ライフサイエンスコーパス: LFA-1

1 LFA-1 also mediates leukocyte adhesion.

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

3 LFA-1 function is regulated through conformational chang

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

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

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

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

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

9 LFA-1-activating antibodies and those inhibitory antibod

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

11 LFA-1/ICAM-1-stimulated human and mouse T-cells were ref

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 or lymphocyte function-associated antigen 1 (LFA-1) expressed on immune cells.

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

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

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

22 in lymphocyte function-associated antigen 1 (LFA-1), which can be induced by selectin engagement.

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

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

25 he integrin lymphocyte functional antigen 1 (LFA-1).

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

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

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

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

30 rin leukocyte function-associated antigen-1 (LFA-1) interaction with its ligand intercellular adhesio

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

32 a(2) integrin, leukocyte function antigen-1 (LFA-1) on white blood cells (WBCs) and causes cell death

33 in lymphocyte function-associated antigen-1 (LFA-1) plays a crucial role within the immune system.

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

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

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

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

38 ts lymphocyte function-associated antigen-1 (LFA-1), a critical adhesion molecule for leukocyte arres

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

40 n, lymphocyte function-associated antigen-1 (LFA-1, CD11a/CD18) using a novel small fluorescent probe

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

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

43 in CD11a/CD18 (leukocyte function antigen-1; LFA-1) to a high-affinity and clustered state that deter

44 BM niche with hematopoietic CXCR4(+)VLA-4(+)LFA-1(+) nursery cells, which provide PC survival factor

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

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

47 tor and the chemokine receptor CCR7 activate LFA-1 through processes known as inside-out signaling.

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

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

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

51 all (ca. 5%) subset of conformational-active LFA-1 nanoclusters preanchored to the cytoskeleton.

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

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

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

55 efined shear stress to low- or high-affinity LFA-1 and imaged the spatiotemporal regulation of bond f

56 Activation of high-affinity LFA-1 by extracellular Ca(2+) resulted in an eightfold i

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

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

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

60 iched within focal clusters of high-affinity LFA-1, which promoted physical linkage with Orai1.

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

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

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

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

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

66 vented in mice doubly deficient in Del-1 and LFA-1 or in Del-1 and the IL-17 receptor.

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

68 djacent pericytes in an ICAM-1-, Mac-1-, and LFA-1-dependent manner.

69 ls' relative expression of CXCR4, VLA-4, and LFA-1, the homing and adhesion molecules that direct/ret

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

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

72 mofetil plus induction with basiliximab and LFA-1 blockade.

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

74 to maintain surface levels of TCR, CD28, and LFA-1.

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

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

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

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

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

80 ere were enhanced and sustained Rap1-GTP and LFA-1 activation as well as prolonged T:APC conjugates.

81 e signals resulted in decreased Rap1-GTP and LFA-1 adhesiveness to ICAM-1, thus impairing T-cell chem

82 hanism by which interaction between LtxA and LFA-1 results in cell death is not well understood.

83 lted in the internalization of both LtxA and LFA-1, with LtxA localizing specifically to the lysosoma

84 pothesized that it cooperates with Orai1 and LFA-1 in signaling local Ca(2+) flux necessary for shear

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

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

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

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

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

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

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

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

93 ells, the combination of belatacept and anti-LFA-1 was able to suppress cytokine production by allore

94 of local inflammatory response and for anti-LFA-1-based therapies.

95 e was coupled with either anti-VLA-4 or anti-LFA-1.

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

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

98 -cell recall effector function, whereas anti-LFA-1 attenuated both trafficking and memory recall effe

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

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

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

102 defects in T cells that prevent appropriate LFA-1 activation and motility.

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

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

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

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

107 Blocking LFA-1 by neutralizing antibody or specific knockdown of

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

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

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

111 In vivo, both LFA-1-dependent slow rolling and Mac-1-dependent crawlin

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

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

114 sing two monoclonal antibodies (R7.1 and CBR LFA-1/1) we further demonstrate that shortening of the C

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

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

117 lease or CD107a expression in CD161(+)CD56(+)LFA-1(+) cells or in mature peripheral blood NK cells.

118 more differentiated cytolytic CD161(+)CD56(+)LFA-1(+) NK cells.

119 between immature noncytolytic CD161(+)CD56(+)LFA-1(-) and more differentiated cytolytic CD161(+)CD56(

120 CD161(+)CD56(+)LFA-1(-) NK cells produce large amounts of CXCL8 after p

121 Within in vitro UCB-derived CD161(+)CD56(+)LFA-1(-) NK cells, CXCL8 release was also induced on ant

122 of CD161 was confined to the CD161(+)CD56(+)LFA-1(-) subset, because it did not induce cytokine rele

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

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

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

126 teins Kindlin-3 and Talin-1 anchor clustered LFA-1 to the cytoskeleton and facilitate the transition

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

128 creased density of Talin-1 and consolidating LFA-1 clusters within sites of contact with ICAM-1.

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

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

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

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

133 Here, we induce differential LFA-1 activation in neutrophils through engagement of th

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

135 soflurane interacts with the full ectodomain LFA-1 and modulates its conformation and function.

136 flurane binding sites on the full ectodomain LFA-1 were probed by photolabeling using photoactivatabl

137 LtxA is unable to kill cells lacking either LFA-1 or cholesterol.

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

141 chanistic data suggest an important role for LFA-1/ICAM-1 interactions in immunoregulation concurrent

142 These cells have high LFA-1 integrin expression and display high spontaneous b

143 to PCC could be blocked by Abs against human LFA-1 and porcine VCAM-1.

144 As an antagonist against human LFA-1 exists and has been used clinically to treat psori

145 rly did not open the actin mesh but could if LFA-1 was coligated.

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

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

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

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

150 -1 and kindlin-3 serve distinct functions in LFA-1 activation.

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

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

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

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

155 Increased expression of SMAD7 and SMURF2 in LFA-1/ICAM-1 cross-linked T-cells resulted in impaired T

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

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

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

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

160 oforms, but not JAK1, mediate CXCL12-induced LFA-1 triggering to a high affinity state.

161 e find that talin-1 is required for inducing LFA-1 extension, which corresponds to intermediate affin

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

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

164 Kindlin-3 was recently reported to initiate LFA-1 clustering in lymphocytes, we hypothesized that it

165 gulating the avidity of the beta(2) integrin LFA-1 in the immunological synapse.

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

167 was not attributed to altered beta2 integrin LFA-1 properties but was instead due to reduced inside-o

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

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

170 8 receptors CXCR1 and CXCR2 and the integrin LFA-1 (alphaLbeta2) were present at the interface betwee

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

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

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

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

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

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

177 eutrophil adhesion dependent on the integrin LFA-1, and by reciprocal higher expression of interleuki

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

179 ccurs through interactions with the integrin LFA-1.

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

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

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

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

184 pt in place of basiliximab, and more intense LFA-1 blockade.

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

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

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

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

189 In contrast to prior models, LFA-1 polarized to T cell-APC contacts in talin1-deficie

190 n were significantly important in modulating LFA-1 function and conformation.

191 recently showed that in quiescent monocytes, LFA-1 preorganizes in nanoclusters proximal to nanoscale

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

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

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

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

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

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

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

199 or siRNA for Galphaq causes accumulation of LFA-1 adhesions and stalled migration.

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

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

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

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

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

205 inery that regulates affinity and avidity of LFA-1 in response to CCR7.

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

207 Blockade of LFA-1, another ICAM-1 receptor, prevented neutrophil adh

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

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

210 duction of the high-affinity conformation of LFA-1 with an open headpiece, which results in neutrophi

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

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

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

214 etween conformation and lateral diffusion of LFA-1 and further underscores the crucial role of mobili

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

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

217 cal activity evaluation of a novel family of LFA-1 antagonists.

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 nce, but in a manner that was independent of LFA-1 integrin activation or adhesion.

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

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

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

225 he crucial role of mobility for the onset of LFA-1 mediated leukocyte adhesion.

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

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

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

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

230 Clustering occurs only in the presence of LFA-1 and cholesterol, and LtxA is unable to kill cells

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 ects both affinity and avidity regulation of LFA-1.

234 nd microparticle formation are the result of LFA-1-mediated adhesion and VLA-3-mediated cell migratio

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

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

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

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

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

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

241 d Galphaq/11 is required for the turnover of LFA-1 adhesion that is necessary for migration.

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

243 recently reported that tensile force acts on LFA-1 bonds inducing their colocalization with Orai1, th

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

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

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

247 Galphaq/11 has an impact on LFA-1 expression at plasma membrane level and also on it

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

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

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

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

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

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

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

255 consequence beta-2 integrins, predominantly LFA-1, are activated.

256 4(+) umbilical cord blood (UCB) progenitors, LFA-1 expression allowed to discriminate between immatur

257 cell expression of Del-1, thereby promoting LFA-1-dependent recruitment of neutrophils.

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

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

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

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

262 mall guanosine triphosphatase Rap1 regulates LFA-1 adhesiveness through one of its effectors, Rap1-in

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

264 ry molecules by siRNA substantially restored LFA-1/ICAM-1-mediated alteration in TGF-beta signaling.

265 ibodies suggested that isoflurane stabilized LFA-1 in the closed conformation.

266 site, and that isoflurane binding stabilizes LFA-1 in the closed conformation.

267 y healthy T cells with CLL cells, subsequent LFA-1 engagement leads to altered Rho GTPase activation

268 Therefore, Del-1 suppressed LFA-1-dependent recruitment of neutrophils and IL-17-tri

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

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

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

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

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

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

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

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

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

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

279 The LFA-1 blockade profoundly attenuated neointimal hyperpla

280 The LFA-1 blockade significantly suppressed the clonal expan

281 cells with each other via interaction of the LFA-1 integrin with ICAM-1.

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

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

284 of inside-out activation ligand, binding to LFA-1 is extremely slow, at least 10 times slower than e

285 complexes require ADAP/SKAP55 for binding to LFA-1 upon CCR7 stimulation.

286 Binding of LtxA to LFA-1 resulted in the internalization of both LtxA and L

287 stead due to reduced inside-out signaling to LFA-1 by activating receptors.

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

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

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

291 t to induce cortical actin remodeling unless LFA-1 was coligated.

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

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

294 is found in discrete sticky patches whereas LFA-1 is expressed over the entire length on slings.

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

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

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

298 Additionally Galphaq co-localizes with LFA-1- and EEA1-expressing intracellular vesicles and pa

299 w here that LtxA interacts specifically with LFA-1 in the active (exposed) conformation.

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