ライフサイエンスコーパス: beryllium

1 rtain HLA-DP alleles allowed presentation of beryllium.

2 electively expanded by a common Ag involving beryllium.

3 ed by the reaction of CD4 T cells to inhaled beryllium.

4 ra deposits using concentrations of meteoric beryllium-10 ((10)Be) adhered to paleolake sediments fro

5 Beryllium-10 (10Be) in excess of that expected from in s

6 We used 115 cosmogenic beryllium-10 ages and 70 radiocarbon ages to constrain t

7 e show that the cosmic ray-produced nuclides beryllium-10 and aluminum-26 can be used to date tills t

8 tes of the cosmogenic nuclides carbon-14 and beryllium-10 and centennial to millennial time scale cha

9 The now extinct short-lived radionuclides beryllium-10 and, possibly, manganese-53 that were prese

10 Beryllium-10 concentrations in soils from the western So

11 Carbon-14 and published beryllium-10 data together suggest that concurrent clima

12 thought, based on 106 cosmogenic ages (from beryllium-10 dating) from moraines in Peru and Bolivia.

13 rial dating with cosmogenic aluminium-26 and beryllium-10 to show that the breccia containing StW 573

14 cosmogenic nuclide production (carbon-14 and beryllium-10) that is thought to reflect variations in s

15 tions of atmospherically produced cosmogenic beryllium-10, carbon, and nitrogen to show that ancient

16 dicative of the in situ decay of short-lived beryllium-10.

17 e particle fluence inferred from the initial beryllium-10/beryllium-9 is sufficient to produce other

18 of the singly ionized radioactive isotope of beryllium, (7)Be, in the near-ultraviolet spectra of the

19 lead ((210)Pb and total Pb), and cosmogenic beryllium-7 ((7)Be) measurements in organic (O) soil hor

20 mas contained 10(5) to 10(6) single-positive beryllium-9 ions (9Be+) at particle densities of 10(8) t

21 uence inferred from the initial beryllium-10/beryllium-9 is sufficient to produce other short-lived n

22 s to that of the particle-reactive tracer (7)beryllium, a consequence of the radionuclides' shared so

23 D4+ T cells, but do so in the absence of the beryllium Ag.

24 regeneration in vivo Moreover, we show that beryllium also inhibits cell migration in vitro using ax

25 the past 7.5 million years, as indicated by beryllium and aluminium isotopes ((10)Be and (26)Al) in

26 d on new measurements of cosmic-ray-produced beryllium and aluminium isotopes ((10)Be and (26)Al) in

27 ated with GDP and gamma-phosphate analogues (beryllium and aluminum fluoride) or when dialyzed into g

28 production of other light elements, such as beryllium and boron, so observations of lithium isotopic

29 ung disorder caused by a hypersensitivity to beryllium and characterized by the accumulation of beryl

30 otype is important in the immune response to beryllium and in progression to beryllium disease.

31 ase (CBD) is caused by workplace exposure to beryllium and is characterized by the accumulation of me

32 characterize the interaction among HLA-DP2, beryllium, and CD4+ T cells, we constructed rHLA-DP2 and

33 facility; and (2) 50 participants from a non-beryllium-associated workplace.

34 nstrate quantum error correction using three beryllium atomic-ion qubits confined to a linear, multi-

35 ed by affixing bridging atoms to attract the beryllium atoms electrostatically or covalently.

36 monolayer, each carbon atom binds with five beryllium atoms in almost the same plane, forming a quas

37 -metal distances (1.728-1.866 A) between two beryllium atoms in different molecular environments, inc

38 nable the synthesis of a broad new family of beryllium-based frameworks with extremely high surface a

39 The first crystalline beryllium-based metal-organic framework has been synthes

40 activated (GTP-bound) form of Cdc42 and that beryllium (Be) can replace aluminum in mediating fluorid

41 Chronic beryllium (Be) disease (CBD) is a multisystem granulomat

42 Chronic beryllium (Be) disease is a granulomatous lung disorder

43 (CBD) is a fibrotic lung disorder caused by beryllium (Be) exposure and is characterized by granulom

44 pecific lymphocyte proliferative response to beryllium (Be) with gamma interferon (IFN-gamma) release

45 ivity of the light elements lithium (Li) and beryllium (Be), which are the first of the metals in the

46 Beryllium (Be)-antigen stimulates tumor necrosis factor-

47 disease characterized by the accumulation of beryllium (Be)-specific CD4(+) T cells in bronchoalveola

48 atous disorder characterized by an influx of beryllium (Be)-specific CD4(+) T cells into the lung.

49 The beryllium (BeF(x)) and aluminium (AlF(4)(-)) containing

50 had a shorter median duration of exposure to beryllium before diagnosis of CBD, and tended to have a

51 cludes betaGlu69 and represents the putative beryllium-binding site.

52 magnetic resonance spectroscopy showed that beryllium binds to the HLA-DP2-derived molecule, with no

53 The carbene-stabilized beryllium borohydride monomer L:Be(BH(4))(2)2 is prepare

54 e carbonaceous chondrite are correlated with beryllium/boron in a manner indicative of the in situ de

55 Exposure to beryllium can lead to sensitization (BeS) and chronic be

56 ical method has been utilized to predict the beryllium chemical shifts of structurally characterized

57 ding spiro-bis(5-methyl-1,9-oxido-phenalenyl)beryllium compound ([2]2Be).

58 The structures of a series of beryllium containing complexes have been optimized at th

59 Medical surveillance in workplaces that use beryllium-containing materials can identify individuals

60 ot even with the very small hydrogen atom or beryllium dication.

61 Interestingly, beryllium did not act as an immunostimulatory agent as i

62 The beryllium dimer has puzzled chemists for roughly 80 year

63 e than 100 theoretical investigations of the beryllium dimer have been published, reporting a wide ra

64 The beryllium dimer is a deceptively simple molecule that, i

65 mple all the bound vibrational levels of the beryllium dimer molecule's electronic ground state.

66 me (ACE) genotype is associated with chronic beryllium disease (CBD) and disease severity, we studied

67 B1 gene (Glu(69)) is associated with chronic beryllium disease (CBD) and possibly beryllium sensitiza

68 ic and clinical similarities between chronic beryllium disease (CBD) and sarcoidosis suggest that sim

69 suggests a genetic predisposition to chronic beryllium disease (CBD) and sarcoidosis, which are clini

70 Chronic beryllium disease (CBD) is a fibrotic lung disorder caus

71 Chronic beryllium disease (CBD) is a granulomatous disorder char

72 Chronic beryllium disease (CBD) is a granulomatous lung disease

73 Chronic beryllium disease (CBD) is a granulomatous lung disorder

74 Chronic beryllium disease (CBD) is a hypersensitivity disorder c

75 Chronic beryllium disease (CBD) is a hypersensitivity granulomat

76 Chronic beryllium disease (CBD) is an occupational lung disorder

77 Chronic beryllium disease (CBD) is associated with the allelic s

78 Chronic beryllium disease (CBD) is caused by beryllium exposure

79 Chronic beryllium disease (CBD) is caused by exposure to berylli

80 Chronic beryllium disease (CBD) is caused by workplace exposure

81 Chronic beryllium disease (CBD) is characterized by a CD4+ T cel

82 Chronic beryllium disease (CBD) is characterized by granulomatou

83 Susceptibility to chronic beryllium disease (CBD) is linked to certain HLA-DP mole

84 Chronic beryllium disease (CBD) provides a human disorder in whi

85 CII allele, HLA-DP2, are at risk for chronic beryllium disease (CBD), a debilitating inflammatory lun

86 ecific granulomatous inflammation of chronic beryllium disease (CBD), and compared it with that in he

87 ies demonstrate associations between chronic beryllium disease (CBD), beryllium sensitization (BeS),

88 beryllium-specific CD4+ T cells and chronic beryllium disease (CBD), which is characterized by the p

89 ronchoalveolar lavage (BAL) cells in chronic beryllium disease (CBD).

90 can lead to sensitization (BeS) and chronic beryllium disease (CBD).

91 time between those who progressed to chronic beryllium disease and those who remained sensitized with

92 biopsies to determine progression to chronic beryllium disease as evidenced by granulomatous inflamma

93 ls with beryllium sensitization have chronic beryllium disease at the time of their initial clinical

94 Chronic beryllium disease is a lung disorder caused by beryllium

95 sion from beryllium sensitization to chronic beryllium disease is unknown.

96 ific TCRs derived from the lung of a chronic beryllium disease patient.

97 ryllium-specific CD4(+) T cells from chronic beryllium disease patients remain CD28-dependent, while

98 lar lavage (BAL) CD4(+) T cells from chronic beryllium disease patients to identify possible therapeu

99 blood and bronchoalveolar lavage of chronic beryllium disease patients up-regulate 4-1BB expression,

100 cell lines derived from the lungs of chronic beryllium disease patients, beryllium presentation to th

101 (+) T cells recruited to the lung in chronic beryllium disease recognize beryllium in an Ag-specific

102 Chronic beryllium disease results from beryllium exposure in the

103 Susceptibility to chronic beryllium disease, a granulomatous lung disease that app

104 osure in the workplace can result in chronic beryllium disease, a granulomatous lung disorder charact

105 for sarcoidosis and, in contrast to chronic beryllium disease, a non-E(69)-containing allele, HLA-DP

106 LA DPB1 locus, a SNP associated with chronic beryllium disease, as well as HLA DPA1 alleles using the

107 We studied this process in chronic beryllium disease, in which the frequency of antigen-spe

108 mmation in the lung of patients with chronic beryllium disease.

109 ould serve as a possible therapy for chronic beryllium disease.

110 ify both beryllium sensitization and chronic beryllium disease.

111 at position 69 (HLA-DPB1(Glu69)) in chronic beryllium disease.

112 response to beryllium and in progression to beryllium disease.

113 orted to be strongly associated with chronic beryllium disease.

114 forms) and aluminum (which can coelute with beryllium during cation exchange chromatography).

115 terval [CI]: 0.68 to 3.66, p = 0.12) for the beryllium-exposed control group, and 1.09 (95% CI: 0.48

116 We enrolled 502 BeS/CBD subjects and 653 beryllium-exposed controls from three beryllium industri

117 (95% CI: 0.48 to 2.46, p = 0.56) for the non-beryllium-exposed controls.

118 tained from BeS (n = 50), CBD (n = 104), and beryllium-exposed nondiseased (Be-nondiseased) (n = 125)

119 Continued research in the beryllium-exposed population will be important for impro

120 sensitization is an adverse health effect in beryllium-exposed workers and merits medical follow-up.

121 ), and compared this with the results for 82 beryllium-exposed workers with no evidence of BH.

122 y differences between the CBD patients and a beryllium-exposed, nondiseased control group.

123 s may have the Glu69 marker, about 30-45% of beryllium-exposed, unaffected individuals carry the same

124 Chronic beryllium disease (CBD) is caused by beryllium exposure and is characterized by granulomatous

125 Beryllium exposure can lead to the development of beryll

126 ryllium disease is a lung disorder caused by beryllium exposure in the workplace and is characterized

127 BD) is a hypersensitivity disorder caused by beryllium exposure in the workplace and is characterized

128 Chronic beryllium disease results from beryllium exposure in the workplace and is characterized

129 Beryllium exposure in the workplace can result in chroni

130 , sex, race or ethnicity, smoking status, or beryllium exposure time between those who progressed to

131 is to increase awareness and knowledge about beryllium exposure, BeS, and CBD.

132 Following beryllium exposure, CD4(+) T cells from blood and bronch

133 and that this drives the strongly insulating beryllium films into a low-temperature 'quantum metal' p

134 gate the electronic properties of disordered beryllium films, with the aim of disentangling the effec

135 rmus aquaticus (Taq) MutS, we found that ADP.beryllium fluoride (ABF), acted as a strong inhibitor of

136 R) domain bound to both a phosphoryl analog [beryllium fluoride (BeF(3)(-))] and Mg(2+), in complex w

137 Beryllium fluoride (BeF(3-)) and aluminum fluoride (AlF(

138 th phosphate analogs (PA), such as vanadate, beryllium fluoride (BeFx) or aluminum fluoride (AlF4-),

139 C4 (LTC(4)) significantly stimulated ABCC10 beryllium fluoride (BeFx)-sensitive ATPase activity.

140 omplexes with aluminum fluoride (E2.AlF) and beryllium fluoride (E2.BeF) as analogs of the E2.P phosp

141 The phosphate analogues beryllium fluoride and aluminum fluoride led to complete

142 e of bovine F1-ATPase inhibited with ADP and beryllium fluoride at 2.0 angstroms resolution contains

143 ha-32P]ADP.Vi and MRP4.8-azido[alpha-32P]ADP.beryllium fluoride can be generated, nucleotide trapping

144 resent the crystal structure of mant-ADP and beryllium fluoride complexed with Dictyostelium discoide

145 -nitrophenyl-N-methyl-aminoethyl-diphosphate.beryllium fluoride have been determined to better than 2

146 NAMPT structures with beryllium fluoride indicate a covalent H247-BeF(3)(-) as

147 ) only when Mg(2+)i was also present; and 4) beryllium fluoride induced maximal IH even in the absenc

148 ATP during hydrolysis in the same order with beryllium fluoride occurring earliest in the ATPase cycl

149 kinesin in the presence of substrate analogs beryllium fluoride or adenylyl-imidodiphosphate.

150 inhibitors, MRP4-ATPase is more sensitive to beryllium fluoride than to orthovanadate.

151 ing cleft closes slightly in the presence of beryllium fluoride trapped MgADP (MgADPBeFx-S1) and most

152 ligands (transported ions, nucleotides, and beryllium fluoride) on IH and, for comparison, on transi

153 With beryllium fluoride, but not phalloidin, this polymerizat

154 stored by larger amounts of wild-type actin, beryllium fluoride, or phalloidin at room temperature, a

155 aps nucleotide in the absence of vanadate or beryllium fluoride, the high to low affinity switch in t

156 ence of the non-hydrolyzable ATP analog, ADP-beryllium fluoride, we observe additional interactions b

157 und with the non-hydrolyzable ATP analog ADP-beryllium fluoride, we studied the NtrC1-sigma(54) AID c

158 to the basal state, particularly when using beryllium fluoride, which mimics the bound phosphate in

159 e specifically, as shown by vanadate-ADP and beryllium fluoride-ADP trapping experiments.

160 increases 8-azido[alpha-32P]ATP binding and beryllium fluoride-induced 8-azido[alpha-32P]ADP trappin

161 hibition 0.19 and 0.25 mm, respectively) and beryllium fluoride-induced 8-azido[alpha-32P]ADP trappin

162 esence of the nonhydrolyzable ATP analog ADP-beryllium fluoride.

163 trapping is approximately 4-fold higher with beryllium fluoride.

164 mm), which is inhibited by orthovanadate and beryllium fluoride.

165 cess using complexes of ADP and aluminium or beryllium fluoride.

166 tabilizers phalloidin and to a lesser extent beryllium fluoride.

167 C but will in the presence of phalloidin or beryllium fluoride.

168 or in the presence of the MgATPase inhibitor beryllium fluoride.

169 e 5'-triphosphate, and adenosine diphosphate beryllium fluoride.

170 upon addition of the phosphomimetic compound beryllium fluoride.

171 Maximal IH through beryllium-fluorinated NKA indicates that this complex mi

172 A new beryllium-free deep-ultraviolet (DUV) nonlinear optical

173 d harmonic generation (SHG) enabled by a new beryllium-free zincoborate-phosphate crystal is reported

174 on dose or cumulative exposures to asbestos, beryllium, hexavalent chromium, or nickel.

175 at, unlike its parent compound BeH2, lithium-beryllium hydride LiBeH3 exhibits a sharp increase in hy

176 rsensitivity granulomatosis characterized by beryllium hypersensitivity (BH) and mediated by CD4+ T c

177 fector memory T cell phenotype and recognize beryllium in a CD28-independent manner.

178 lung in chronic beryllium disease recognize beryllium in an Ag-specific manner and express Th1-type

179 D4(+) T cell lines specifically responded to beryllium in culture in the presence of antigen-presenti

180 iferate and secrete IFN-gamma in response to beryllium in culture.

181 during hydrolysis is 2.6 angstroms from the beryllium in the beta(DP) subunit and 3.8 angstroms away

182 Due to the persistence of beryllium in the lung after the cessation of exposure, a

183 llium disease (CBD) is caused by exposure to beryllium in the workplace, and it remains an important

184 ts demonstrate that in the presence of APCs, beryllium induced strong proliferation responses of BAL

185 addition of anti-PD-1 ligand mAbs augmented beryllium-induced CD4+ T cell proliferation, and an inve

186 on BAL T cells was associated with increased beryllium-induced cell death.

187 Thus, the PD-1 pathway is active in beryllium-induced disease and plays a key role in contro

188 Genetic susceptibility to beryllium-induced disease is strongly associated with HL

189 nd the ability of Treg cells to modulate the beryllium-induced granulomatous immune response.

190 te the role of coinhibitory receptors in the beryllium-induced immune response, we examined the expre

191 B ligand-4-1BB interaction partially blocked beryllium-induced proliferation of BAL CD4(+) T cells, a

192 LA-DR or anti-OX40 ligand Ab mainly affected beryllium-induced proliferation responses with little im

193 eting CD4 T cells in blood in the absence of beryllium-induced proliferation, and overall, the correl

194 ssion on beryllium-specific CD4+ T cells and beryllium-induced proliferation.

195 er costimulatory molecules are essential for beryllium-induced T cell function in the lung.

196 of CTLA-4 signaling in blood cells inhibited beryllium-induced T cell proliferation while having no e

197 disease and plays a key role in controlling beryllium-induced T cell proliferation.

198 nd 653 beryllium-exposed controls from three beryllium industries who gave informed consent for parti

199 otls to wild-type hosts, we demonstrate that beryllium inhibits fibroblast migration during limb and

200 antum Fourier transform in a system of three beryllium ion qubits (two-level quantum systems) confine

201 niversal geometric pi-phase gate between two beryllium ion-qubits, based on coherent displacements in

202 defined by two hyperfine ground states of a beryllium ion; the cat state corresponds to an entangled

203 lattice of hundreds of spin-half particles (beryllium ions stored in a Penning trap).

204 nstrate our method experimentally with three beryllium ions.

205 Beryllium is associated with a human pulmonary granuloma

206 helialization, suggesting that the effect of beryllium is cell type-specific.

207 ogenesis of CBD and provide insight into how beryllium is recognized in human disease.

208 g disease that appears in workers exposed to beryllium, is modified by genetic variants of the HLA-DP

209 ell death during regeneration in response to beryllium, it did disrupt cell proliferation in mesenchy

210 We evaluated the beryllium lymphocyte proliferation test (BeLPT), broncho

211 The beryllium lymphocyte proliferation test is the cornersto

212 The blood beryllium lymphocyte proliferation test is used in medic

213 A confirmed abnormal beryllium lymphocyte proliferation test without evidence

214 isease severity, including chest radiograph, beryllium lymphocyte proliferation, and spirometry.

215 s, consisting of: (1) 50 participants from a beryllium machining facility; and (2) 50 participants fr

216 The unique properties associated with beryllium metal ensures the continued use in many indust

217 Lithium-beryllium metal hydrides, which are structurally related

218 dy, we show that exposing amputated limbs to beryllium nitrate disrupts blastema formation and causes

219 f 1,3,5-benzenetribenzoic acid (H(3)BTB) and beryllium nitrate in a mixture of DMSO, DMF, and water a

220 A new standard for beryllium NMR in nonaqueous solvents has been suggested.

221 rast, exposing full-thickness skin wounds to beryllium only causes a delay in skin regeneration.

222 exposed mice transgenic (Tg) for HLA-DP2 to beryllium oxide (BeO) via oropharyngeal aspiration.

223 NIST) Standard Reference Material (SRM) 1877 Beryllium Oxide Powder.

224 e present in the involved skin of a positive beryllium patch test and thus mirror the granulomatous p

225 cted amounts of spiro-bis(9-oxidophenalenone)beryllium [PLY(O,O)]2Be leads to the formation of a seri

226 idue of the MHC class II beta-chain dictates beryllium presentation and potentially, disease suscepti

227 sting a critical role for this amino acid in beryllium presentation to Ag-specific CD4+ T cells.

228 Thus, we hypothesized that beryllium presentation to CD4+ T cells was dependent on

229 lungs of chronic beryllium disease patients, beryllium presentation to those cells was independent of

230 e residues of the DP beta-chain required for beryllium presentation.

231 ation and IL-2 secretion upon re-exposure to beryllium presented by APCs.

232 mobilization of large numbers of pathogenic beryllium-reactive T cells into the circulating pool.

233 ressing mutated HLA-DP2 and -DR13 molecules, beryllium recognition was dependent on the glutamic acid

234 y was to characterize activation pathways of beryllium-responsive bronchoalveolar lavage (BAL) CD4(+)

235 lation was observed between the frequency of beryllium-responsive bronchoalveolar lavage (BAL) CD4(+)

236 In this study, we show that the majority of beryllium-responsive CD4(+) T cells in BAL have lost CD2

237 In contrast, the frequency of beryllium-responsive CD4(+) T cells in the blood of thes

238 Beryllium-responsive CD4(+) T cells in the bronchoalveol

239 Beryllium-responsive CD4(+) T cells in the lung are CD28

240 g no effect on the proliferative capacity of beryllium-responsive CD4(+) T cells in the lung.

241 omatous inflammation and the accumulation of beryllium-responsive CD4(+) T cells in the lung.

242 ortant role of 4-1BB in the costimulation of beryllium-responsive CD4(+) T cells in the target organ.

243 ve lost CD27 expression, whereas a subset of beryllium-responsive cells in blood retains expression o

244 rmore, CTLA-4 expression was greatest in the beryllium-responsive subset of CD4(+) T cells that retai

245 Beryllium-responsive, HLA-DP2-restricted CD4(+) T cells

246 Enhanced proliferation of a beryllium-responsive, HLA-DP2-restricted T cell line was

247 gulate 4-1BB expression, and the majority of beryllium-responsive, IFN-gamma-producing CD4(+) T cells

248 rom control and CBD subjects to evaluate the beryllium salt-specific production of endogenous IL-10 a

249 ith CBD and normal individuals, we evaluated beryllium salt-stimulated T lymphocyte proliferation and

250 These cells respond vigorously to beryllium salts in culture by producing proinflammatory

251 Interestingly, beryllium salts interfered with an IL-10-stimulated decr

252 ons between chronic beryllium disease (CBD), beryllium sensitization (BeS), and HLA-DPB1 alleles with

253 chronic beryllium disease (CBD) and possibly beryllium sensitization (BeS).

254 sed in medical surveillance to identify both beryllium sensitization and chronic beryllium disease.

255 Approximately 50% of individuals with beryllium sensitization have chronic beryllium disease a

256 We conclude that beryllium sensitization is an adverse health effect in b

257 ation; however, the rate of progression from beryllium sensitization to chronic beryllium disease is

258 Fifty-five individuals with beryllium sensitization were monitored with a range of 2

259 Thirty-eight of the 55 (69%) remained beryllium sensitized without disease after an average fo

260 onchoalveolar lavage (BAL) CD4+ T cells from beryllium-sensitized and CBD subjects.

261 We monitored a cohort of beryllium-sensitized patients at 2-year intervals, using

262 in samples from bedrock fluvial terraces, 10-beryllium shows that both the Susquehanna and Potomac Ri

263 We have shown that circulating beryllium-specific CD4(+) T cells from chronic beryllium

264 and is characterized by the accumulation of beryllium-specific CD4(+) T cells in the lung and granul

265 ium and characterized by the accumulation of beryllium-specific CD4(+) T cells in the lung.

266 ine staining, we found that the frequency of beryllium-specific CD4(+) T cells in the lungs (bronchoa

267 es that complete the alphabetaTCR ligand for beryllium-specific CD4(+) T cells suggests a unique role

268 Using beryllium-specific CD4+ T cell lines derived from the lu

269 relation was seen between PD-1 expression on beryllium-specific CD4+ T cells and beryllium-induced pr

270 lium exposure can lead to the development of beryllium-specific CD4+ T cells and chronic beryllium di

271 In most CBD patients, the majority of beryllium-specific CD4+ T cells in blood expressed an ef

272 -4Ig that inhibited the CD28-B7 interaction, beryllium-specific CD4+ T cells in lung were still able

273 Exposure of beryllium-specific CD4+ T cells to BeSO4 -pulsed, plate-

274 In addition, pretreatment of beryllium-specific CD4+ T cells with BeSO4-pulsed, plate

275 direct correlation between the percentage of beryllium-specific CD4+ T(EM) cells in blood and T cell

276 Few, if any, beryllium-specific CD8(+) T cells were identified.

277 expressing molecules are capable of inducing beryllium-specific proliferation and IFN-gamma expressio

278 We isolated beryllium-specific T cell lines from the lungs of affect

279 in blood, with the highest expression on the beryllium-specific T cell subset.

280 B7 interaction markedly reduced responses of beryllium-specific T cells in blood.

281 at, in CBD, failure of IL-10 to modulate the beryllium-specific, cell-mediated immune response would

282 omatous inflammation and the accumulation of beryllium-specific, HLA-DP2-restricted CD4+ T lymphocyte

283 Our data demonstrate that beryllium-stimulated bronchoalveolar lavage cells produc

284 We conclude that, in the CBD-derived, beryllium-stimulated cell-mediated immune response, low

285 ss exogenous rhIL-10 partially inhibited the beryllium-stimulated production of IL-2, IFN-gamma, and

286 CD4+ T cells in blood of CBD patients after beryllium stimulation.

287 lood cells to proliferate in the presence of beryllium strongly correlated with the fraction expressi

288 We show here that when beryllium sulfate (BeSO(4)) was added during in vivo sen

289 xpressed a Th1-type phenotype in response to beryllium sulfate (BeSO(4)).

290 patients studied had a positive response to beryllium sulfate application and a negative patch test

291 Patch testing of CBD patients with beryllium sulfate results in granulomatous inflammation

292 to secrete Th1-type cytokines in response to beryllium, they showed less proliferative capacity and w

293 Overall, the DP alleles that presented beryllium to disease-specific T cell lines match those i

294 ability of these HLA-DP molecules to present beryllium to pathogenic CD4(+) T cells.

295 as as molecular switch was demonstrated by a beryllium trifluoride anion titration assay, which allow

296 addition of exogenous inorganic phosphate or beryllium trifluoride to ADP filaments, however, decreas

297 The response to beryllium was nearly completely and selectively blocked

298 of microtubules by displacing fluoride from beryllium was ruled out from the 9Be and 19F NMR spectra

299 A-DPB1 sequence motifs in current and former beryllium workers implicated a glutamic acid residue at

300 rmation for prospective, current, and former beryllium workers must be weighed against the potential