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 includes five small three-helix-bundle domains that

3 SpA induction of sTNFR1 shedding required the entire IgG

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

5 SpA is also a potent activator of tumor necrosis factor

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

7 SpA PB mononuclear NK cells from SpA patients showed gre

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

9 SpA treatment also induced a persistent loss of splenic

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

11 SpA(KKAA) MAbs promoted opsonophagocytic killing of MRSA

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

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

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

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

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

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

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

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

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

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

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

23 Staphylococcal protein A (SpA) is a cell-wall-bound pathogenicity factor from the

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

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

26 Staphylococcal protein A (SpA) is representative of a new class of Ags, the B cell

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

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

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

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

31 ), and/or modified staphylococcal protein A (SpA), a 45-kilodalton bacterial "superantigen" that reac

32 Staphylococcal protein A (SpA), a bacterial membrane protein, and protein Fv (Fv b

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

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

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

36 Staphylococcal protein A (SpA), acting as a B cell superantigen, binds to the Fab

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

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

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

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

41 l mimic for Staphylococcus aureus Protein A (SpA).

42 was identified as staphylococcal protein A (SpA).

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

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

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

46 VH3-depleted hIgG and then were administered SpA i.d.

47 t untreated rabbits, which were administered SpA intradermally (i.d.), do not develop a cutaneous inf

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

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

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

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

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

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

54 of denatured Ig suggested that both pFv and SpA interact with conformationally dependent V(H) sites,

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

56 reatment to quantitated outcomes for PsA and SpA.

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

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

59 the inflammatory arthritis conditions RA and SpA.

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

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

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

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

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

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

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

67 evelopment of criteria for classifying axial SpA.

68 s efficacy of biologic agents in early axial SpA.

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

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

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

72 by the new classification criteria for axial SpA.

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

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

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

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

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

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

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

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

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

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

83 -2DS1, and -2DS5 in AAU patients with axial SpA, which have been implicated in NK cell activation.

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

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

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

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

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

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

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

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

92 41, there was a decrease in mean whole blood SpA and ChT:T (P =.07 and.11, respectively).

93 For both SpA and pFv, binding is less frequent among IgG than IgM

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

95 dulates the inflammatory response induced by SpA.

96 tion of a prominent inflammatory response by SpA was dependent upon the presence of VH3+ molecules in

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

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

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

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

101 Current SpA treatments only provide partial symptomatic and func

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

103 (21-3 x 382-2)F(1) , only the males develop SpA, and neither sex develops gut inflammation.

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

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

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

107 apoptosis and migration to VSMC loss during SpA remodeling.

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

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

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

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

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

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

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

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

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

117 For example, SpA reacts with the Fabs of most human Igs using heavy c

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

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

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

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

122 acteristic lesions are actually specific for SpA.

123 posterior element lesions being specific 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 nd RF- RA, respectively, versus 3% and 9% in SpA and UA patients, respectively; P < 0.0001).

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

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

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

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

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

152 .4 ng/microl in RA samples, 4.3 ng/microl in SpA samples, and <0.9 ng/microl in OA samples.

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

154 link gut inflammation and joint pathology in SpA.

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

156 ized towards a type 17 immunity programme in SpA.

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

158 expanding area of translational research in SpA.

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

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

161 consistent feature of new-onset synovitis in SpA, but are a minor feature of RA.

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

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

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

165 ential to recruit maternal immune cells into SpAs.

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

167 al blood from patients with JRA and juvenile SpA was cloned and sequenced.

168 atients with pauciarticular JRA and juvenile SpA while single large Vbeta8-specific expansions were f

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

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

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

172 ential for implementing peptidoglycan-linked SpA superantigen activity.

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

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

175 t consumption and C3a production only in Mod SpA-treated serum reconstituted with a VH3+, SpA-binding

176 Addition of Mod SpA to human serum led to complement consumption and the

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

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

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

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

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

182 ze the Fcgamma and Fab binding activities of SpA.

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

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

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

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

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

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

189 requisites for the subsequent development of SpA.

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

191 Patients with a previous diagnosis of SpA were excluded.

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

193 n younger subjects were highly diagnostic of SpA.

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

195 , the Z domain (an analog of the B domain of SpA), has been determined by simulated annealing with re

196 cture of an engineered IgG-binding domain of SpA, the Z domain (an analog of the B domain of SpA), ha

197 conserved in the five homologous domains of SpA.

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

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

200 xation elements between the B domain (Fb) of SpA and the Fc fragment of IgG were identified from the

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

202 v. with human IgG (hIgG), i.d. injections of SpA induced an inflammatory response with the classical

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

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

205 planation for the anatomical localization of SpA.

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

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

217 les did in fact react with Lc1 and B6 and/or SpA, but not with control mAbs of irrelevant specificity

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

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

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

230 dence that an interaction of the B cell SAg, SpA, with its reactive (VH3+) IgGs leads to an immune co

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 ly determined X-ray structure of the similar SpA B domain in complex with the Fc fragment of a human

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

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

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

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

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

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

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

241 eceding the development of spondylarthritis (SpA).

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

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

244 r understanding of the spondylarthropathies (SpA).

245 Study Group criteria for spondylarthropathy (SpA), and 75 (36%) were classified as having undifferent

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

247 pauciarticular/juvenile spondylarthropathy (SpA), respectively.

248 erhaps other subtypes of spondylarthropathy (SpA).

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

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

251 of preradiographic axial spondyloarthritis (SpA).

252 ntial pathogenic roles in spondyloarthritis (SpA).

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

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

255 p of disorders termed spondyloarthropathies (SpAs).

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

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

258 in cases pFv binding is more permissive than SpA binding.

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

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

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

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

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

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

265 Six of the SpA patients had bone marrow edema that was maximal at e

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

267 All 10 of the SpA patients, but only 4 of the 10 RA patients, had foca

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

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

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

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

272 spectratypes are also available through the SpA interface.

273 ngly, was not a feature specific only to the SpA group.

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

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

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

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

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

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

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

281 linically significant AU have an undiagnosed SpA.

282 SpA-treated serum reconstituted with a VH3+, SpA-binding, IgM protein.

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

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

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

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

287 nts with recent-onset knee effusion (10 with SpA and 10 with RA) were evaluated using fat-suppressed

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

289 of the ligands binds IgG competitively with SpA in solution and when immobilized on agarose beads, w

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

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

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

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

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

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

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

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

298 and mechanisms of synovitis in patients with SpA.

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

300 tients with polyarticular JIA and those with SpA.

301 guishable from clinical signs of humans with SpAs.