ライフサイエンスコーパス: OAS

1 OAS produces a unique oligonucleotide second messenger,

2 al gene, 2',5'-oligoadenylate synthetase 1a (OAS), were determined by real-time reverse-transcriptase

3 d expression of IFN-beta, IFN-lambda1/IL-29, OAS and viperin in asthmatics compared with healthy subj

4 We show that the induction of 2,5 OAS in response to IFN-gamma is BRCA1 and STAT1 dependen

5 -gamma-induced apoptosis is dependent on 2,5 OAS induction.

6 proliferation, transient transfection of 2,5 OAS into breast cancer cell lines results in decreased c

7 2,5 OAS is the only known upstream regulator of RNaseL, a re

8 targets, 2,5 oligoadenylate synthetase (2,5 OAS), is a mediator of BRCA1/IFN-gamma-induced apoptosis

9 IFN-gamma to transcriptionally activate 2,5 OAS, leading to the downstream activation of RNaseL and

10 ion, the expression of the IFN-inducible 2-5 OAS gene was significantly reduced in HUT78R cells, sugg

11 sis, we characterize the activation of 2'-5' OAS in lungs from mice exposed to CS and viral pathogen-

12 -5' oligoadenylate synthetase (OAS), a 2'-5' OAS-like (OASL) gene, galectin-9, myxovirus protein A (M

13 cells is to sequester dsRNA away from 2'-5' OAS.

14 ) and 2',5'-oligoadenylate synthetase (2',5'-OAS) were down-regulated in IFN-alpha-treated HEV-A549 c

15 N-alpha-stimulated genes encoding PKR, 2',5'-OAS, and myxovirus resistance A.

16 cells and induction of PD-1, PD-L1, and 2,5-OAS-1 in the liver.

17 levels of intrahepatic PD-1, PD-L1, and 2,5-OAS-1 messenger RNAs correlated with peak titers of HCV.

18 SG-15, ISG-54, ISG-56, ISG-60, STAT1, IRF-9, OAS, and Mx1.

19 eins, of which the major isoforms, OAS-TL A, OAS-TL B, and OAS-TL C, catalyze the formation of Cys by

20 e that sulfate reduction and O-acetylserine (OAS) production together limit cysteine synthesis.

21 present in PC3 cells that bind and activate OAS.

22 in 2 (PCBP2) that bind and potently activate OAS.

23 ion, as well as to provide dsRNA to activate OAS.

24 NA containing modified nucleosides activates OAS less efficiently and induces limited rRNA cleavage.

25 vitro transcribed, unmodified RNA activates OAS, induces RNase L-mediated ribosomal RNA (rRNA) cleav

26 actions capable of binding to and activating OAS.

27 We sequenced each exon within all OAS and RNASEL genes in 33 individuals hospitalized with

28 Our results indicate that higher IFN-alpha, OAS, CXCL9, and CXCL10 mRNA expression in LN was associa

29 e activation of endogenous p69-OAS and of an OAS-Luc reporter and a synergistic activation of a GAS-L

30 s, but our study shows that the OAS-TL A and OAS-TL B of both halophytes are enzymes that also degrad

31 ch pollen is a common sensitizing agent, and OAS results when patients consume certain fruits, vegeta

32 the major isoforms, OAS-TL A, OAS-TL B, and OAS-TL C, catalyze the formation of Cys by combining O-a

33 Furthermore, higher expression of CXCL10 and OAS in peripheral blood could potentially serve as a dia

34 d (v) 'no-panallergen PFS': mild disease and OAS triggered by kiwifruit.

35 d to 129 SvEv mice, while prolactin mRNA and OAS mRNA levels were suppressed.

36 interferon-stimulated gene produces MxA and OAS.

37 The immunologic surrogates, neopterin and OAS, were induced at all doses with a sustained concentr

38 NA and can prevent activation of the PKR and OAS pathways.

39 ons of host defense proteins such as PKR and OAS that have been previously synthesized and merely awa

40 emical analyses of recombinant plant SAT and OAS-TL indicate that the reversible association of the p

41 e interaction between mitochondrial SAT3 and OAS-TL C in planta by FRET and establish the role of the

42 s regulated by the CysE-dependent signal and OAS were identified in P. stuartii and E. coli.

43 inetic parameters for cysteine synthesis and OAS: acetate lyase activity yield, within error, identic

44 ons, deletions, or nonsense mutations in any OAS or RNASEL gene.

45 ar complex, which is the origin of assembly (OAS) in RCNMV that selectively recruits and orients CP s

46 ch pollen rhinoconjunctivitis and associated OAS to apple were included in an open, randomized, contr

47 ufficient to compensate for inadequate basal OAS levels.

48 that the Us11 protein is sufficient to block OAS activation in extracts from uninfected, interferon-t

49 malian cells depleted 2-5A levels induced by OAS activation with poly(rI):poly(rC), preventing RNase

50 the result of high l-Cys degradation rate by OAS-TLs, whereas the greater organic-S and biomass accum

51 efficient Cys synthesis than total cellular OAS-TL activity in leaves.

52 intravascular drug delivery, and controlled OAS treatment of calcific plaques resulted in greater dr

53 Compared to controls, OAS-treated femoropopliteal segments exhibited 180mum th

54 ed by pretreatment at pH 8.5, which converts OAS to NAS.

55 regulation of interferon-inducible cytokines OAS and CXCL10/IP-10 compared with control mice treated

56 A sequences of the rat, cattle, pig, and dog OAS genes were amplified, sequenced and compared with ea

57 While two tandemly duplicated OAS-like (OASL) genes were identified in the dog genome,

58 Products of the CysE enzyme (OAS, N-acetyl-L-serine [NAS], O-acetyl-L-threonine, and

59 ntitumor drug bleomycin produces exclusively OAS in the form of C-4-keto-C-1-aldehydes in unbroken DN

60 nes were detected in the pig genome and five OAS genes were found in both the cattle and dog genomes.

61 s compensated by an increase in affinity for OAS, leading to the observed second-order rate constant,

62 e to the WT and loss-of-function mutants for OAS-TLs in the cytosol, plastids, and mitochondria.

63 tegy based on stringent affinity of RNAs for OAS.

64 Four OAS genes were detected in the pig genome and five OAS g

65 e OASS-catalyzed elimination of acetate from OAS.

66 The elimination of acetic acid from OAS is thought to proceed via an anti-E2 mechanism, and

67 Furthermore, in the absence of a functional OAS pathway, corneal HSV-1 Ag expression was more widesp

68 wild-type mice or mice lacking a functional OAS pathway, these results suggest that PKR is the domin

69 that the presence of at least one functional OAS-TL isoform is essential for the proper function of t

70 ptional upregulation of IFN-responsive genes OAS and ISG54 (encoding 2'-5' oligoadenylate synthetase

71 red with CSC-bound SAT and explains the high OAS export rate of WT mitochondria in the presence of cy

72 -acetyl-serine(thiol)lyase (OASTL) homologs, OAS-B, which is an authentic OASTL, and CS26, which has

73 Three forms of human OAS have been described corresponding to proteins of 40/

74 of the gene encoding the large form of human OAS.

75 izing 2-5As and differs from the other human OAS family members by having two C-terminal ubiquitin-li

76 ed among the different isoforms of the human OAS family, reflecting the evolutionary link among them.

77 The human OAS-like (OASL) protein, however, does not harbor the ca

78 r prostate cancer, we sought to determine if OAS activators are present in prostate cancer cells.

79 immune regulatory genes (e.g., IFI27, IFI44, OAS, and BST2) was increased.

80 representative IFN-stimulated genes (IFIT3, OAS, LMP2, TGTP, and USP18) in both neonatal and adult b

81 clease domain is preferentially conserved in OAS derivatives that lack an active nucleotidyltransfera

82 fluorescent paclitaxel penetrated deeper in OAS-treated femoropopliteal segments compared to control

83 wever, participants with larger increases in OAS level exhibited greater decreases in plasma viral lo

84 and mice; the functions of these inactivated OAS derivatives remain unknown.

85 In peripheral blood, increased OAS and CXCL10 expression were elevated in SIV(+) monkey

86 So far, the significance of individual OAS-TL-like enzymes is unresolved.

87 propose that OAS1D suppresses the interferon/OAS/RNase L-mediated cellular destruction by interacting

88 -like proteins, of which the major isoforms, OAS-TL A, OAS-TL B, and OAS-TL C, catalyze the formation

89 ; (iii) 'LTP PFS': living in Southern Italy, OAS triggered by hazelnut and peanut; (iv) 'PR-10 PFS':

90 in RNA reduce 2-5A pathway activation joins OAS and RNase L to the list of RNA sensors and effectors

91 rine)E(t), V/K(AcCoA)E(t), V(2)/E(t), V(2)/K(OAS)E(t), and V/K(CoA)E(t) are 3300 +/- 180 s(-1), (9.6

92 rections, as well as the V/K(serine) and V/K(OAS), decrease at low pH, exhibiting a pK of approximate

93 The V/K(OAS), which reflects the first half-reaction, is identic

94 virus antagonize the oligoadenylate-RNase L (OAS-RNase L) pathway.

95 rase (SAT) and O-acetylserine (thiol) lyase (OAS-TL) in the cytosol, plastids, and mitochondria of pl

96 ajor function of O-acetyl-Ser-(thiol) lyase (OAS-TL; EC 2.5.1.47) is the formation of l-Cys, but our

97 genes encode for O-acetylserine(thiol)lyase (OAS-TL)-like proteins, of which the major isoforms, OAS-

98 Generation of all major OAS-TL double loss-of-function mutants in combination wi

99 sis was not affected by the absence of major OAS-TLs, indicating significant transport of Cys into th

100 siveness of Cys synthesis by the three major OAS-TLs and ruled out alternative sulfur fixation by oth

101 her two human DNA repair enzymes can mediate OAS excision in vitro: Ape1 protein (the main human abas

102 The predominant role of mitochondrial OAS synthesis was validated in planta by feeding [(3)H]s

103 of episodic positive selection in the mouse OAS-like proteins with inactivated nucleotidyltransferas

104 uced mRNA expression of antiviral genes MX1, OAS, and ISG56 but not IFN-beta.

105 The ability of OAS to activate the cma37::lacZ fusion was abolished by

106 abidopsis was found to cause accumulation of OAS, Cys, and glutathione, mimicking the biochemical cha

107 roduct is able to counteract the activity of OAS, a third cellular protein critical for host defense.

108 ha-aminoacrylate intermediate on addition of OAS, suggesting that K42 is involved in the abstraction

109 ha-aminoacrylate intermediate on addition of OAS.

110 Comparative sequence analysis of OAS, poly(A)-polymerases, TRF4/sigma-family polymerases,

111 bstituted enzyme suggest that the binding of OAS as it forms the external Schiff base is such that th

112 In the 7 cases of OAS, detection rate of allergen-specific IgE to shrimp w

113 an a similar linear sequence is the cause of OAS.

114 nse revealed that the high concentrations of OAS, Cys, and GSH observed in this hyperaccumulator coin

115 The first half-reaction, conversion of OAS to the alpha-aminoacrylate intermediate and acetate,

116 rases, suggest that the C-terminal domain of OAS and their homologs might have nuclease activity.

117 We compared the effect of OAS gene family variants on 2 DENV serotypes in cell cul

118 dditionally, our studies provide evidence of OAS in the acute-phase dengue virus immune response, pro

119 -C plants showed the SAT-dependent export of OAS.

120 with relatively high levels of expression of OAS genes, which are necessary but not sufficient for in

121 Feeding of OAS to the PaAPR-expressing plants caused cysteine and g

122 asis for future work examining the impact of OAS phenotype antibodies on protective immunity and dise

123 L following infection, despite induction of OAS expression.

124 Inhibition of OAS specifically requires the Us11 dsRNA-binding domain,

125 interferon and the consequent high levels of OAS mRNA induced in these cell types.

126 express significantly higher basal levels of OAS transcripts than nonmyeloid cells.

127 relates with high basal expression levels of OAS, as found in myeloid cells.

128 relates with high basal expression levels of OAS, as found in myeloid cells.

129 es revealed that subcellular localization of OAS-TL proteins is more important for efficient Cys synt

130 servations help define mammalian pathways of OAS repair, point to interactions that might coordinate

131 possibly involved in the physiopathology of OAS and (ii) CD68+ macrophages likely critical in allerg

132 cleaves 2',5'-oligoadenylate, the product of OAS, to prevent activation of the cellular endoribonucle

133 plotype in the transcriptional regulation of OAS genes at baseline and infected conditions.

134 , hepatocytes express undetectable levels of OASs and RNase L, which likely explains the lack of RNas

135 r regular apple consumption has an effect on OAS and immune parameters of Mal d 1 or Bet v 1 allergy.

136 Only OAS was capable of activating the cma37::lacZ fusion.

137 led out alternative sulfur fixation by other OAS-TL-like proteins.

138 ced an additive activation of endogenous p69-OAS and of an OAS-Luc reporter and a synergistic activat

139 ed by hazelnut and peanut; (iv) 'PR-10 PFS': OAS triggered by Rosaceae; and (v) 'no-panallergen PFS':

140 es known to encode antagonists of the potent OAS-RNase L antiviral pathway, highlighting its importan

141 which the wild-type virus blocks the potent OAS-RNase L antiviral pathway.

142 atalyzes the acetylation of l-Ser to produce OAS, which acts as both a key positive regulator of sulf

143 ermediate collapses, generating the products OAS and CoASH.

144 The presence of cysteine resulted in reduced OAS export in mitochondria of oastl-C mutants but not in

145 In addition, the reduced OAS expression may result in modulation of prolactin rec

146 does not consistently improve apple related OAS symptoms, we evaluated whether regular apple consump

147 Upon sensing double-stranded RNA, OAS produces 2',5'-oligoadenylates (2-5A), which activat

148 Upon binding target RNA, OAS is activated to produce 2'-5'-linked oligoadenylates

149 manner to stimulate the production of select OAS moieties.

150 thesis of l-cysteine from O-acetyl-l-serine (OAS) and inorganic bisulfide.

151 cysteine and acetate from O-acetyl-L-serine (OAS) and sulfide.

152 the beta-acetoxy group of O-acetyl-L-serine (OAS) by a thiol to give L-cysteine.

153 replacement of acetate in O-acetyl-L-serine (OAS) by sulfide to give L-cysteine.

154 ubstitution of acetate in O-acetyl-L-serine (OAS) by sulfide via a ping-pong kinetic mechanism .

155 the beta-acetoxy group of O-acetyl-L-serine (OAS) is replaced by bisulfide to give L-cysteine and ace

156 on of the acetyl group of O-acetyl-L-serine (OAS) to form the alpha-aminoacrylate intermediate.

157 the beta-acetoxy group of O-acetyl-l-serine (OAS) with inorganic bisulfide.

158 of glutathione, Cys, and O-acetyl-l-serine (OAS), in shoot tissue, are strongly correlated with the

159 e conversion of serine to O-acetyl-L-serine (OAS).

160 mvent the effects of original antigenic sin (OAS) in certain circumstances.

161 s are reminiscent of original antigenic sin (OAS), given that the patients had prior dengue virus exp

162 address the issue of original antigenic sin (OAS): the phenomenon where the induced antibody shows hi

163 deoxyribose generates oxidized abasic sites (OAS) that may constitute one-third of ionizing radiation

164 e often an associated oral allergy syndrome (OAS) to apple, which contains the cross-reactive allerge

165 (ii) 'profilin PFS': oral allergy syndrome (OAS) triggered by Cucurbitaceae; (iii) 'LTP PFS': living

166 e diagnosed as having oral allergy syndrome (OAS), and only few cases of FDEIA are reported.

167 patients with/without oral allergy syndrome (OAS), at baseline and after 5 months of sublingual aller

168 to be responsible for oral allergy syndrome (OAS), in which sensitization to airborne allergens cause

169 genes p56- and p69-oligoadenylate synthase (OAS).

170 The 2',5'-oligoadenylate (2-5A) synthetase (OAS)-RNase L system is a mechanism for restricting viral

171 NA activation of 2'-5' oligo (A) synthetase (OAS), it is likely that the primary role of dsRNA bindin

172 (NOS2) and 2', 5' oligoadenylate synthetase (OAS) 1 induction in response to virus or IFNgamma.

173 urements of 2',5'-oligoadenylate synthetase (OAS) activity, and induction levels of interferon-induci

174 d equivalent 2'5' oligoadenylate synthetase (OAS) and MX1 gene expression in this cell type.

175 ced enzymes 2'-5'-oligoadenylate synthetase (OAS) and RNase L are key components of innate immunity i

176 sistance 1 (Mx1), oligoadenylate synthetase (OAS) and viperin in unstimulated sputum cells in 57 asth

177 PKR and the 2'-5' oligoadenylate synthetase (OAS) are both activated by double-stranded RNA (dsRNA) p

178 2',5'-Oligoadenylate synthetase (OAS) enzymes and RNase-L constitute a major effector arm

179 The oligoadenylate synthetase (OAS) enzymes are cytoplasmic dsRNA sensors belonging to

180 < 0.01); and 2'5'-oligoadenylate synthetase (OAS) had a 163 (+/-120.6) pmol/dl increase (P < 0.01).

181 The 2'-5' oligoadenylate synthetase (OAS) locus encodes for three OAS enzymes (OAS1-3) involv

182 e Mx(+) and 2'-5' oligoadenylate synthetase (OAS) proteins was not regulated, whereas expression of d

183 poptosis-1, 2'-5' oligoadenylate synthetase (OAS), a 2'-5' OAS-like (OASL) gene, galectin-9, myxoviru

184 isoform of 2'-5'-oligoadenylate synthetase (OAS), a member of the OAS/RNase L system of innate viral

185 m levels of 2'-5' oligoadenylate synthetase (OAS), a validated interferon response marker.

186 ene product 2'-5' oligoadenylate synthetase (OAS), and the chemokines CXCL9 and CXCL10 in the slow pr

187 olymerases, 2'-5' oligoadenylate synthetase (OAS), and yeast Trf4p .

188 eron (IFN-alpha), oligoadenylate synthetase (OAS), CXCL9, and CXCL10-was positively associated with d

189 ies such as 2'-5' oligoadenylate synthetase (OAS), stimulated trans-acting factor of 50 kDa (STAF-50)

190 by PKR and 2'-5' oligoadenylate synthetase (OAS), which respectively inactivate the translation init

191 o block the 2',5'-oligoadenylate synthetase (OAS)-RNase L (RNase L) antiviral pathway.

192 The oligoadenylate synthetase (OAS)-RNase L pathway is a potent antiviral activity.

193 The oligoadenylate synthetase (OAS)-RNase L pathway is a potent interferon (IFN)-induce

194 n inducible 2',5'-oligoadenylate synthetase (OAS)-RNase L pathway to facilitate hepatitis development

195 nterferon-induced oligoadenylate synthetase (OAS)-RNase L pathway.

196 R (PKR) and 2'-5' oligoadenylate synthetase (OAS).

197 opterin and 2'-5' oligoadenylate synthetase (OAS).

198 stimulating 2'5'-oligoadenylate synthetase (OAS).

199 ance of the 2'-5' oligoadenylate synthetase (OAS)/RNase L and double-stranded RNA (dsRNA)-dependent p

200 ed that the 2'-5' oligoadenylate synthetase (OAS)/RNase L system, an innate immune antiviral pathway,

201 sed expression of oligoadenylate synthetase (OAS)1a mRNA in the eye.

202 in 2 (Mx2), 2',5'-oligoadenylate synthetase (OAS-1), Virus inhibitory protein (viperin), ISG15 and IS

203 d gene (ISG; MX1, oligoadenylate synthetase [OAS], IFIT-1) response in the same cell types.

204 s the 2',5'-oligoadenylate (2-5A) synthetase(OAS)/RNase L system, a component of the interferon-induc

205 2'-5' Oligoadenylate synthetases (OAS) are a family of enzymes, which are best known for t

206 CL-10, CXCL-11), oligoadenylate synthetases (OAS) genes, and selectively activated activating transcr

207 The 2'-5' oligoadenylate synthetases (OAS) represent a family of interferon (IFN)-induced prot

208 -inducible 2',5'-oligoadenylate synthetases (OAS) upon activation by viral double-stranded RNA (dsRNA

209 ), but not 2',5'-oligoadenylate synthetases (OAS), in vaginal tissue.

210 dsRNA-activated oligoadenylate synthetases (OAS), which produce signaling 2',5'-linked RNA molecules

211 ble 2',5'-oligoadenylate (2-5A) synthetases (OASs) and ribonuclease (RNase) L are components of a pot

212 wed by addition of RNA-1 to form a synthetic OAS to direct the virion-like assembly by RCNMV CP.

213 treated using an orbital atherectomy system (OAS) under simulated blood flow and fluoroscopy.

214 counteract PKR, HSV-1 functions that target OAS have not been described.

215 DNA polymerase beta excised the 5'-terminal OAS formed by Ape1 incision at a rate similar to its rem

216 merase beta-mediated excision of 5'-terminal OAS was stimulated by Ape1 as it is for unmodified abasi

217 Fpg (MutM) protein also excised 5'-terminal OAS, but in our hands, the RecJ protein did not.

218 Examination of phylogenetic trees shows that OAS inactivation in mammals occurred on several independ

219 Results suggest that OAS activation may occur in prostate cancer cells in viv

220 The OAS-inhibiting activity is generated late in the virus'

221 eficient nsp15, activated MDA5, PKR, and the OAS/RNase L system, resulting in an early, robust induct

222 diesterases (2',5'-PDEs) that antagonize the OAS-RNase L pathway, and we report here that these prote

223 evidence that a Neandertal haplotype at the OAS locus was subjected to positive selection in the hum

224 te a signal of adaptive introgression at the OAS locus.

225 ulation of dsRNA in HCMV-infected cells, the OAS pathway remains inactive, even in HCMV[DeltaI/DeltaT

226 Upon binding to viral dsRNA, the OAS enzymes synthesize 2'-5' linked oligoadenylates (2-5

227 re, we investigated a potential role for the OAS-RNase L system in the restriction of retrotransposon

228 Different receptors from the OAS family contain one, two, or three copies of the 2-5A

229 strong evidence of positive selection in the OAS region is still lacking.

230 enzyme, while decreases of > 200-fold in the OAS: acetate lyase activity and a 30-fold decrease in V

231 mutant exhibits a > 50-fold increase in the OAS:acetate lyase activity and a 17-fold decrease in V f

232 The dramatic change in the OAS:acetate lyase activity of OASS-A in the C42S and C42

233 t in the downstream effector molecule of the OAS pathway, RNase L, were no more sensitive to ocular H

234 his Article, an oligonucleotide mimic of the OAS sequence was attached to Au, CoFe2O4, and CdSe nanop

235 Covalent linkage of the OAS to nanoparticles directs RNA-dependent encapsidation

236 However, the role of the OAS-like domain of OASL remains unclear.

237 Furthermore, the structure of the OAS-like domain shows that OASL has a dsRNA binding groo

238 Here we present the crystal structure of the OAS-like domain, which shows a striking similarity with

239 challenge the notion that activation of the OAS-RNase L pathway requires virus to induce type I IFN,

240 oadenylate synthetase (OAS), a member of the OAS/RNase L system of innate viral resistance.

241 Inhibition of PDE12 may up-regulate the OAS/RNase-L pathway in response to viral infection resul

242 commitment to catalysis, indicating that the OAS external Schiff base preferentially partitions towar

243 We demonstrate that the OAS-like domain can bind dsRNA and that mutating key res

244 ation of l-Cys, but our study shows that the OAS-TL A and OAS-TL B of both halophytes are enzymes tha

245 in the absence of exogenous IFN, whereas the OAS pathway appears to respond to exogenous IFN, contrib

246 tectable levels of RNase L as well as by the OASs expressed in hepatocytes.

247 ate synthetase (OAS) locus encodes for three OAS enzymes (OAS1-3) involved in innate immune response.

248 Thus, OAS does not seem to be a common occurrence in normal, h

249 Thus, OAS is sticky, and a value of 1.5 is calculated for the

250 alpha-aminoacrylate intermediate compared to OAS being released from enzyme.

251 ues from patients with OAS, when compared to OAS- patients (P < 0.05).

252 slightly lower rate (70-100 s-1) compared to OAS.

253 lated sulfite and thiosulfate in response to OAS feeding.

254 induce type I IFN, which in turn upregulates OAS gene expression, as well as to provide dsRNA to acti

255 e compared to a value of 1.81 +/- 0.04 using OAS-3,3-d2 for alpha-DKeq for the first half-reaction.

256 ndary deuterium kinetic isotope effect using OAS-3,3-d2 is 1.11 +/- 0.06 obtained by direct compariso

257 The value of D(V/KOAS) using OAS-2-d is dependent on pH from 5.8 to 7.0 with independ

258 factor eIF2alpha via phosphorylation, while OAS induces the endonuclease RNase L to degrade RNA.

259 In contrast with OAS-B, the loss of CS26 function resulted in dramatic ph

260 The anti-HIV-1 effect correlated with OAS protein levels (weeks 1 and 2) and IFIG induction le

261 In patients with OAS to apple, tolerance can be safely induced with slowl

262 LCs found in oral tissues from patients with OAS, when compared to OAS- patients (P < 0.05).

263 ells were identical in patients with/without OAS, except lower numbers of CD207+ LCs found in oral ti