ライフサイエンスコーパス: HEL

1 r interactions with antibody in the HyHEL-63/HEL complex, alanine substitution of Lys96 results in a

2 und HEL in the wild type and mutant HyHEL-63/HEL complexes reveals that the side-chain conformation o

3 ics of specific interactions in the HyHEL-63/HEL interface, double mutant cycles were constructed to

4 mined the crystal structures of the HyHEL-63/HEL Lys96Ala and HyHEL-63/HEL Lys97Ala complexes to 1.80

5 es of the HyHEL-63/HEL Lys96Ala and HyHEL-63/HEL Lys97Ala complexes to 1.80 and 1.85 A resolution, re

6 In the 7/8 HEL group, patients with 3 or more LEL mismatches scored

7 are associated with lower survival after 7/8 HEL matched transplantation.

8 sks in donor-recipient pairs matched for 7/8 HEL.

9 n correlates with improved presentation of a HEL-derived epitope.

10 The interaction of a TgB cell with a HEL-bearing DC triggered strong Ca2+ transients in the B

11 The addA(NUC) and addA(HEL) mutants colonized the stomach less efficiently than

12 Extracts with AddA(HEL)B lacked detectable helicase and nuclease activity.

13 egulatory T cells in mice when administering HEL, indicating that the T cell responses were mediated

14 MyD88-independent, evident within 24 h after HEL immunization, and restricted to the CD11b/c(+) APC s

15 mice that express soluble HEL as a self Ag (HEL-Ig mice) decreases B cell mIgM expression, responsiv

16 Induction of autoantibodies against HEL was not dependent on coadministration of strong adju

17 HEL, induced high-titer Ab responses against HEL in both soluble HEL Tg mice and double Tg mice that

18 ntional methods for immune responses against HEL.

19 Although HEL hot spot residues Lys96 and Lys97 make similar inter

20 calization of ICP0 in cells (e.g., HEp-2 and HEL) that are poor transgene expressers.

21 l IFN stimulated genes (ISGs) in HEL-299 and HEL-TERT cells.

22 g white lysozyme (HEL) antibody HyHEL-63 and HEL.

23 lass I cross-presentation of soluble HEL and HEL in late endosomal liposomes.

24 ed cells in recipients injected with PTX and HEL were substantially reduced by treatment with Abs aga

25 s infection alone induced no detectable anti-HEL, subsequent RBC transfusion induced 100- to 1000-fol

26 In mice transgenic for soluble HEL, anti-HEL B cells capable of editing showed evidence for both

27 bility of HEL-conjugated VLPs to induce anti-HEL Abs in tolerant mice was dependent on the presence o

28 nsfusion induced 100- to 1000-fold more anti-HEL in mice that had been previously infected compared w

29 HEL stimulation in presence of soluble anti-HEL IgM antibodies.

30 membrane HEL in a setting in which the anti-HEL L chain was "knocked-in" at the endogenous L chain l

31 ese three antibodies with the native antigen HEL and with Japanese quail egg white lysozyme (JQL), a

32 Immunization with multivalent VLP-arrayed HEL, but not a trivalent form of HEL, induced high-titer

33 ling energy, 3.0 kcal/mol, was found between HEL residue Lys97 and HyHEL-63 residue V(H)Asp32, which

34 entarity-determining regions but still binds HEL with nanomolar affinity by means of a binding interf

35 C subsets in the presentation of blood-borne HEL.

36 ee HEL in different crystal forms onto bound HEL in the wild type and mutant HyHEL-63/HEL complexes r

37 in cultures of naive CD4 cells activated by HEL/APC.

38 and downstream signaling in HEL92.1.7 cells (HEL) and primary cells from polycythemia vera (PV) patie

39 In addition, human erythroleukaemic cells (HEL cells) were used as a model for erythroid precursor

40 differentiated human erythroleukemia cells (HEL) using SEEL using the sialyltransferases ST6Gal1 and

41 utant viruses in human embryonic lung cells (HEL) or HEK293T cells derived from normal tissues.

42 present Ag despite low levels of circulating HEL.

43 (3MA) blocked presentation of citrullinated HEL peptides, but presentation of unmodified peptides wa

44 In in vitro studies, VLP-conjugated HEL was more potent than trivalent HEL in up-regulating

45 repeated encounters between TgB cells and DC-HEL that are best described by a "kiss-run and engage" m

46 ed at contact sites between TgB cells and DC-HEL, and both cell types rearranged their actin cytoskel

47 ) transgenic mice and DC pulsed with HEL (DC-HEL) in collagen matrices.

48 secretion in Stat6-sufficient and deficient HEL-Ig mice.

49 MHC class II processing of a GILT-dependent HEL epitope.

50 MHC class II processing of a GILT-dependent HEL epitope.

51 IFI16 is stable in STING-depleted HEL cells infected with wild-type virus.

52 -specific antibodies reactive with different HEL epitopes significantly increased the suppressive eff

53 mature features and in both cases displayed HEL peptides as well as SDS-stable MHC class II molecule

54 ainst modifications of a chemically dominant HEL peptide as well as a minor HEL peptide, bound to the

55 E/HEL-Tg mice produced antibody in response to antigen, in

56 In addition, E/HEL-Tg mice produced more antibody and an increased perc

57 MP2A allows B cells to respond to antigen, E/HEL-Tg mice were immunized with hen egg lysozyme.

58 ls that are specific for hen egg lysozyme (E/HEL-Tg).

59 body responses in vivo and in vitro in the E/HEL-Tg system.

60 Eleven HEL residues in contact with HyHEL-63 in the crystal str

61 roid ratio in the bone marrow by eliminating HEL cell engraftment in this tissue.

62 In contrast, liposome-encapsulated HEL targeted to early endosomes entered the MHC class I

63 e JAK2(V617F)-positive human erythroleukemia HEL cell line.

64 tate (PMA)-stimulated human erythroleukemia (HEL) and CHRF 288-11 cells, which have megakaryocytic ch

65 Jak2-V617F expressing human erythroleukemia (HEL) cell line by promoting marked cell cycle arrest and

66 When the human erythroleukemia (HEL) cell line is induced to differentiate with 12-O-tet

67 nous alphaIIbbeta3 in human erythroleukemia (HEL) cells and beta1 integrin activation in macrophage-l

68 d human platelets and human erythroleukemia (HEL) cells, which express integrin alphaIIbbeta3, to inv

69 JAK2V617F-expressing human erythroleukemia (HEL) cells.

70 e marrow-derived DC also processed exogenous HEL.

71 cytomegalovirus (MCMV) engineered to express HEL induced extensive proliferation of transferred naive

72 RhHEL-Tg mice expressed HEL mRNA in their thymus, and the tolerogenic mechanism

73 ic, inducing inflammation in eyes expressing HEL.

74 s and induce inflammation in eyes expressing HEL.

75 etermined by the ability of LMP2A-expressing HEL-specific B cells to proliferate and induce NF-kappaB

76 B lymphoma-expressing HEL cells presented citrullinated peptides only after br

77 are injected into recipient mice expressing HEL in their eyes.

78 ) peptide were injected into mice expressing HEL on beta cells and the other using T cells in the non

79 Tg mice expressing HEL under control of the rhodopsin promoter (RhHEL-Tg) w

80 Tg mice expressing HEL under control of the rhodopsin promoter develop a to

81 In transgenic mice expressing HEL, the T cells to the modified epitopes escaped negati

82 mice were also mated with Tg mice expressing HEL-specific receptor on their T lymphocytes and the dou

83 h wild-type polyoma virus or RBCs expressing HEL alone.

84 g., HEp-2, human embryonic lung fibroblasts (HEL), and HeLa] and low in others (e.g., Vero cells).

85 d affinity difference, superposition of free HEL in different crystal forms onto bound HEL in the wil

86 trast, type A pMHC complexes are formed from HEL protein in late vesicles after editing by H2-DM.

87 n contrast, presentation of type A pMHC from HEL and from peptide was minimally affected by TLR ligan

88 mechanisms of generation of type B pMHC from HEL protein with TLR stimulation did not involve H2-DM o

89 at type B pMHC complexes were presented from HEL protein only after stimulation of dendritic cells (D

90 pMHC complexes, which are not presented from HEL.

91 uclease (NUC) domains and the AddA helicase (HEL) domain by site-directed mutagenesis.

92 .5, or IE9 proteins during infection of HFF, HEL, or U373MG cells.

93 ot form a salt bridge in any of the three HH-HEL complexes.

94 ray structure of the well-characterized HH10-HEL complex as template.

95 xes, and the x-ray crystal structure of HH10-HEL complex.

96 exes: theoretical models of HH8-HEL and HH26-HEL complexes, and the x-ray crystal structure of HH10-H

97 that HH8-HEL has the lowest number and HH26-HEL has the highest number of intra- and intermolecular

98 ot networked, and are weak, whereas, in HH26-HEL, an intramolecular salt-bridge triad at the binding

99 The modeled HH26-HEL structure predicts the recently determined x-ray str

100 tes in the intermolecular pentad in the HH26-HEL complex.

101 The binding site salt bridges in HH8-HEL are not networked, and are weak, whereas, in HH26-HE

102 7 forms an intermolecular salt bridge in HH8-HEL, and participates in the intermolecular pentad in th

103 protein complexes: theoretical models of HH8-HEL and HH26-HEL complexes, and the x-ray crystal struct

104 Our results show that HH8-HEL has the lowest number and HH26-HEL has the highest n

105 By using murine FDC-P1-EPOR and human HEL and SET-2 cell lines, we found that JAK2(V617F)-indu

106 Murine (32D, M1) and human (HEL, U937, and UKE-1) leukemic cell lines and freshly is

107 Using CCR7(-/-)Ig(HEL)-transgenic B cells we find that localization to the

108 ficant suppression of JAK/STAT activation in HEL cells at a concentration equivalent to that seen in

109 e kinase following FcgammaRIIA activation in HEL cells.

110 negative selection and regulatory T cells in HEL TCR transgenic mice, indicating a redundant role of

111 Surprisingly, knocking-down EpoR in HEL cells did not alter Akt activity or cell adhesion to

112 ther phorbol 12,13-dibutyrate or ethanol, in HEL cells endogenously expressing AC7, was not through t

113 When expressed in HEL cells, T482A/S484A kindlin-3 decreased soluble ligan

114 ell lines, inhibition of colony formation in HEL cells, and analysis of apoptosis.

115 High levels of Rap1-GTP were found in HEL and BaF3 cells expressing JAK2V617F compared with Ba

116 -1 ICP0 mutant was inhibited by IFN-gamma in HEL-30 cells and was less effective than wild-type virus

117 in viral late gene expression and growth in HEL cells, despite having distinctly different effects o

118 rs of CD8alpha(+) cDCs, were not impaired in HEL presentation by I-A(k) molecules of thymic APCs.

119 ) Th9 cells induced moderate inflammation in HEL-expressing recipient eyes but only when producing hi

120 of four model IFN stimulated genes (ISGs) in HEL-299 and HEL-TERT cells.

121 while it was observed both early and late in HEL cells.

122 eased with time and was considerably less in HEL cells than in Vero cells.

123 iency of SEEL for both sialyltransferases in HEL cells was greatly increased with prior neuraminidase

124 ion in Vero cells, but only at late times in HEL cells.

125 of IE19 protein expression in HCMV-infected HEL cells.

126 All thymic APCs acquired the injected HEL, with the plasmacytoid dendritic cell being the best

127 ues 476-485 of kindlin-3 was introduced into HEL cells and platelets; adhesion and spreading of both

128 he majority of newly generated MHC-II I-A(k)-HEL(46-61) complexes are expressed in sub-100-nm microcl

129 We now show that stimulatory MHC-II I-A(k)-HEL(46-61) complexes that move from intracellular antige

130 In this study, we showed that keratinocytes (HEL-30) were refractory to IFN-gamma induction of an ant

131 In this model, wild-type MCMV, lacking HEL, did not induce overt uveitis, suggesting that disea

132 The latter HEL result is higher than elastic limits for any BMG rep

133 results indicating a Hugoniot Elastic Limit (HEL) to be 8.58 +/- 0.53 GPa for SAM2X5-600 and 11.76 +/

134 tant-expressing erythroid leukemia cell line HEL with a small molecule Jak2 inhibitor was associated

135 hly expressed HLA-A, -B, -C, and -DRB1 loci (HEL) is associated with worse outcomes in hematopoietic

136 tured cells, including human embryonic lung (HEL) cells, we used our engineered viral mutants to map

137 T) gene into a primary human embryonic lung (HEL-299) cell strain, which is known to respond to the t

138 A mouse model utilizing hen egg lysozyme (HEL) "anergic" B cells was studied.

139 ressing high affinity anti-hen egg lysozyme (HEL) Ag receptors exposed in vivo to membrane HEL in a s

140 ble-transgenic for soluble hen egg lysozyme (HEL) and an Ig that recognizes HEL with a high affinity

141 express a soluble form of hen egg lysozyme (HEL) and in which B cell tolerance to HEL is maintained

142 genic Th cells specific to hen egg lysozyme (HEL) are adoptively transferred to recipients and induce

143 ransgenic mice specific to hen egg lysozyme (HEL) are polarized with IL-6/TGF-beta and, concurrently,

144 mHEL mice express surface hen egg lysozyme (HEL) as a transmembrane protein.

145 e to low levels of soluble hen egg lysozyme (HEL) both in vivo and in vitro as determined by the abil

146 SLPI and to both human and hen egg lysozyme (HEL) but not to lactoferrin.

147 h express BCRs specific to hen egg lysozyme (HEL) display diminished responsiveness to HEL stimulatio

148 complement fragment C3d to hen egg lysozyme (HEL) enhanced the immunogenicity of HEL 10,000-fold.

149 ossing STAT5b-CA mice with hen egg lysozyme (HEL) H chain transgenic mice.

150 families of peptides from hen egg lysozyme (HEL) presented by MHC class II I-A(k) molecules.

151 imaged B cells (TgB) from hen egg lysozyme (HEL) transgenic mice and DC pulsed with HEL (DC-HEL) in

152 specific B cells in Ig(Tg) hen egg lysozyme (HEL) transgenic mice inhabit the spleen but undergo AICD

153 transgenic mice expressing hen egg lysozyme (HEL) under a retina-specific promoter.

154 ance in Tg mice expressing hen egg lysozyme (HEL) under control of the rhodopsin promoter.

155 D4 cells, specific against hen egg lysozyme (HEL), are injected into recipient mice expressing HEL in

156 nized with pDNA encoding a hen egg lysozyme (HEL)-IgFc fusion protein (JwHEL)+JwIL4 and pIL10 or left

157 ersistent cross-linking of hen egg lysozyme (HEL)-specific B cell membrane Ig (mIg) in double transge

158 ary B cells that express a hen egg lysozyme (HEL)-specific BCR, we found that oligomeric HEL more eff

159 eon cytochrome c (PCC) and hen egg lysozyme (HEL).

160 ng disulfide bonds such as hen egg lysozyme (HEL).

161 ace between the anti-hen egg white lysozyme (HEL) antibody HyHEL-63 and HEL.

162 ide from the protein hen egg white lysozyme (HEL) generates different conformational isomers of the p

163 e created expressing hen egg-white lysozyme (HEL) in a pancreas-specific fashion.

164 d II presentation of hen egg-white lysozyme (HEL) in different forms, soluble and liposome encapsulat

165 mprey immunized with hen egg white lysozyme (HEL) in unbound and antigen-bound forms.

166 bound peptides from hen egg white lysozyme (HEL) injected intravenously.

167 tured series of anti-hen egg white lysozyme (HEL) mouse IgG1, were constructed with either complete o

168 cells specific for a hen-egg white lysozyme (HEL) peptide were injected into mice expressing HEL on b

169 ng residues 48-61 of hen egg white lysozyme (HEL) presented by I-A(k) gives rise to two T cell popula

170 the 48-62 epitope of hen egg white lysozyme (HEL) presented by I-A(k).

171 mmunization with the hen egg-white lysozyme (HEL) protein induces T cells to various of its peptide d

172 ssing of the protein hen egg-white lysozyme (HEL) resulted in citrullination of peptides presented on

173 main in complex with hen egg-white lysozyme (HEL) reveals a minimal antigen-binding domain that conta

174 the same epitope on hen egg white lysozyme (HEL), and share >90% sequence homology.

175 tides of the protein hen egg-white lysozyme (HEL), consisting of nitration of tyrosines and modificat

176 cterized epitopes on hen egg white lysozyme (HEL).

177 of the model protein hen egg white lysozyme (HEL).

178 cells to their target Ag, hen egg lysozyme [HEL] and APCs).

179 o another TCR system (anti-hen egg lysozyme [HEL] TCR/HEL mice) where similarly extensive thymic dele

180 pressing a B-cell epitope (hen egg lysozyme [HEL]) fused to (OVA)(323-339).

181 xpressing the HOD antigen (hen egg lysozyme [HEL]-ovalbumin-human transmembrane Duffy(b)) were transf

182 that are (insulin) or not (hen egg lysozyme; HEL) expressed by ss-cells have proven useful in dissect

183 In the 8/8 matched HEL group, LEL mismatches were not associated with any a

184 EL) Ag receptors exposed in vivo to membrane HEL in a setting in which the anti-HEL L chain was "knoc

185 required for editing in response to membrane HEL was approximately 6 h.

186 ally dominant HEL peptide as well as a minor HEL peptide, bound to the class II histocompatibility mo

187 n culture or in vivo, generated the modified HEL epitopes that stimulated the T cells.

188 ouble Tg mice that also express a monoclonal HEL-specific BCR.

189 A blend of monoclonal HEL-specific antibodies reactive with different HEL epit

190 o the HOD antigen, whereas single-monoclonal HEL antibodies were less effective despite the use of sa

191 Although monomeric HEL efficiently engages the BCR, presentation of HEL-der

192 than did monovalent HEL, although monovalent HEL, unlike monovalent Fab fragments of anti-Ig, readily

193 tion and internalization than did monovalent HEL, although monovalent HEL, unlike monovalent Fab frag

194 Adoptively transferred naive HEL-specific CD4(+) T cells proliferated in the eye drai

195 rated in vivo after immunization with native HEL molecules or were generated ex vivo by peroxynitrite

196 to foreign epitopes on VLPs, the ability of HEL-conjugated VLPs to induce anti-HEL Abs in tolerant m

197 Activation of HEL-specific T cells allows them to secrete IFN-gamma an

198 to thymic expression of minuscule amounts of HEL.

199 CK2 inhibitors potently induce apoptosis of HEL cells and PV cells.

200 ne or together with selected combinations of HEL-specific antibodies, and the resulting suppressive e

201 lymphocyte response to low concentrations of HEL.

202 hese mice was shown to be thymic deletion of HEL-specific T cells by the following observations in th

203 h lines of double-Tg mice showed deletion of HEL-specific T cells, demonstrated by reduction in numbe

204 senting both major and minor determinants of HEL over a 100-fold range of Ag dose, and 3) that B cell

205 egrinbeta3 and CD44, upon differentiation of HEL cells to adherent megakaryocytes.

206 Such DC showed a slight enhancement of HEL catabolism, but peptide release was not evident.

207 parently as a result of thymic expression of HEL and deletion of T cells specific to this antigen.

208 VLP-arrayed HEL, but not a trivalent form of HEL, induced high-titer Ab responses against HEL in both

209 marrow chimeras indicates that both forms of HEL are produced by irradiation-resistant thymic stromal

210 ysozyme (HEL) enhanced the immunogenicity of HEL 10,000-fold.

211 RmHP.111 mice had levels of HEL per cell similar to that of the established ILK-3 st

212 High levels of HEL were expressed in the eye compared to low expression

213 se two lines of Tg mice with the 3A9 line of HEL-specific TCR Tg mice, to produce double-Tg mice.

214 unized with HEL results in selective loss of HEL antigen from donor RBCs without affecting other bloo

215 i by the TUNEL assay, as well as for loss of HEL-specific T cells, by flow cytometry and proliferativ

216 d109 genomes at late times postinfection of HEL cells.

217 The presence of HEL mRNA in mouse thymi was determined by RT-PCR.

218 Cross-presentation of HEL in early endosomal liposomes had several unique feat

219 together, MHC class I and II presentation of HEL occurred through pathways having distinct molecular

220 efficiently engages the BCR, presentation of HEL-derived epitopes is impaired compared to oligovalent

221 generated intracellularly upon processing of HEL from that formed with exogenous peptide.

222 lls that see the peptide after processing of HEL, need to recognize all three TCR contact residues.

223 oarrays to examine the transcript profile of HEL cells after induction of MEF expression.

224 The residues of HEL (Tyr20, Lys96, and Lys97) most important for binding

225 clusters that juxtapose hot spot residues of HEL, resulting in energetic complementarity across the i

226 Stimulation of HEL cells with agonists significantly increased kindlin-

227 imed type B T cells in vivo, and transfer of HEL-bearing allogeneic dendritic cells activated type B

228 In contrast, treatment of HEL cells with the antioxidant N-acetylcysteine decrease

229 erated ex vivo by peroxynitrite treatment of HEL.

230 (HEL)-specific BCR, we found that oligomeric HEL more efficiently promoted both BCR activation and in

231 Furthermore, oligovalent HEL induced more pronounced rearrangement of MHC class I

232 Soluble HEL or HEL targeted to a late endosomal compartment only allowe

233 ed for their ability to recognize insulin or HEL as foreign, rather than autoantigens.

234 Polyclonal HEL antibodies dramatically inhibited the antibody respo

235 The immature DC from spleen processed HEL and displayed the chemically dominant epitope as evi

236 egg lysozyme (HEL) and an Ig that recognizes HEL with a high affinity to characterize the mechanisms

237 ly reduced in its replication in restrictive HEL-299 cells and murine embryonic fibroblasts (MEFs).

238 We show that the resulting HEL-TERT cell line is capable of replicating beyond 100

239 her transgenic mouse (ML-5) containing serum HEL also showed the ability to process and present Ag de

240 Soluble HEL or HEL targeted to a late endosomal compartment only

241 ter Ab responses against HEL in both soluble HEL Tg mice and double Tg mice that also express a monoc

242 double transgenic mice that express soluble HEL as a self Ag (HEL-Ig mice) decreases B cell mIgM exp

243 EL transgenic mice that also express soluble HEL, lack of Itpkb converts anergy induction to deletion

244 In mice transgenic for soluble HEL, anti-HEL B cells capable of editing showed evidence

245 ed MHC class I cross-presentation of soluble HEL and HEL in late endosomal liposomes.

246 enic signal induced by low levels of soluble HEL.

247 rrying the BCR-specific IgHEL and/or soluble HEL (sHEL) transgenes were generated by breeding IgHEL-t

248 tic APCs from RmHP.111 x 3A9 mice stimulated HEL-reactive cells to a much greater degree than those f

249 TCR system (anti-hen egg lysozyme [HEL] TCR/HEL mice) where similarly extensive thymic deletion also

250 HC complexes, we find the following: 1) that HEL in the draining lymph node gets concentrated in a li

251 The HEL cell line, in which constitutive JAK/STAT pathway ac

252 The HEL transgene enforces allelic exclusion, preventing rea

253 train-softening, retains strength beyond the HEL.

254 r, whereas HEL-specific T cells dominate the HEL-flu inflammatory site in the lung.

255 corporation lowered binding affinity for the HEL antigen.

256 imulated with LPS or when separated from the HEL-presenting cells by a semipermeable membrane.

257 istidine complexes, were much greater in the HEL cells than in the erythrocyte.

258 circulation and initiate inflammation in the HEL-expressing recipient eyes.

259 tified according to number of matches in the HEL.

260 emarkable reduction in the proportion of the HEL-specific T cells, and (3) loss of lymphocyte respons

261 odies that block each other's binding to the HEL protein did not increase suppression.

262 te differential tolerogenic effects of these HEL forms on B cells specific to this Ag.

263 HH8 binding to HEL is least sensitive toward mutations in the epitope a

264 plasma cells after immunization compared to HEL-Tg littermates, suggesting that LMP2A increased the

265 In contrast to HEL cells, IFI16 was undetectable in STING-depleted HEp-

266 similar to findings in culture, exposure to HEL in these eyes arrested the IL-9 production in Th9 ce

267 f endogenous expression in HL-60 relative to HEL and CHRF.

268 well as by reduced proliferative response to HEL in vitro.

269 by reduced cellular and humoral responses to HEL, as well as by the failure of ocular inflammation to

270 e (HEL) display diminished responsiveness to HEL stimulation in presence of soluble anti-HEL IgM anti

271 ozyme (HEL) and in which B cell tolerance to HEL is maintained by anergy.

272 RhHEL-Tg mice developed tolerance to HEL, shown by reduced cellular and humoral responses to

273 5, which represent less than 1% of the total HEL peptides.

274 By tracking HEL, and the ensuing peptide/MHC complexes, we find the

275 ith Listeria monocytogenes of the transgenic HEL mice generated APC containing the modifications.

276 er model of lysozyme-specific Ig transgenic (HEL immunoglobulin transgene (MD4) strain) B cells.

277 onjugated HEL was more potent than trivalent HEL in up-regulating surface activation markers on purif

278 ins detected varies between undifferentiated HEL cells and those differentiated to megakaryocytes, wi

279 orylation in the presence of JAK2V617F using HEL and BaF3 cell lines as well as RBCs from patients wi

280 induced by JAK2 inhibition in JAK2 V617F(+) HEL and SET-2 cells.

281 ted with HEL epitope-tagged influenza virus (HEL-flu).

282 Moreover, immunization with VLP-HEL reversed B cell anergy in vivo in an adoptive transf

283 ) induced, in vivo, complete deletion of VLR(HEL)Tmu-expressing B cells.

284 The VLRA-HEL complex demonstrates that certain VLRAs, like gammad

285 ppressed to a similar degree in STAT5b-CA vs HEL mice.

286 - and ethylene-dependent RNAs (PDF1.2, VSP1, HEL, THI2.1, FAD3, ERS1, ERF1) were repressed or not mod

287 When HEL cells were stimulated with thrombopoietin or phorbol

288 -BCG inflammatory site in the liver, whereas HEL-specific T cells dominate the HEL-flu inflammatory s

289 abundant in the liver than the lung, whereas HEL-flu infection is localized to the lung.

290 pathogenicity, however, when cocultured with HEL/APC.

291 id develop in recipient mice coinjected with HEL and any one of the seven TLR ligands.

292 esponding crystal structures in complex with HEL were essentially indistinguishable from the unsubsti

293 ex, and 10 HyHEL-63 residues in contact with HEL, were individually truncated to alanine in order to

294 and, concurrently, are activated either with HEL presented by APCs, or with anti-CD3/CD28 Abs.

295 lammation to develop after immunization with HEL.

296 fusion of mHEL RBCs into mice immunized with HEL results in selective loss of HEL antigen from donor

297 gged BCG (PCC-BCG) and acutely infected with HEL epitope-tagged influenza virus (HEL-flu).

298 Treatment of recipient mice with HEL alone stimulated proliferation of the transferred ce

299 yme (HEL) transgenic mice and DC pulsed with HEL (DC-HEL) in collagen matrices.

300 In B6.Sle2(z)HEL(Ig).sHEL BCR-transgenic mice, Sle2(z) did not breach