ライフサイエンスコーパス: SpA

1 SpA binds the Fcgamma domains of IgG and protects staphy

2 SpA derived iNKT and gammadelta-T cells showed unique an

3 SpA includes five small three-helix-bundle domains that

4 SpA induction of sTNFR1 shedding required the entire IgG

5 SpA is a web-accessible system for the management, visua

6 SpA is also a potent activator of tumor necrosis factor

7 SpA is known to bind to IgG Fc, which impedes phagocytos

8 SpA PB mononuclear NK cells from SpA patients showed gre

9 SpA stimulated a RhoA/ROCK/MLC cascade, resulting in the

10 SpA treatment also induced a persistent loss of splenic

11 SpA(+) but not SpA(-) mutants stimulated activation of E

12 SpA(KKAA) MAbs promoted opsonophagocytic killing of MRSA

13 SpA, the best-studied B-cell SAg, reacts with the Fabs o

14 SpA-like inflammation, but not osteoproliferation, was d

15 ormed a descriptive longitudinal study of 10 SpA patients, all of whom had active inflammatory back p

16 In total, 294 SpAs were studied, and only one apoptotic VSMC was ident

17 with extensive bone edema but none of the 5 SpA patients with mild bone edema were HLA-B27 positive

18 The interaction between a SpA domain and the Fc fragment of IgG was partially eluc

19 interfacial residues, and displacement of a SpA side chain by an Fc side chain in a molecular-recogn

20 Nontoxigenic protein A (SpA(KKAA)), when used as an immunogen in mice, stimulate

21 ding properties of staphylococcal protein A (SpA) can be attributed to the presence of five highly ho

22 d pyronins and added to unlabeled Protein A (SpA) from S. aureus.

23 ctor of S. aureus, staphylococcal protein A (SpA) in the presence of electroactive redox couple ferri

24 sorting for reduced deposition of protein A (SpA) into the staphylococcal envelope.

25 Staphylococcal protein A (SpA) is a cell-surface component of Staphylococcus aureu

26 Staphylococcal protein A (SpA) is an important virulence factor from Staphylococcu

27 Staphylococcal protein A (SpA) is anchored to the cell wall envelope of Staphyloco

28 Staphylococcal protein A (SpA) is representative of a new class of antigens, the B

29 ual surface-linked Staphylococcus protein A (SpA) molecules and to characterize the strength of the n

30 us expresses the virulence factor Protein A (SpA) on all clinical isolates, and SpA has been shown in

31 Staphylococcus aureus protein A (SpA) plays a critical role in the induction of inflammat

32 CD4(+) T cells and staphylococcal protein A (SpA), a cell wall-anchored surface molecule that binds F

33 Protein A (SpA), a highly conserved and abundant surface protein of

34 ough expression of staphylococcus protein A (SpA), a surface protein that drives polyclonal B cell ex

35 d surface component of S. aureus, protein A (SpA), contributes to its success as a pathogen by both a

36 gBDs) derived from Staphylococcus protein A (SpA), Streptococcus protein G (SpG), and Finegoldia (for

37 is decorated with staphylococcal protein A (SpA), which captures the Fcgamma portion of immunoglobul

38 was identified as staphylococcal protein A (SpA).

39 e antibody-binding staphylococcal protein A (SpA).

40 nt surface-exposed Staphylococcal protein A (SpA).

41 we tested the hypothesis that EVTs activate SpA endothelial cells to secrete chemokines that have th

42 to compare MRI patterns of disease in active SpA, degenerative arthritis (DA), and malignancy.

43 measured by specific chymotryptic activity (SpA) and chymotryptic/tryptic activity (ChT:T).

44 solated monoclonal antibodies (MAbs) against SpA(KKAA) that, by binding to the triple-helical bundle

45 e (TnA) and the area subpallialis amygdalae (SpA).

46 area were held in the optical trap while an SpA-coated substrate was scanned beneath them at a dista

47 y was undertaken to determine whether EO and SpA in male (21-3 x 382-2)F(1) rats are causally related

48 eatment of patients with co-incident IBD and SpA and for the repurposing of therapeutics from one dis

49 ions of Tregs and dendritic cells to IBD and SpA have been assessed in both animal models of disease

50 rotein A (SpA) on all clinical isolates, and SpA has been shown in mice to expand and ablate variable

51 yond anti-tumor necrosis factors for PsA and SpA.

52 reatment to quantitated outcomes for PsA and SpA.

53 s and FLS, particularly in those from RA and SpA patients.

54 ites were not significant between the RA and SpA patients.

55 the inflammatory arthritis conditions RA and SpA.

56 duction of surfactant proteins SpC, SpB, and SpA, decline of lung compliance, transient fibrosis, and

57 Decidual spiral arteriole (SpA) remodeling is essential to ensure optimal uteroplac

58 During human uterine spiral artery (SpA) remodeling, vascular smooth muscle cells (VSMCs) ar

59 infused protein A of Staphylococcus aureus (SpA) and followed the fate of peripheral B cells express

60 toxin protein A from Staphylococcus aureus (SpA) interacts with B cell antigen receptors encoded by

61 mpact of protein A of Staphylococcus aureus (SpA), a virulence factor with targeted B cell antigen re

62 measure for ankylosing spondylitis and axial SpA, the ASDAS, new measures for the heterogeneous clini

63 evelopment of criteria for classifying axial SpA.

64 s efficacy of biologic agents in early axial SpA.

65 The patients were evaluated for axial SpA based on their histories using published criteria.

66 al Society classification criteria for axial SpA heralds a new era for the identification of early di

67 lopment of classification criteria for axial SpA will aid in the identification of patients suitable

68 by the new classification criteria for axial SpA.

69 MRI in axial SpA is the most rapidly expanding area of translational

70 the high diagnostic utility of MRI in axial SpA, with severe or multiple RLs evident on MRI being ch

71 (DW) MRI reflects disease activity in axial SpA.

72 33) and patients with nonradiographic axial SpA (10 of 24) and higher in AS patients (18 of 19).

73 5) or in patients with nonradiographic axial SpA (P = 0.007).

74 negative patients with nonradiographic axial SpA were lower than those of AS patients (P = 0.01).

75 ose from patients with nonradiographic axial SpA, and those from AS patients.

76 s with AAU, 71 (49.6%) had features of axial SpA.

77 Preradiographic axial SpA refers to patients with SpA who exhibit signs and sy

78 Patients with axial SpA can have remarkably similar clinical features and di

79 ination was decreased in subjects with axial SpA compared with subjects with AAU without axial SpA (P

80 -2DS1, and -2DS5 in AAU patients with axial SpA, which have been implicated in NK cell activation.

81 ivating KIRs in subjects with AAU with axial SpA, which reached statistical significance for 2DS5 (P

82 d disease activity in individuals with axial SpA.

83 ompared with subjects with AAU without axial SpA (P = 0.022; P(c) = NS; OR, 0.43; 95% CI, 0.21-0.88).

84 KIR3DL2(+) T cells from B27(+) SpA patients proliferated more in response to Ag present

85 DL2-expressing leukocytes observed in B27(+) SpA may be explained by the stronger interaction of KIR3

86 , an alternative binding interaction between SpA and the Fab-region of immunoglobulin domains encoded

87 o the well-characterized interaction between SpA and the Fc-region of human IgG, an alternative bindi

88 Many genetic risk factors are shared between SpA and IBD, and changes in the composition of gut micro

89 most common diagnostic confusion was between SpA and DA, since both had RLs present and the presence/

90 rs (BCRs) with VH regions capable of binding SpA.

91 41, there was a decrease in mean whole blood SpA and ChT:T (P =.07 and.11, respectively).

92 cterize structurally the interface formed by SpA repeats and type-3 V(H)-domains, we have studied the

93 dulates the inflammatory response induced by SpA.

94 l artery-associated trophoblast giant cells (SpA-TGCs) surrounding maternal blood vessels and severel

95 on of spiral artery trophoblast giant cells (SpA-TGCs) that invade and remodel maternal blood vessels

96 ident distally only in patients with chronic SpA (9 of 17 patients, compared with none of 20 patients

97 sitis (20 with early SpA and 17 with chronic SpA) and 10 normal control subjects underwent ultrasound

98 Current SpA treatments only provide partial symptomatic and func

99 therapeutic blockade substantially decreases SpA severity.

100 avenues for research to understand defective SpA remodeling and consequent pregnancy pathology.

101 (21-3 x 382-2)F(1) , only the males develop SpA, and neither sex develops gut inflammation.

102 HLA-B27-transgenic rodents develop SpAs, implicating HLA-B27 in the etiology of these disor

103 erefore, although most gorillas that develop SpAs express an MHC class I molecule with striking diffe

104 In studies of different SpA forms, the magnitude of the induced deletion directl

105 apoptosis and migration to VSMC loss during SpA remodeling.

106 nd Achilles tendon enthesitis (20 with early SpA and 17 with chronic SpA) and 10 normal control subje

107 nthesis, were evident in patients with early SpA and in normal control subjects.

108 Bone erosion in patients with early SpA occurred at either the proximal insertion or the sup

109 compared with none of 20 patients with early SpA; P < 0.0001).

110 We believe that the reported ELP-SpA fusion will find applications not only as a powerful

111 The resulting ELP-SpA fusion was shown to preserve the ability to reversib

112 hase-separation immunoassay based on the ELP-SpA format was established for paclitaxel (taxol) with I

113 mains as efficiently as by either the entire SpA or the intact IgG binding region.

114 identified intricate crosstalk between EVTs, SpA cells, and decidual immune cells that governs their

115 n of IL-23 resulted in a severe experimental SpA, confirmed a fundamentally different immunobiology t

116 und that within minutes of in vivo exposure, SpA became surface associated with B lymphocytes and ind

117 report the 2.3-A structure of a fully folded SpA domain in complex with Fc.

118 Arthritis International Society criteria for SpA were recruited from four rheumatology centers betwee

119 Spondylarthropathy Study Group criteria for SpA, without evidence of ankylosing spondylitis, psorias

120 suggests a probable binding orientation for SpA- and V(H)3-domains.

121 acteristic lesions are actually specific for SpA.

122 posterior element lesions being specific for SpA.

123 ntial as an orally delivered therapeutic for SpA.

124 ingle RLs were of low diagnostic utility for SpA, but >or=3 RLs (likelihood ratio [LR] 12.4) and seve

125 Dendritic cells from SpA patients may also contribute to disease by producing

126 SpA PB mononuclear NK cells from SpA patients showed greater cytotoxicity than those from

127 FLS from SpA and RA patients supported increased pseudoemperipole

128 he interaction between NK cells and FLS from SpA patients results in a proinflammatory response.

129 were observed surrounding and separate from SpA walls in partially remodeled vessels; the highest le

130 y to play a major role in loss of VSMCs from SpAs during remodeling in normal pregnancy, but VSMCs ap

131 Inc., Wayne, PA, under license from Giuliani SpA, Milan, Italy) is a novel, once-daily, high-strength

132 However, SpA did not mediate binding of nonimmunoglobulin compone

133 acterize the strength of the noncovalent IgG-SpA bond.

134 rein tetrapeptide-tetraglycyl [L-Ala-D-iGln-(SpA-Gly5)L-Lys-D-Ala-Gly4] linked to its C-terminal thre

135 In SpA, an increased number of PB and SF NK and CD4+ T cell

136 PJ versus 114 mm2 at the SPP [P = 0.010]; in SpA, mean synovitis area 214 mm2 at the CPJ versus 143 m

137 e expression of abnormal forms of HLA-B27 in SpA may have a pathogenic role through interaction with

138 GMP accumulate in the BM in SpA and, unexpectedly, at extramedullary sites: in the i

139 ify Blimp1-dependent transcripts enriched in SpA-TGCs.

140 seen adjacent to tendon/ligament entheses in SpA.

141 sociation with Achilles tendon enthesitis in SpA is anatomically uncoupled from bone formation-the 2

142 The driving forces in SpA pathophysiology are now becoming clear; these data m

143 by NK cell and FLS coculture was greatest in SpA patients.

144 me which has been increasingly implicated in SpA pathology.

145 s little evidence that they are important in SpA.

146 NK cells and CD4 lymphocytes is increased in SpA and ERA.

147 IL-15 on FLS was significantly increased in SpA and RA patients, but not OA patients.

148 Current dogma is that inflammation in SpA initiates in the gut and leads to joint inflammation

149 The gut-joint axis of inflammation in SpA is further reinforced by similarities in immunopatho

150 eripheral osteoproliferative inflammation in SpA.

151 hours, a sequence of events was initiated in SpA-binding splenic B cells, with rapid down-regulation

152 ations for understanding bone involvement in SpA and for the SpA concept in general, especially the h

153 unction of NK and T cells bearing KIR3DL2 in SpA.

154 This response was much more marked in SpA and RA patients as compared with OA patients.

155 .4 ng/microl in RA samples, 4.3 ng/microl in SpA samples, and <0.9 ng/microl in OA samples.

156 rmed the diagnostic utility of spinal MRI in SpA and have described highly specific lesions such as i

157 link gut inflammation and joint pathology in SpA.

158 We thus conclude that disease patterns in SpA are related to normal enthesis structure and biomech

159 ized towards a type 17 immunity programme in SpA.

160 binding Fc, including a general reduction in SpA conformational heterogeneity, freezing out of polyro

161 expanding area of translational research in SpA.

162 e NK and innate lymphoid immune responses in SpA and other related diseases.

163 expression of IFN response genes or STAT1 in SpA synovial macrophages.

164 nsight into the reason the target tissues in SpA are apparently so diverse.

165 transmembrane (tm) versus soluble (s) TNF in SpA versus RA together with a decrease in the enzymatic

166 uld be elicited by any one of the individual SpA IgG binding domains as efficiently as by either the

167 inished formation of B cell memory; instead, SpA reduced the proliferative capacity of PCs that enter

168 ential to recruit maternal immune cells into SpAs.

169 ulated mice were challenged with an isogenic SpA-deficient S. aureus mutant, cells proliferated in th

170 of this domain in the context of full-length SpA in the cell remains unexplored.

171 Therefore, B-cell SAgs like SpA have great potential to elicit inflammatory response

172 expansion occurred with peptidoglycan-linked SpA from the bacterial envelope but not with recombinant

173 ential for implementing peptidoglycan-linked SpA superantigen activity.

174 Genetic and mechanistic evidence links SpA with inflammatory bowel disease (IBD) and psoriasis,

175 hese Blimp1(+) cells give rise to the mature SpA-TGCs, canal TGCs, and glycogen trophoblasts.

176 Moreover, SpA cross-links B-cell receptors to modify host adaptive

177 SpA(+) but not SpA(-) mutants stimulated activation of EGFR and along w

178 ciple is to take advantage of the ability of SpA to bind a variety of antibodies with high affinity,

179 played greatly reduced envelope abundance of SpA and surface proteins with YSIRK signal peptides.

180 a and the V(H)3(+) Fab binding activities of SpA and provide protection from staphylococcal abscess f

181 ze the Fcgamma and Fab binding activities of SpA.

182 suggest that the superantigenic activity of SpA leads to immunodominance, limiting host responses to

183 g spondylitis, and the broader categories of SpA may be present in 1-2% of the general population, mo

184 Upon cessation of SpA exposure, the representation of conventional splenic

185 reviously considered to be characteristic of SpA could also be found frequently in patients with DA a

186 SpG (SpG(C3)) followed by domains B and D of SpA, suggesting that SpG(C3) is particularly useful to e

187 These results support the designation of SpA as a multiple independently-folding domain (MIFD) pr

188 requisites for the subsequent development of SpA.

189 linical variables including the diagnosis of SpA according to Assessment of SpondyloArthritis Interna

190 Patients with a previous diagnosis of SpA were excluded.

191 oderate grade were also highly diagnostic of SpA (LR 14.5).

192 n younger subjects were highly diagnostic of SpA.

193 is required for terminal differentiation of SpA-TGCs and defines a lineage-restricted progenitor cel

194 The effects of SpA during natural infection, however, have not been add

195 The effects of SpA on PC fate were limited to the secondary response, b

196 onsible for the key pathological features of SpA.

197 4beta7 in IBD can lead to onset or flares of SpA.

198 g spondylitis (AS) is the prototypic form of SpA in which progressive disease can lead to fusion of t

199 ng TNF and IL-23 in IBD and in some forms of SpA.

200 G), followed by intraperitoneal injection of SpA, showed neutrophil influx into the peritoneal cavity

201 reaction was dependent on the interaction of SpA with VH3+ IgG.

202 previously reported that the interaction of SpA with VH3+ immunoglobulin molecules leads to activati

203 e clearly enriched within inflamed joints of SpA patients where they act as major IL-17 secretors.

204 planation for the anatomical localization of SpA.

205 n controlling the clinical manifestations of SpA that is resistant to disease-modifying antirheumatic

206 ited disease progression in animal models of SpA.

207 essential mechanism triggering the onset of SpA.

208 role of these events in the pathogenesis of SpA.

209 better understanding of the pathogenesis of SpA.

210 to better understand the pathophysiology of SpA to develop more specific and effective treatments fo

211 e approximation of the A-B or B-C portion of SpA.

212 fusions to the intact IgG binding region of SpA and to each of the individual binding domains, we fo

213 ein hydrolase, contributes to the release of SpA by removing amino sugars [i.e., N-acetylmuramic acid

214 led description of the tertiary structure of SpA domains in complex with Fc and the structural change

215 tages, enthesitis may be the only symptom of SpA, particularly in patients lacking the HLA-B27 recept

216 17A-blocking antibodies for the treatment of SpA.

217 imates, including gorillas, develop signs of SpAs indistinguishable from clinical signs of humans wit

218 VH3 clan IgG from S. aureus-infected or SpA-treated animals was not pathogen-specific, suggestin

219 In patients with RA or SpA, the area of synovitis was significantly larger imme

220 esponse in mice inoculated with wild-type or SpA-deficient S. aureus mutant.

221 with recent Salmonella infection, ReA, other SpA, and rheumatoid arthritis (RA).

222 G to specific lysines of its binding partner SpA but not to bovine serum albumin (BSA) as a nonbindin

223 (69.8% vs. 27.3%, P < 0.0001) and peripheral SpA (21.9% vs. 11.1%, P < 0.0001) than patients with rec

224 % of patients presented axial and peripheral SpA according to ASAS criteria, respectively.

225 ssification criteria of axial and peripheral SpA as well as the CASPAR criteria for PsA, a new compos

226 biologic treatments of axial and peripheral SpA, and new drugs beyond anti-tumor necrosis factors fo

227 The receptor SpA was attached to BioPE-DOTAP binary lipid bilayer tet

228 bacterial envelope but not with recombinant SpA, and optimally required five tandem repeats of its I

229 ases cleave the anchor structure of released SpA to modify host immune responses.

230 and CXCL6 by endothelial cells in remodeling SpAs, and their cognate receptors are present in both dN

231 sion in freshly isolated RA and seronegative SpA synovial macrophages.

232 f 5 patients with RA and 3 with seronegative SpA (2 with psoriatic arthritis and 1 with ankylosing sp

233 The spondylarthritides (SpA) are strongly associated with possession of HLA-B27.

234 RA and 18 patients with spondylarthritides (SpA) were lysed immediately after isolation or were cult

235 ith RA, 20 patients with spondylarthritides (SpA), and 20 patients with osteoarthritis (OA).

236 for the diagnosis of axial spondylarthritis (SpA), but it is unknown whether characteristic lesions a

237 tural killer (NK) cells in spondylarthritis (SpA) patients.

238 sis at different stages of spondylarthritis (SpA) with microanatomic studies of normal cadaveric enth

239 ted in the pathogenesis of spondylarthritis (SpA), yet the molecular mechanisms are incompletely defi

240 eceding the development of spondylarthritis (SpA).

241 itis (RA) and seronegative spondylarthritis (SpA).

242 systemic JIA, and 19 with spondylarthritis [SpA]) and 830 healthy control subjects; all were ages 5-

243 r understanding of the spondylarthropathies (SpA).

244 lantar fasciitis; 17 had spondylarthropathy (SpA)-associated disease, and 11 had mechanically induced

245 erhaps other subtypes of spondylarthropathy (SpA).

246 ted the research map in spondyloarthritides (SpA) in recent months.

247 itis and other forms of spondyloarthritides (SpA).

248 Spondyloarthritis (SpA) represents a family of inflammatory diseases of the

249 iatic arthritis (PsA) and spondyloarthritis (SpA).

250 matoid arthritis (RA) and spondyloarthritis (SpA).

251 ammatory lesions in axial spondyloarthritis (SpA) has not been well established.

252 of preradiographic axial spondyloarthritis (SpA).

253 lammation in experimental spondyloarthritis (SpA).

254 ntial pathogenic roles in spondyloarthritis (SpA).

255 strongly associated with spondyloarthritis (SpA), as exemplified by the high prevalence of inflammat

256 ch is not associated with spondyloarthritis (SpA), is also a ligand for KIR3DL2.

257 rmed the seronegative spondyloarthropathies (SpA) include ankylosing spondylitis (AS), psoriatic arth

258 atoid disorders, i.e. spondyloarthropathies (SpAs), particularly peripheral spondyloarthropathies.

259 p of disorders termed spondyloarthropathies (SpAs).

260 The spondyloarthropathies (SpAs) are a group of interrelated inflammatory disorders

261 the development of novel therapies to target SpA and related inflammatory disorders.

262 Here we demonstrate that SpA is released with murein tetrapeptide-tetraglycyl [L-

263 In this murine study, we show that SpA altered the fate of plasmablasts and plasma cells (P

264 s was not pathogen-specific, suggesting that SpA cross-linking of VH3 idiotype B-cell receptors and a

265 the immune response is the synovium but the SpA disorders target the tendon, ligament, and joint cap

266 standing bone involvement in SpA and for the SpA concept in general, especially the hypothesis that e

267 The level of MARCO in the SFMC from the SpA patient group was low.

268 nts (IRE P = 0.054, ME P = 0.018) and in the SpA patients (IRE P = 0.002, ME P = 0.001).

269 All 6 of the SpA patients with extensive bone edema but none of the 5

270 n 12 of the RA samples (60%), in none of the SpA samples, and in 1 OA sample.

271 tected in 18 of the RA samples, in 16 of the SpA samples, and in none of the OA samples.

272 appear to migrate away from the wall of the SpA, an effect enhanced by the presence of EVT cells.

273 ndividual binding domains, we found that the SpA IgG binding domains also mediate binding to human ai

274 spectratypes are also available through the SpA interface.

275 This is in contrast to the SpA-Fc interface which is predominantly hydrophobic in n

276 K (dNK) cells and macrophages infiltrate the SpAs and are proposed to initiate remodeling before colo

277 Thus, SpA(KKAA) MAbs may be useful for the prevention and ther

278 oad data from their spectratype analyzers to SpA, which saves the raw data and user-defined supplemen

279 reus antigens, only high-affinity binding to SpA was observed.

280 nation of an X-ray structure of IgG bound to SpA revealed that the fluorophore was selectively transf

281 ammadelta-T cells, but their contribution to SpA is still unclear.

282 mune cells that governs their recruitment to SpAs in the early stages of remodeling and has identifie

283 linically significant AU have an undiagnosed SpA.

284 The physician diagnosis was SpA in 64 subjects, DA in 45 subjects, malignancy in 45

285 the protein-protein interface may occur when SpA binds its multiple binding partners.

286 The mechanisms whereby SpA is released from the bacterial surface to access the

287 To determine whether SpAs in gorillas have a similar HLA-B27-related etiology

288 oints in 24 patients (13 with RA and 11 with SpA) was undertaken.

289 peripheral blood (PB) from 35 patients with SpA and 5 patients with juvenile enthesitis-related arth

290 Thirty-seven patients with SpA and Achilles tendon enthesitis (20 with early SpA an

291 evident in 64.7% (11 of 17) of patients with SpA and in 45% (5 of 11) of those with mechanically indu

292 s identified in 9 (53%) of the patients with SpA but in none (0%) of those with mechanically induced

293 diographic axial SpA refers to patients with SpA who exhibit signs and symptoms of axial involvement,

294 s and FLS were obtained from 6 patients with SpA, 4 patients with rheumatoid arthritis (RA), and 8 pa

295 luid from patients with RA and patients with SpA, but not in OA samples.

296 ubclinical gut inflammation in patients with SpA.

297 est in patients with RA and in patients with SpA.

298 JIA, those with systemic JIA, and those with SpA.

299 tients with polyarticular JIA and those with SpA.

300 guishable from clinical signs of humans with SpAs.