ライフサイエンスコーパス: IgA

1 IgA endomysial antibodies tests were associated with hig

2 IgA is predominantly recognized to play an important rol

3 IgA nephropathy (IgAN) is a common chronic glomerular di

4 IgA nephropathy (IgAN) is the most common form of primar

5 IgA nephropathy (IgAN) is the most prevalent among prima

6 IgA nephropathy (IgAN), characterized by mesangial IgA1

7 IgA nephropathy frequently leads to progressive CKD.

8 IgA nephropathy is thought to be associated with mucosal

9 IgA protease B1 and B2-expressing strains showed greater

10 IgA proteases B1 and B2 cleave LAMP1 and mediate intrace

11 IgA proteases B1 and B2 cleave LAMP1.

12 IgA subclasses have been linked to protection against re

13 IgAs in the liver could mediate clearance of gut-derived

14 IgAs were not specific to individual bacterial taxa but

15 intestinal expressions of Ki67, MUC2, ZO-1, IgA, mucin and lower barrier permeability than those in

16 308 IgA vasculitis patients and 1,018 healthy controls from

17 dy therefore highlights modulation of IL-33, IgA, IL-1alpha, and the microbiota as a potential therap

18 population in the small intestine of C57BL/6.IgA(-/-) mice compared with wild-type mice, which was fu

19 munogenicity endpoints were anti-P2-VP8-P[8] IgA and IgG and neutralising antibody seroresponses and

20 Large quantities of immunoglobulin A (IgA) are constitutively secreted by intestinal plasma ce

21 The salivary immunoglobulin A (IgA) level was measured by an enzyme-linked immunosorben

22 nts, whereas antirotavirus immunoglobulin A (IgA) levels were not.

23 s M. tuberculosis-specific immunoglobulin A (IgA) secretion to respiratory airways and lung expressio

24 mpared serum antirotavirus immunoglobulin A (IgA) seroconversion (>/=20 U/mL) and geometric mean conc

25 Immunoglobulin A (IgA), the major class of antibody secreted by the gut mu

26 The genetic component of Immunoglobulin-A (IgA) vasculitis is still far to be elucidated.

27 An aberrant IgA responsiveness to the gut microbiota during infancy

28 s infants transition from passively acquired IgA present in breast milk to host-derived IgA.

29 e magnitude of ADCC not only increased after IgA removal but also correlated with CD4(+) T-cell prese

30 e activation in HIV-1+ infants did not alter IgA responses associated with protection from rotavirus

31 Altered IgA recognition patterns in children with allergy were o

32 ic mean titer [GMT], 1,704) were found among IgA-deficient individuals than among healthy blood donor

33 e results demonstrate that engineering of an IgA antibody can significantly improve its pharmacokinet

34 IgE, IgA/IgE, and IgA2/IgE ratios for EW and IgA/IgE ratio for OVA were found to be significantly ele

35 We discuss molecules-mucus glycans and IgA-that affect microbe adhesion and identify testable p

36 ng reduced liver and serum levels of IgA and IgA deposits in liver and prevented liver injury.

37 ed 2 procedures for diagnosis: total-IgA and IgA-TTG (the TTG-IgA procedure), as well as IgG-DGL with

38 found the heritability of serum gd-IgA1 and IgA levels to be 80% (95% confidence interval, 66% to 89

39 In contrast to IgM cross-reactivity, IgG and IgA antibodies against ZIKV nonstructural protein 1 (NS1

40 lasmonic-gold platform for measuring IgG and IgA antibodies and IgG avidity against both Zika virus (

41 adjuvants boosted anti-hemagglutinin IgG and IgA antibody levels.

42 lveolar lavage fluid, total anti-IAV IgG and IgA titers and virus-neutralizing antibody titers but no

43 Anti-MVA IgG and IgA were detected in cervicovaginal fluid after a second

44 s exhibited mucosal antigen-specific IgG and IgA with the IgA responses 30-fold greater than systemic

45 nd SF of RA patients contained IgM, IgG, and IgA RFs.

46 E but substantially reduced IgG3, IgG2b, and IgA serum levels.

47 chains of IgG1a (IGHG1a), IgG2 (IGHG2), and IgA (IGHA), and the light chains (lambda and kappa).

48 One graft loss, mediated by non-HLA IgM and IgA antibodies, occurred.

49 duced significantly more PC-reactive IgM and IgA.

50 least, detection of Toxoplasma IgG, IgM, and IgA and a comprehensive review of maternal history, incl

51 iently decreased the frequency of memory and IgA(+) B cells.

52 iters and avidity indices of IgG in sera and IgA in tracheal, lung, and intestinal secretions, signif

53 toire or the link between immune stimuli and IgA structure.

54 t mice had normal production of antiparasite IgA, butex vivo T cell recall responses were impaired.

55 oating of the Bacteroides genus), as well as IgA recognition patterns, differed between healthy child

56 PP DCs augment IgA production by integrin alphavbeta8-mediated activati

57 ents with end-stage kidney disease caused by IgA nephropathy are transplanted every year, and each of

58 of HA1 binding in plasma was contributed by IgA antibodies.

59 terize the bacterial recognition patterns by IgA in stool samples collected at 1 and 12 months of age

60 nusual feature of the antigen recognition by IgA 5I2 is the predominant involvement of the CDR light

61 Human gut bacterial taxa targeted by IgA in the setting of barrier dysfunction are capable of

62 We evaluated cervicovaginal IgA in Partners PrEP Study participants using a subtype

63 S- and flagellin-specific Ig concentrations (IgA and IgG) were measured with the use of an ELISA.

64 Consequently, IgA-positive patients achieved complete remission less f

65 s include a rare variant at RUNX3 decreasing IgA levels by shifting isoform proportions (rs188468174[

66 Deposited IgA has been reported as polymeric, J chain associated,

67 d IgA present in breast milk to host-derived IgA.

68 ve been associated with allergy development, IgA responses to the gut microbiota have not yet been st

69 ty members play a dominant role in dictating IgA responses.

70 Moreover, the bacterial targets of early IgA responses (including coating of the Bacteroides genu

71 Our aim was to determine if elevated IgA anti-tTG were associated with increased mortality ri

72 nsitivity and specificity of tTG IgA and EMA IgA assays in identifying patients with celiac disease w

73 e found that tests for serum tTG IgA and EMA IgA levels had low sensitivity (below 50%) in detection

74 say (95% CI, 0.41-0.60) and 0.45 for the EMA IgA assay (95% CI, 0.34-0.57).

75 say (95% CI, 0.79-0.87) and 0.91 for the EMA IgA assay (95% CI, 0.87-0.94).

76 ied S. sanguinis strains have genes encoding IgA proteases, mitogenic factor deoxyribonucleases, nick

77 was confirmed using an assay for endomysial IgA.

78 markedly reduced IgE production and enhanced IgA production.

79 s cocultured with LGG significantly enhanced IgA responses.

80 irus-specific antibody responses, especially IgA levels and hemagglutination inhibition (HAI) titers,

81 Relative increases in IgG4-EW, IgA-EW, and IgA2-EW were observed in responders (P = 0.0

82 compared with the same strain that expressed IgA protease B1 (P = .006) or B2 (P = .015).

83 , had increased levels of systemic and fecal IgA, and were highly susceptible to chemical-induced col

84 Anti-LPS and anti-flagellin IgA and IgG concentrations increased over the first year

85 longitudinal study of COPD were analyzed for IgA protease expression, survival in human respiratory e

86 s of celiac disease assay using an assay for IgA against tissue transglutaminase; in subjects with po

87 Conventional methods for IgA N- and O-glycosylation analysis are tedious, thus li

88 ontrol group, patients who were negative for IgA aB2GP1 (n=974).

89 group 2 patients who were positive only for IgA aB2GP1 (n=240); and control group, patients who were

90 riking association with the KEGG pathway for IgA production (pathway P < 0.0001), with 22 of the 30 a

91 Patients who were positive for IgA aB2GP1 only are at risk of experiencing thrombosis i

92 1.2%); 8 of 830 children tested positive for IgA against tissue transglutaminase (1.0%; 95% confidenc

93 shed: group 1 patients who were positive for IgA anti-beta2-glycoprotein I (aB2GP1) and B2A-CIC (n=12

94 of 6032, 85 participants tested positive for IgA anti-tTG (1.4 %) and 5947 tested negative.

95 nsplantation, 401 patients were positive for IgA-aB2GPI (29.2%, group 1), and the remaining patients

96 eened for IgA anti-tTG, and if positive, for IgA endomysial antibodies.

97 years old or above, which were screened for IgA anti-tTG, and if positive, for IgA endomysial antibo

98 disease based on results of serum tests for IgA against tissue transglutaminase and endomysium or on

99 ould become the first specific treatment for IgA nephropathy targeting intestinal mucosal immunity up

100 om 62 to more than 12000 participants) found IgA tissue transglutaminase was associated with high acc

101 ases affecting the glomerulus, such as FSGS, IgA nephropathy, lupus nephritis, and diabetic nephropat

102 tients with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN), membranoproliferative GN (MPGN)

103 In conclusion, anti-FVIII IgA represents a potential novel biomarker that could be

104 Anti-FVIII IgA was the strongest negative predictor of recurrence-f

105 roups 1 and 2, plasma immunoglobulin (Ig) G, IgA, and neutralizing antibody responses at week 2 were

106 d transgenic mice, we traced newly generated IgA-secreting cells at steady state and after oral immun

107 e in vivo induced the production of anti-GFP IgA antibodies, demonstrating in vivo transfection and e

108 ary isolate and found that women on PrEP had IgA with higher average human immunodeficiency virus typ

109 We investigated interfaces from human IgA CH3, IgD CH3, IgG1 CH3, IgM CH4, T-cell receptor (TC

110 urrently not known whether and how the human IgA subclasses IgA1 and IgA2 contribute to the clinical

111 IgG4/IgE, IgA/IgE, and IgA2/IgE ratios for EW and IgA/IgE ratio fo

112 Stimulated ILC2s also induced IgM, IgG, IgA, and IgE production by B cells.

113 es were characterized by CTH522-specific IgG/IgA antibodies, together with CTH522-specific interferon

114 ls and promoted the production of IgM, IgG1, IgA, and IgE by these cells in vitro.

115 at component-resolved analysis of IgE, IgG4, IgA, IgA1, and IgA2 may identify potential biomarkers of

116 Specific and total IgG1, IgG4, IgA, and IgE from plasma as well as culture supernatants

117 The mean intensities of immune IgA, IgG, and C3 deposits were lower in the group with h

118 tions cannot be attributed to differences in IgA levels or bacterial load between the 2 groups.

119 The role of immunosuppression in IgA nephropathy (IgAN) is controversial.

120 CT B subunit-specific serum IgG response in IgA(-/-) mice after CT immunization was microbiota depen

121 ticity, and the differential CT responses in IgA(-/-) and wild-type mice disappeared after intestinal

122 odies assigned salient pathogenetic roles in IgA nephropathy.

123 Hematuria is a cardinal symptom in IgA nephropathy, but its influence on the risk of diseas

124 of adaptive immune cell responses, including IgA affinity maturation and secretion, and a recently de

125 ng that 1 in every 600 Caucasian children is IgA deficient.

126 s anti-beta-2 glycoprotein-I of IgA isotype (IgA-aB2GP1) have been linked to thrombotic events and mo

127 We also show that serum lacking IgA antibodies is sufficient to block NoV VLP binding to

128 ivation genes and induced significantly less IgA production.

129 beta7 and CCR9 gut-homing receptors on local IgA-expressing B cells.

130 Strains that lost IgA protease expression showed reduced survival in host

131 y T cells and a higher production of luminal IgA.

132 Assays to measure IgA-TTG, IgG-DGL, and endomysium antibodies were perform

133 ng a gut-specific gene signature with memory IgA(+) B cells, memory IgM(+) B cells were related to so

134 Correspondingly, less specific IgE- and more IgA-secreting cells resided in the spleen in the 9cRA gr

135 Mucosal IgA or secretory IgA (SIgA) are structurally equipped to

136 We newly identified mucosal IgA-producing plasma cells (PCs) as one major iNOS(+) ce

137 d plasma antibodies and induction of mucosal IgA responses at potential SIV entry sites are associate

138 detected in serum and human anti-RSV mucosal IgA was detected in bronchioalveolar lavage fluid for up

139 ited high levels of antigen-specific mucosal IgA and large numbers of local antigen-reactive B cells,

140 e profiled the reactivities of single murine IgA plasma cells by cloning and characterizing large num

141 epithelial cells than strains expressing no IgA protease (P < .001) or IgA protease A1 or A2 (P < .0

142 M. genitalium-specific IgG, but not IgA, was detected in cervical secretions of serum antibo

143 ion of ADCC-mediating IgG antibodies but not IgA.

144 ansplantation with asystolic donors.Notably, IgA-aB2GP1 was an independent risk factor for graft thro

145 The variants of NTHi IgA proteases play distinct roles in pathogenesis of inf

146 presence of circulating immune complexes of IgA bound to beta2-glycoprotein I (B2A-CIC) has been ass

147 analysis for patients with concentrations of IgA against tissue transglutaminase (IgA-TTG) >10-fold t

148 hrough host cells selected for expression of IgA proteases B1 and B2 but not A1.

149 ersistence of NTHi selects for expression of IgA proteases B1 and B2.

150 monstrate that the immunological function of IgA is substantially more extensive than previously cons

151 IgA1 mesangial deposition is the hallmark of IgA nephropathy and Henoch-Schonlein purpura, the onset

152 in about 6-8% of the disease heritability of IgA nephropathy (IgAN), suggesting that there are still

153 Antibodies anti-beta-2 glycoprotein-I of IgA isotype (IgA-aB2GP1) have been linked to thrombotic

154 lamentous bacteria in the small intestine of IgA(-/-) mice.

155 xcluded due to incomplete data, low level of IgA, or poor-quality biopsies.

156 ol feeding reduced liver and serum levels of IgA and IgA deposits in liver and prevented liver injury

157 els of binding IgG antibodies, low levels of IgA antibodies, and high levels of antibody-dependent ce

158 tients at 6 months or later and in levels of IgA in 3 of 10 patients at 18 months or later.

159 HDM-specific levels of IgA in serum were similar to levels measured in nonaller

160 ikely a consequence of the reduced levels of IgA in the gut.

161 7orf99(-/-) mouse exhibits reduced levels of IgA in the serum, gut, feces, and lactating mammary glan

162 VA)-, and ovomucoid (OVM)-specific levels of IgA, IgA1, and IgA2 were quantified by ELISA.

163 t increase the PPV of samples with levels of IgA-TTG >/=10-fold the ULN.

164 pective study concluded that measurements of IgA-TTG and total IgA, or IgA-TTG and IgG against deamid

165 d fewer Peyer's patches and lower numbers of IgA-secreting cells.

166 athway has a key role in the pathogenesis of IgA nephropathy (IgAN).

167 little remains known about the potential of IgA to actively contribute to induction of inflammation,

168 ported a correlation between the presence of IgA autoantibodies and worse disease course.

169 Furthermore, the presence of IgA-aB2GP1 was associated with early graft loss and dela

170 , during childhood had a lower proportion of IgA bound to fecal bacteria at 12 months of age compared

171 issues contained a significant proportion of IgA-producing plasma cells that shared phenotypic and fu

172 We sought to determine the proportions of IgA coating together with the characterization of the do

173 ops in early infancy and the relationship of IgA epitope recognition with development of cow's milk a

174 The repertoire of IgA bound to gut bacteria reflects both T-cell-dependent

175 Little is known about the different roles of IgA protease variants in NTHi infection.

176 the receptor that regulates the secretion of IgA into the intestinal lumen, the polymeric immunoglobu

177 imab, at least at this stage and severity of IgA nephropathy, may reflect a failure of rituximab to r

178 tissues, we found the liver to be a site of IgA production by B cells, derived from gut-associated l

179 was observed, in contrast to avid uptake of IgA complexes.

180 ymerization, deposition might also depend on IgA carrying specific variable domains.

181 a may have a significant favorable effect on IgA nephropathy outcomes.

182 ins expressing no IgA protease (P < .001) or IgA protease A1 or A2 (P < .001).

183 at measurements of IgA-TTG and total IgA, or IgA-TTG and IgG against deamidated gliadin (IgG-DGL) cou

184 onal gammopathy multiple myeloma with IgG or IgA MGUS clones were subsequently identified from the th

185 Thirty-seven SAE-specific, IgG- or IgA-expressing B cells were isolated and yielded 6 anti-

186 ith wild-type mice, but not those of IgG1 or IgA.

187 Plasma IgA levels specific for antigens in rotavirus vaccine an

188 sion were found only after removal of plasma IgA from 12-month PHI samples: the magnitude of ADCC not

189 Patient plasma IgA RF and IgM RF showed a strong correlation.

190 Here, we demonstrate that plasma IgA is a factor capable of modifying the magnitude of Ig

191 lobulin receptor (pIgR) transports polymeric IgA and IgM across epithelia to mucosal secretions, wher

192 iving homeostatic production of polyreactive IgAs with innate specificity to microbiota.

193 PP IgA class switching requires innate lymphoid cells, whic

194 In conclusion, pretransplant IgA-aB2GP1 was the main risk factor for graft thrombosis

195 least 18 years with biopsy-confirmed primary IgA nephropathy and persistent proteinuria despite optim

196 originated from Peyer's patches and produced IgAs reactive to commensal bacteria.

197 f liver-resident immunoglobulin-A-producing (IgA(+)) cells.

198 ive Therapy for the Treatment of Progressive IgA Nephropathy (STOP-IgAN) Trial, 162 patients with IgA

199 domized 34 adult patients with biopsy-proven IgA nephropathy and proteinuria >1 g/d, maintained on an

200 with suppression of neutrophil recruitment, IgA secretions, Th2 responses, and delayed bacterial cle

201 erial defenses, i.e., phagocyte recruitment, IgA secretion, and Muc5b expression.

202 responses, including phagocyte recruitment, IgA secretion, and mucous cell metaplasia.

203 was correlated with SIV Env-specific rectal IgA, rectal memory B cells, and total rectal plasma cell

204 system dysfunction, which manifests as renal IgA deposition that leads to impairment and end-stage re

205 body seroconversion and evaluating rotavirus IgA/IgG seroresponses in MR + HRV recipients.

206 d in levels of serum antibodies and salivary IgA to influenza A(H3N2) and influenza B virus strains a

207 Influenza virus-specific salivary IgA levels correlated with serum HI responses, making th

208 Uremia did not affect secretory IgA release into the ileum lumen or mucosal leukocyte su

209 ns that complements the mucous and secretory IgA Ab-mediated system in the protection of intestinal m

210 intestinal T-cell populations, and secretory IgA expression.

211 examined the relationship between secretory IgA (SIgA) on the mucosal surface of small airways and p

212 and sufficient to transfer delayed secretory IgA expression.

213 Mucosal IgA or secretory IgA (SIgA) are structurally equipped to resist chemical

214 4 in the text) HIV antigen through secretory IgA (SIgA) in nasal mucosae in mice.

215 In mice where B cells cannot access the SED, IgA responses against oral antigen and gut commensals ar

216 Serum IgA seroresponses were observed in 38 (81%, 95% CI 67-91

217 in healthy individuals, we determined serum IgA and gd-IgA1 levels by ELISA in a sample of 148 healt

218 dence that immune complex formation of serum IgA plays an important role in orchestration of inflamma

219 icient mice showed increased polymeric serum IgA on exposure to pathogens.

220 allenge transiently increased specific serum IgA, IgE, and IgG1 serum levels (2.0- and 8.9-fold).

221 ibody responses except for suppressing serum IgA responses.

222 previously considered and suggest that serum IgA-induced inflammation plays an important role in orch

223 how that opsonization of bacteria with serum IgA induced cross-talk between FcalphaRI and different T

224 , memory IgM(+) B cells were related to some IgA(+) clonotypes and switched to IgA in response to T c

225 Furthermore, although some IgAs acquired somatic mutations, these did not substanti

226 roteins in these families, although specific IgA in breast milk was not proportionally up-regulated.

227 en, a substantial number of antigen-specific IgA-secreting cells was found in the liver.

228 ion results in downregulation of CM-specific IgA antibody levels in BM, but not in serum, suggesting

229 p < 0.01) and the magnitudes of Env-specific IgA (p = 0.01) and IgG (p < 0.05) in rectal secretions.

230 st to the rare vaccine-elicited Env-specific IgA in infants, rgp120 vaccine-elicited Env-specific IgA

231 strategy to enhance protective Env-specific IgA in milk, which is subsequently transferred to the in

232 nce of vaccine-elicited mucosal Env-specific IgA responses in combination with high-avidity systemic

233 Remarkably, high-magnitude Env-specific IgA responses were observed in milk, surpassing those in

234 ines also elicited modest serum Env-specific IgA responses.

235 i.n.) boost induced robust milk Env-specific IgA responses.

236 nfants, rgp120 vaccine-elicited Env-specific IgA was frequently detected in adults.

237 examined how infants' food epitope-specific IgA develops in early infancy and the relationship of Ig

238 Increased binding of serum epitope-specific IgA to CM in mothers of infants with CMA may reflect inh

239 nt had increased binding of epitope-specific IgA to CM proteins compared to those with a non-CMA infa

240 Epitope-specific IgA was detectable in infants' sera starting at less tha

241 sought to investigate whether food-specific IgA epitope profiles differ intra-individually between m

242 ockroach allergen, alpha-1,3-glucan-specific IgA-secreting cells are present in the lungs of mice imm

243 ergy via pulmonary alpha-1,3-glucan-specific IgA-secreting cells.

244 s work provides evidence that gp120-specific IgA was capable of modifying ADCC responses during natur

245 We measured specific IgA to a series of overlapping peptides in major CM alle

246 palmitic acid and PEG induced PLA2-specific IgA and increased Foxp3(+) Treg frequencies and TGF-beta

247 lising activity and poliovirus type-specific IgA were measured in stool after a monovalent OPV type 2

248 d method for larger patient cohorts to study IgA N- and O-glycosylation changes in pathologies.

249 vaccinations had identical IgG but superior IgA responses.

250 aying an unexpected increase in the systemic IgA responses.

251 ainst TG2 are a hallmark of CD, and anti-TG2 IgA-producing gut PCs accumulate in patients upon gluten

252 -containing diet who tested positive for TGA-IgA from November 2011 through May 2014, seen at 33 pedi

253 l findings from 16 antibody tests (8 for TGA-IgA, 1 for TGA-IgG, 6 for IgG against deamidated gliadin

254 Patients with only a low level of TGA-IgA (threefold or less the ULN) but no other results ind

255 Findings from local laboratories of TGA-IgA 10-fold or more the ULN, a positive result from the

256 Diagnosis based on level of TGA-IgA 10-fold or more the ULN, a positive result from the

257 levels of antibodies, but when levels of TGA-IgA were 10-fold or more the ULN, PPVs ranged from 99.63

258 bulin A against tissue-transglutaminase (TGA-IgA) 10-fold or more the upper limit of normal (ULN), co

259 Although it has recently become clear that IgA also mediates other immunological processes, little

260 In conclusion, our study suggests that IgA vasculitis is an archetypal HLA class II disease.

261 The IgA test is used by some laboratories as an additional m

262 ong naive B cells and were selected into the IgA repertoire upon recirculation in Peyer's patches.

263 information concerning the influence of the IgA repertoire or the link between immune stimuli and Ig

264 reducing the IgE response but promoting the IgA response.

265 demonstrated previously that triggering the IgA Fc receptor (FcalphaRI) on neutrophils results in ne

266 observed already at 1 month of age, when the IgA antibodies are predominantly maternally derived in b

267 ucosal antigen-specific IgG and IgA with the IgA responses 30-fold greater than systemic levels.

268 erization of the dominant bacteria, bound to IgA or not, in infant stool samples in relation to aller

269 increased richness and diversity compared to IgA-only-coated or uncoated bacteria.

270 capable of robust cytokine-dependent CSR to IgA results in reduced, but not abolished, CSR.

271 This enhanced switch to IgA production in the absence of CLCa was attributable t

272 ed to some IgA(+) clonotypes and switched to IgA in response to T cell-independent or T cell-dependen

273 GF-beta1 complexes with isotype switching to IgA production.

274 luded that measurements of IgA-TTG and total IgA, or IgA-TTG and IgG against deamidated gliadin (IgG-

275 t microbiota diversity and low mucosal total IgA levels in infancy have been associated with allergy

276 ers recorded symptoms; measurements of total IgA, TGA, and EMA; and histopathology findings from duod

277 However the total IgA levels post-VirHRV challenge in the intestine and pr

278 validated 2 procedures for diagnosis: total-IgA and IgA-TTG (the TTG-IgA procedure), as well as IgG-

279 ions of IgA against tissue transglutaminase (IgA-TTG) >10-fold the upper limit of normal (ULN) and if

280 ssess the sensitivity and specificity of tTG IgA and EMA IgA assays in identifying patients with celi

281 on a GFD, we found that tests for serum tTG IgA and EMA IgA levels had low sensitivity (below 50%) i

282 low levels of sensitivity: 0.50 for the tTG IgA assay (95% CI, 0.41-0.60) and 0.45 for the EMA IgA a

283 high levels of specificity: 0.83 for the tTG IgA assay (95% CI, 0.79-0.87) and 0.91 for the EMA IgA a

284 In a prospective study, we validated the TTG-IgA procedure and the TTG-DGL procedure in identificatio

285 The TTG-IgA procedure identified patients with celiac disease wi

286 or diagnosis: total-IgA and IgA-TTG (the TTG-IgA procedure), as well as IgG-DGL with IgA-TTG (TTG-DGL

287 ochemical properties compared with wild-type IgA.

288 cific B cells isolated from breast milk were IgA isotype, in stark contrast to the overwhelming predo

289 by a mean of 57% after adding 9cRA, whereas IgA was strongly induced (20-fold), and IgG1 levels rema

290 e aim of this study was to determine whether IgA could modify the magnitude of ADCC in HIV infection,

291 ad to tissue damage, we investigated whether IgA immune complexes in plasma and synovial fluid of RA

292 replicated 5 known variants associating with IgA, IgG or IgM levels or with composite immunoglobulin

293 TTG-IgA procedure), as well as IgG-DGL with IgA-TTG (TTG-DGL procedure).

294 genetic or pharmacological interference with IgA(+) cell generation attenuates liver carcinogenesis a

295 nsplant rates were highest for patients with IgA nephropathy (IgAN) (referent) and lower for all othe

296 ,131 patients with GN studied, patients with IgA nephropathy (IgAN) had the lowest mortality rates an

297 istently, kidney biopsies from patients with IgA nephropathy and diabetic nephropathy exhibited subst

298 We followed a cohort of 112 patients with IgA nephropathy for a mean+/-SEM period of 14+/-10.2 yea

299 he drug to the distal ileum in patients with IgA nephropathy.

300 ockade, reduced proteinuria in patients with IgA nephropathy.