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 Beryllium-7 has two advantages: First, this radionuclide

21 Second, beryllium-7 is a product of cosmic rays which are themse

22 This study shows whether beryllium-7 observed concentration changes are correlate

23 genic radionuclide measured at ground-level, beryllium-7, is utilized as a proxy to study atmospheric

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

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

26 The microstructural response of beryllium after neutron irradiation at various temperatu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 h known toxicity (antimony, arsenic, barium, beryllium, cadmium, cesium, lead, mercury, platinum, tha

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

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

60 ene], prepared by oxidation of a zero-valent beryllium complex with 2,2,6,6-tetramethylpiperidin-1-ox

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

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

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

64 These deuterons impinge on a beryllium converter to generate neutrons.

65 the high-energy deuteron bombardment of the beryllium converter.

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

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

68 The beryllium dimer has puzzled chemists for roughly 80 year

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

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

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

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

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

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

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

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

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

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

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

80 Chronic beryllium disease (CBD) is a hypersensitivity granulomat

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

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

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

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

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

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

87 Chronic beryllium disease (CBD) is characterized by granulomatou

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

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

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

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

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

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

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

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

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

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

98 Chronic beryllium disease is a lung disorder caused by beryllium

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

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

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

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

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

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

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

106 Chronic beryllium disease results from beryllium exposure in the

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

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

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

110 mong BAL cells of patients with sarcoidosis, beryllium disease, and hypersensitivity pneumonitis.

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

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

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

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

115 ify both beryllium sensitization and chronic beryllium disease.

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

117 response to beryllium and in progression to beryllium disease.

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

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

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

121 (95% CI: 0.48 to 2.46, p = 0.56) for the non-beryllium-exposed controls.

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

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

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

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

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

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

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

129 Beryllium exposure can lead to the development of beryll

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

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

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

133 Beryllium exposure in the workplace can result in chroni

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 upon addition of the phosphomimetic compound beryllium fluoride.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

203 nstrate our method experimentally with three beryllium ions.

204 Beryllium is associated with a human pulmonary granuloma

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

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

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

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

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

210 The beryllium lymphocyte proliferation test is the cornersto

211 The blood beryllium lymphocyte proliferation test is used in medic

212 A confirmed abnormal beryllium lymphocyte proliferation test without evidence

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

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

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

216 Lithium-beryllium metal hydrides, which are structurally related

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

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

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

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

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

222 ctron energy-loss spectroscopy, we show that beryllium oxide crystallizes in the planar hexagonal str

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 Herein we report a paramagnetic beryllium radical cation, [(CAAC)(2)Be](+*) (2) [CAAC =

233 ck charged radical and the first crystalline beryllium radical.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

253 nd BAL cells from patients with sarcoidosis, beryllium sensitivity, or hypersensitivity pneumonitis a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 -4Ig that inhibited the CD28-B7 interaction, beryllium-specific CD4+ T cells in lung were still able

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

298 The response to beryllium was nearly completely and selectively blocked

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