 HIV-posit

93 we evaluated two rapid lateral flow assays (LFA) for detection of Mycobacterium leprae-specific anti

94 ) lateral flow immunochromatographic assays (LFA) are used to screen for serum TSH concentration >5 m

95 over the currently available antibody-based LFA systems for influenza viruses, which offer discrimin

96 there exists a molecular cross-talk between LFA-1 and Notch1 through the Akt/ERK-GSK3beta signaling

97 Blocking LFA-1 by a neutralizing Ab or specific inhibition of Not

98 Furthermore, blocking LFA-1-induced MTOC polarization through ZAP70 inhibition

99 LFA-1 and inhibit alpha4beta1, inhibit both LFA-1 and alpha4beta1, inhibit LFA-1 but not alpha4beta1

100 umor cells and decreased recruitment of both LFA-1 and lipid rafts to the immunological synapse, whic

101 ine requirements and can be distinguished by LFA-1 expression.

102 erse range of downstream signaling cascades, LFA-1 stimulation in T lymphocytes modulates gene-transc

103 They also expressed CXCR3/CCR5/LFA-1 trafficking/tissue-resident phenotypes and consist

104 s a newly recognized regulator of TCR, CD28, LFA-1, and GLUT1 endosome-to-membrane recycling.

105 on of the structurally related protein CD58 (LFA-3) is associated with disease remission in MS.

106 Most purified CD56(+)CD117(+)CD7(+/-)LFA-1(-) remained as ILC22 cells and never became cNK ce

107 cNK cells showed a CD56(+)CD117(+)CD7(+/-)LFA-1(high) phenotype and expressed surface receptors, c

108 ed within the CD56(+)CD117(high)CD94(-)CD7(-)LFA-1(-) fraction and produced IL-22, IL-8, and granuloc

109 nlicensed NK cells that did form conjugates, LFA-1-dependent granule polarization was similar to that

110 entical to those applied to the conventional LFA strip sensor.

111 100 muL of the sample, whereas conventional LFA captures less than 1% of the target.

112 CrAg LFA and LA titers were correlated but were not directly

113 From August 2013 to August 2014, CRAG LFA (IMMY, Norman, Oklahoma) tests were performed on fin

114 infection for 20 patients (52.6%), and CrAg LFA titers in serum and CSF samples ranged from 1:5 to >

115 ryptococcal antigen lateral flow assay (CrAg LFA) was evaluated for the diagnosis of cryptococcosis i

116 ng to LP, the cerebrospinal fluid (CSF) CrAg LFA was positive.

117 nt with targeted therapy and decreasing CrAg LFA titers.

118 The remaining 13 patients had CrAg LFA titers of 1:2 (n = 11) or 1:5 (n = 2) and were ultim

119 rovement (n = 2), leading to an overall CrAg LFA false-positive rate of 34%.

120 between whole blood, serum, and plasma CRAG LFA results demonstrates that fingerstick CRAG is a reli

121 reviews for all patients with positive CrAg LFA results between June 2014 and December 2016.

122 le cases of low-titer (</=1:5) positive CrAg LFA results in patients for whom cryptococcosis was ulti

123 gate the accuracy of low-titer positive CrAg LFA results, we performed chart reviews for all patients

124 n for patients with first-time positive CrAg LFA titers of 1:2.

125 The CRAG LFA is an accurate diagnostic assay for CSF and should b

126 or histopathological confirmation, the CrAg LFA results were considered true-positive results for 5

127 We evaluated the accuracy of the CRAG LFA using fingerstick whole blood compared with serum/pl

128 rom 3,969 patients were tested with the CrAg LFA, and 55 patients (1.5%) tested positive.

129 Despite excellent performance of the CrAg LFA, we have observed multiple cases of low-titer (</=1:

130 in inhibition of Rap1 activity and decreased LFA-1-mediated adhesion.

131 alency and further promotes ligand-dependent LFA-1 activation.

132 Using different LFA-1 monoclonal antibodies, we have been able to study

133 The affinity of different (LFA-1) derived peptides also depends on the pH, although

134 The daughter CD8(+) T cells with disparate LFA-1 expression showed different patterns of migration

135 ITP-enhanced LFA (ITP-LF) also shows up to 30% target extraction from

136 to detect targets in situ; however, existing LFA formats (predominantly sandwich assays) are not suit

137 dances between the 3 assays were as follows: LFA-PCR, 92.2%; LFA-RPLA, 94.8%; and PCR-RPLA, 97.4%.

138 ely, our results define unique functions for LFA-1 in the Tfh cell effector program and suggest that

139 verall, our findings outline a new model for LFA-1 in which the integrin can mediate both adhesion an

140 first time membrane components required for LFA in milk system was optimized.

141 all expressed GNB isoforms are required for LFA-1 activation.

142 4%(n = 15) were detected by UCP-LFA and Gold-LFA, respectively.

143 entified by UCP-LFA and 78%(n = 133) by Gold-LFA.

144 mmunogold OnSite Leprosy Ab Rapid test [Gold-LFA] and the quantitative, luminescent up-converting pho

145 The lateral flow immunoassay (LFA) is one of the most widely used point-of-care diagno

146 Lateral flow immunoassays (LFA) are one of the most prevalent point-of-care (POC) d

147 tic leukemia (CLL) exhibit globally impaired LFA-1-mediated migration and that this defect is mediate

148 pression of SOS1, ARHGEF1, and DOCK2 impairs LFA-1-mediated rapid T lymphocyte adhesion as well as un

149 The improved LFA holds great potential for diseases diagnostics, food

150 ow of pH range for potential applications in LFA-1 related tumor therapy and autoimmune disease treat

151 edge, most likely resulting from a defect in LFA-1 release required for forward movement.

152 ude that P-Rex1 serves distinct functions in LFA-1 and Mac-1 activation.

153 vity is reduced, resulting in an increase in LFA-1 adhesion compared to that for syngeneically activa

154 indicate that HPK1 is critically involved in LFA-1-mediated PMN trafficking during acute inflammation

155 e prepared and used as labelling material in LFA.

156 s, and other kinases to ultimately result in LFA-1 activation.

157 o-related gene) channel, which, when used in LFA, provides a highly sensitive (zero false negatives o

158 particles provide an opportunity to increase LFA sensitivity and impart novel capabilities.

159 eased over the 20-s contact time, indicating LFA-1-mediated adhesion strengthening in primary effecto

160 cell subsets vary in their ability to induce LFA-1 binding activity after activating receptor stimula

161 n tyrosine kinases control chemokine-induced LFA-1- and VLA-4-mediated adhesion as well as human T ly

162 okinesis (DOCK)2 GEFs mediate CXCL12-induced LFA-1 activation in human primary T lymphocytes.

163 inhibit both LFA-1 and alpha4beta1, inhibit LFA-1 but not alpha4beta1, or not affect LFA-1 or alpha4

164 a-secretase inhibitor substantially inhibits LFA-1/ICAM-1-mediated activation of Notch signaling.

165 The alphaLbeta2 integrin LFA-1 is known to play a key role in T lymphocyte migrat

166 icular, redistribution of the beta2 integrin LFA-1 to the immunological synapse is compromised in Cav

167 eficient NK cells were dependent on integrin LFA-1 but not on DNAM-1 or NKG2D.

168 8 receptors CXCR1 and CXCR2 and the integrin LFA-1 (alphaLbeta2) were present at the interface betwee

169 VS and show that cross-linking the integrin LFA-1 alone is sufficient to induce active T cell polari

170 In this study, we report that the integrin LFA-1 cross-linking with its ligand ICAM-1 in human PBMC

171 ng B-cell migration, as well as the integrin LFA-1 for stromal guidance.

172 The integrin LFA-1 is essential for efficient activation and for cyto

173 stimulation of T-cells through the integrin LFA-1 or the chemokine receptor CXCR4, Rab5a is phosphor

174 Here, we show that the integrin LFA-1 triggers organelle polarization and viral protein

175 ccurs through interactions with the integrin LFA-1.

176 or more active conformations of the integrin LFA-1.

177 by Treg cells was due, in part, to integrin LFA-1-mediated interactions between Treg cells and dendr

178 Notably, CsA inhibited integrin-LFA-1-dependent and NFAT-independent adhesion of T cells

179 The analysis of beta2 integrins LFA-1 and macrophage-1 Ag (Mac-1) showed that in CD45E61

180 , which in turn activate multiple integrins (LFA-1, VLA-4), adhesion molecules (ICAM-1, MadCAM-1) and

181 sensitivity by integrating sponge shunt into LFA to decrease the fluid flow rate.

182 Intracellular LFA-1 quickly translocated to the cell surface with anti

183 rtantly, the redistribution of intracellular LFA-1 at the contact with APC was maintained during cell

184 an important regulator of the intracellular LFA-1 translocation.

185 LAM LFA had a sensitivity of 50% for definite and probable h

186 LAM LFA had a sensitivity of 68% for the composite standard

187 LAM LFA had a sensitivity of 75% for definite histopathologi

188 LAM LFA in CSF is a useful additional diagnostic tool.

189 We performed LAM LFA (on unprepared and supernatant CSF after heating and

190 r biomarker, using its physiological ligand, LFA-1.

191 Using the developed three-line LFA sensor, 50 clinical samples were measured at a detec

192 his study, we report the use of a three-line LFA strip sensor, adding an antigen line to the conventi

193 an antigen line to the conventional two-line LFA sensor, for detecting CRP within a broad concentrati

194 Moreover, LFA-1 affinity triggering by CXCL12 is impaired by SOS1,

195 bition of Pyk2 caused cells to form multiple LFA-1-rich tails at the trailing edge, most likely resul

196 hosphatase SHP-1 in the regulation of murine LFA-1-mediated adhesion in an allograft setting.

197 of a dilution step for samples with negative LFA results and the presence of yeasts on microscopy.

198 endothelial ICAM-1 and ICAM-2 and neutrophil LFA-1 and Mac-1.

199 showed that in CD45E613R mutant neutrophils LFA-1 adhesiveness was impaired, and avidity was enhance

200 We present a new LFA design that probes the dissociation of aptamers from

201 ce resonance energy transfer (FRET) with new LFA-1-specific fluorescent probes showed that triggering

202 drugs restricts the quantitation ability of LFA strips.

203 Cav1-knockout T cells, as is the ability of LFA-1 to form high-avidity interactions with ICAM-1.

204 e characterized by distinct accumulations of LFA-1-ICAM-1 in the lamella and TCR-MHC in the uropod, c

205 Activation of LFA-1 is a multistep process that depends on several pro

206 otential also show the highest activation of LFA-1, which correlated with the expression of the small

207 We have found that the binding affinity of LFA-1 whole protein and ICAM-1 increases significantly a

208 the T cell receptor for agonist pMHC and of LFA-1 (lymphocyte function-associated antigen 1) for ICA

209 kindlin 3 that is enhanced by the binding of LFA-1 to intercellular adhesion molecule 1 (ICAM-1).

210 loss of CD18 expression, the beta2 chain of LFA-1 and Mac-1 integrins.

211 duction of the high-affinity conformation of LFA-1 obligatory for leukocyte arrest.

212 aintaining the high affinity conformation of LFA-1, for increasing valency by recruiting LFA-1 to the

213 ary to induce high-affinity conformations of LFA-1 and VLA-4 that recognize their endothelial cell li

214 icient mice and involves the contribution of LFA-1 (lymphocyte-associated antigen 1) and alpha4 integ

215 A common criticism of LFA tests is that they have poor detection limits compar

216 ISG15 engagement of LFA-1 led to the activation of SRC family kinases (SFKs)

217 Thus, the coordinated expression of LFA-1 and DNAM-1 is a central component of NK cell educa

218 hannels inhibited, the high-affinity form of LFA-1 failed to become active, and T cells failed to mig

219 evented the generation of activated forms of LFA-1.

220 egulation led to a significant impairment of LFA-1 activation, which was demonstrated in vitro and in

221 ivision and led to an unequal inheritance of LFA-1 in divided T cells.

222 Tfh cell differentiation, and inhibition of LFA-1 abolished Tfh cell generation and prevented protec

223 The low detection limit of LFA and associated long equilibration times are due to k

224 ITP improves the LoD of LFA to the level of some lab-based immunoassays, such as

225 e to improve the limit of detection (LoD) of LFA by 400-fold for 90 s assay time and by 160-fold for

226 kine-induced activation of the Rho module of LFA-1 affinity triggering is dependent on JAK activity,

227 mation, along with decreased polarization of LFA-1, F-actin, and cytolytic granules toward the cytoto

228 ta demonstrate that an intracellular pool of LFA-1 in naive CD8(+) T cells plays a key role in T cell

229 reserve a significant intracellular pool of LFA-1 in the uropod during migration.

230 isms underlying the therapeutic potential of LFA-1 blockade in preventing chronic rejection are not f

231 Our data suggest that regulation of LFA-1 is one reason for the different activity of NK cel

232 novel key role of SHP-1 in the regulation of LFA-1-mediated adhesion may provide a new insight into T

233 ures, but the poor analytical sensitivity of LFA restricts its application.

234 potential therapeutic value of a new set of LFA-1 inhibitors, whose further development is facilitat

235 d an accumulation of surface Env at sites of LFA-1 engagement, with intracellular Env localized to a

236 We find that the very first stage of LFA-1-mediated attaching is unable to proceed in the abs

237 ell recognition, the conformational state of LFA-1 changed in educated NK cells, associated with rapi

238 ced by cytokines and leads to suppression of LFA-1 activity.

239 Specifically, triggering of LFA-1 to high-affinity state is prevented by PTPRG activ

240 Although clinical use of LFA-1 antagonists is limited by toxicity related to immu

241 nd in contrast to Th1 cells, Tregs depend on LFA-1 for their entry into the CNS in the absence of Itg

242 the Notch pathway activation is dependent on LFA-1/ICAM-1-induced inactivation of glycogen synthase k

243 onstrained ICAM-1 mobility opposes forces on LFA-1 exerted by the T cell cytoskeleton, whereas ICAM-1

244 LAD-III B cells to adhere to and migrate on LFA-1 ligand ICAM-1, potentially by altering the dynamic

245 not other integrins, such as alpha5beta1 or LFA-1, or a variety of membrane proteins.

246 teraction of either CD103 with E-cadherin or LFA-1 with ICAM-1.

247 ion assay showed that engagement of CD103 or LFA-1, together with TCR, enhances the strength of the T

248 ctional coupling between T Cell receptors or LFA-1 and the actin cytoskeleton.

249 , L-selectin and Mac-1 but not P-selectin or LFA-1.

250 Additionally, we show that our LFA design is not confined to the specific proteins used

251 tant arrest, whereas Mac-1 was dominant over LFA-1 in mediating neutrophil polarization on the BBB in

252 Pretreatment LFA titers correlated with quantitative cultures (R(2) =

253 ne signaling with timing coherent with rapid LFA-1 affinity activation.

254 acts as a ligand for the leukocyte receptor LFA-1.

255 LFA-1, for increasing valency by recruiting LFA-1 to the immunological synapse, and ultimately for p

256 rk generates mechanical forces that regulate LFA-1 activity at the immunological synapse.

257 f Talin-1, an adaptor protein that regulates LFA-1 affinity, dictated Tfh versus Th2 effector cell di

258 ssociated with higher screening plasma/serum LFA titers.Among the 28 CrAg-positive patients, mortalit

259 Finally, short-term LFA-1 blockade promoted long-term donor-specific regulat

260 We argue that LFA-1 contact with a cognate ligand, such as ICAM-1, ind

261 ce of inside-out integrin signaling but that LFA-1-mediated firm adhesion under conditions of shear f

262 es coupled with inhibitors demonstrated that LFA-1-induced polarization was dependent on the T cell k

263 flection fluorescence imaging indicated that LFA-1 and both chemokine receptors redistributed into cl

264 Taken together, these data reveal that LFA-1 is a key determinant in inducing dynamic T cell re

265 Here, we show that LFA-1 can mediate both adhesion and de-adhesion, depende

266 Our data show that LFA-1 has a low ligand-binding activity in resting human

267 ng a cell aggregation assay, suggesting that LFA-1 derived peptides show great potential for peptide

268 The LFA-1 blockade prevented acute rejection and preserved p

269 The LFA-1 blockade profoundly attenuated neointimal hyperpla

270 The LFA-1 blockade significantly suppressed the clonal expan

271 through a collimating lens to illuminate the LFA.

272 n line between test and control lines in the LFA sensor.

273 Analytical results revealed that the LFA has almost the same detection sensitivity as that of

274 s into a thin band and transport them to the LFA capture line, resulting in a dramatic increase in th

275 ncident light and angles of detection to the LFA were measured.

276 Together, the LFA and injectable synthetic biomarkers, which could be

277 with the ischemic brain endothelium via the LFA-1/ICAM-1 pathway and platelets and these findings we

278 When the LFA was paired with Gram staining, a sensitivity of 100%

279 that of the interaction (of ICAM-1) with the LFA-1 whole protein.

280 The limit of detection of this LFA was 0.13 ng/mL IgE, approximately 100 times lower th

281 Taken together, LFA-1 blockade inhibits initial endogenous alloreactive

282 pposed by immobilized ICAM-1, which triggers LFA-1 activation through a combination of induced fit an

283 = 161) of MB patients were identified by UCP-LFA and 78%(n = 133) by Gold-LFA.

284 n = 14) and 44%(n = 15) were detected by UCP-LFA and Gold-LFA, respectively.

285 up-converting phosphor anti-PGL-I test [UCP-LFA].

286 rly higher sensitivity obtained with the UCP-LFA assay.

287 Therefore, the UCP-LFA platform, which allows multiplexing with differentia

288 t can be interpreted as a previously unknown LFA-1 conformation.

289 as compared to 10(4) copies/ml in unmodified LFA.

290 testing of HBV as compared to the unmodified LFA.

291 otes the conjugate formation by upregulating LFA expression on NK cells and by inducing ICAM-1 expres

292 These included 16 also positive by urine LFA (2.5% of total screened) and 7 by serum LA (1.1% of

293 Using LFA, we performed small molecule screens on three differ

294 ls enables neutrophils to adhere firmly, via LFA-1-mediated binding to ICAM-1 constitutively expresse

295 However, stromal network guidance was LFA-1 independent, uncoupling integrin-dependent migrati

296 and discusses molecular mechanisms by which LFA-1 signaling influence T lymphocyte differentiation i

297 eling to the VS and suggest a model in which LFA-1 engagement triggers active polarization of the MTO

298 DNAM-1 interacts with LFA-1, a critical molecule for immunological synapse for

299 were CrAg positive in serum and plasma with LFA.

300 The results show that with LFA-1 antibodies, we can activate LFA-1 and inhibit alph