ライフサイエンスコーパス: tryptase

1 uding mast cell-restricted proteases such as tryptase.

2 h was proteolytically activated by mast cell tryptase.

3 oteins by MCs and their activation by the MC tryptase.

4 Hsp27, Hsp40, Hsp70, and Hsp90 with CD68 and tryptase.

5 relates with mast cell burden as assessed by tryptase.

6 pression, storage, and enzymatic activity of tryptase.

7 eficial and adverse functional roles for the tryptase.

8 a nonpulmonary cause was stained for MCs and tryptase.

9 he human version of mast cell tryptase, beta-tryptase.

10 hiMC, CE also caused a reduced expression of tryptase.

11 ease of the vasoactive mediators chymase and tryptase.

12 m naturally in individuals who express alpha-tryptase.

13 detection of potentially relevant changes in tryptases.

14 2.14, 95% CI 1.42-3.22), a concentration of tryptase 125 ng/mL or higher (1.81, 1.20-2.75), a leukoc

15 s equation (peak MCT should be>1.2x baseline tryptase+2 mg/L) has been proposed to interpret acute MC

16 levels should be greater than ([1.2xbaseline tryptase] + 2] mug/L to be considered a clinically signi

17 Mean DAO (132 ng/mL) and tryptase (304 ng/mL) concentrations increased 187- and 4

18 tively, over baseline values (DAO 0.7 ng/mL, tryptase 76 ng/mL) during severe anaphylaxis.

19 beta-Tryptase, a homotetrameric serine protease, has four ide

20 Tryptase, a major secretory product of human mast cells

21 Imatinib also reduced levels of serum tryptase, a marker of mast-cell activation, to a greater

22 Human beta-tryptase, a tetrameric trypsin-like serine protease, is

23 nce homed to the pleural space, MCs released tryptase AB1 and IL-1beta, which in turn induced pleural

24 whereas the bivalent IgG fully inhibits beta-tryptase activity in a hinge-dependent manner.

25 Active beta-tryptase allele count correlates with blood tryptase lev

26 arrying null, one or two copies of the alpha-tryptase allele.

27 ings (n = 1350) were genotyped for the alpha-tryptase alleles, using high-resolution melting assays.

28 Injected tryptase alone was sufficient to induce plasma loss from

29 caused by increased alpha-tryptase-encoding Tryptase-alpha/beta1 (TPSAB1) copy number resulting in e

30 Chymase, but not MC tryptase, also degraded other alarmins, i.e. biglycan, H

31 ion in the tryptases is extensive, and alpha-tryptase, an allelic variant of the more extensively stu

32 Both alpha-tryptase and beta-tryptase are preferentially expressed

33 Tryptase and carboxypeptidase A3 expression in epithelia

34 lymphopoietin combined with IL-33 increased tryptase and carboxypeptidase A3 immunostaining in mast

35 e correlations analysis identified mast cell tryptase and CCL26, a chemokine for mast cells, as genes

36 Tryptase and cysteinyl leukotriene (cysLT) levels were m

37 Urinary eicosanoids, plasma tryptase and cytokine levels, platelet-leukocyte aggrega

38 ons increased during VIT (P < .001) although tryptase and IgE were unaltered.

39 of multiple copies of TPSAB1 encoding alpha-tryptase and increased risk for severe anaphylaxis.

40 S-tryptase and KIT D816V allele burden were monitored.

41 Tryptase and thrombin are upregulated in wound healing a

42 Together, these results suggest that tryptase and thrombin may be an initial trigger to overr

43 We report that tryptase and thrombin potentiate human fibrocyte differe

44 Reaction grade, tryptase and UMH changes were compared with statistical

45 ha-tryptase had higher basal serum levels of tryptase and were more symptomatic than those with allel

46 leased substances (histamine, serotonin, and tryptase) and the pattern of activated itch-sensory neur

47 ase of IL-33 and its correlation with early (tryptase)- and late-phase markers (IL-13 levels, eosinop

48 Murine IL-33 is also cleaved by mast cell tryptase, and a tryptase inhibitor reduced IL-33-depende

49 Furthermore, serglycin, tryptase, and carboxypeptidase A messenger RNA transcrip

50 primary human mast cells and express CD117, tryptase, and FcepsilonRI.

51 Plasma DAO, tryptase, and histamine concentrations of four severe an

52 Conversely, chymase (P<0.001), tryptase, and Mmp9 (P<0.01) mRNA levels were significant

53 nts with mastocytosis were assayed for IL-6, tryptase, and sIL-6R.

54 c lesions, mast cells degranulate to release tryptase, and thrombin mediates blood clotting in early

55 This anti-tryptase antibody potently blocks tryptase enzymatic act

56 A 2.15 angstrom crystal structure of a beta-tryptase/antibody complex coupled with biochemical studi

57 for GA, that MC degranulation and MC-derived tryptase are central to disease progression.

58 Both alpha-tryptase and beta-tryptase are preferentially expressed by human mast cell

59 oglycan and one of its associated proteases, tryptase, are known to regulate cell death by promoting

60 acy of MIMA was higher compared with that of tryptase (area under the curve 0.93 vs 0.74; P = .011).

61 ata provide a foundation for developing anti-tryptase as a clinical therapy for severe asthma.

62 hrough a secretory granule-derived serglycin-tryptase axis as a novel principle for histone modificat

63 was shown that the absence of the serglycin-tryptase axis resulted in altered chromatin composition.

64 rimary proteolytic targets for the serglycin-tryptase axis.

65 ely resembles the human version of mast cell tryptase, beta-tryptase.

66 ar permeability was induced by pooled mature tryptases but not alpha- or beta-tryptase homotetramers.

67 alpha/beta-Tryptase, but not homotetramer, activates protease-activ

68 ot compensate for their loss of the membrane tryptase by increasing their expression of other granule

69 lls can produce and secrete C3, whereas beta-tryptase can act on C3 to generate C3a and C3b, raising

70 These findings introduce tryptase-catalyzed histone clipping as a novel epigeneti

71 ms of protease content (tryptase-only [MCT], tryptase + chymase [MCTC]) and tumour necrosis factor-al

72 preformed compounds, including proteases of tryptase-, chymase-, and carboxypeptidase A3 type that a

73 ere used for measurement of CD11c, CD3, CD4, tryptase, claudin-1, occludin, E-cadherin, and vascular

74 rine proteases such as trypsin and mast cell tryptase cleave protease-activated receptor-2 (PAR2) at

75 be considered, regardless of the basal serum tryptase concentration.

76 A striking finding was decreased tryptase content in mast cells with copper overload, whe

77 verload, whereas copper starvation increased tryptase content.

78 Associations of alpha-tryptase copy number with serum IgE levels, atopy scores

79 ophil (P < 0.01) counts increased and plasma tryptase correlated with eosinophil counts (Pearson r =

80 , we evaluated whether histone truncation by tryptase could have an impact on epigenetic events in ma

81 ulfill any diagnostic SM criteria (excluding tryptase criterion).

82 Intriguingly, tryptase deficiency resulted in defective proteolytic mo

83 ptidase A3, cathepsin G, granzyme B, and the tryptases derived from the TPSAB1, TPSB2, TPSD1, and TPS

84 t a medical evaluation that included a serum tryptase determination, allele-specific quantitative PCR

85 eveloped by using clinical findings, a serum tryptase determination, and ASqPCR.

86 t a medical evaluation that included a serum tryptase determination, mutational analysis for KIT D816

87 in cases of severe anaphylaxis: basal serum tryptase determination, physical examination for cutaneo

88 mpling times, and the possible use of mature tryptase determination.

89 T were analyzed for immune cell populations, tryptase, ECP, and sIgE.

90 Plasma tryptase elevation during aspirin-induced respiratory re

91 is is indicative of a severe reaction, serum tryptase elevation, and mast cell clonality.

92 sociated with inherited differences in alpha-tryptase-encoding copies at TPSAB1.

93 usively associated with duplication of alpha-tryptase-encoding sequence in TPSAB1, and affected indiv

94 T)-a genetic trait caused by increased alpha-tryptase-encoding Tryptase-alpha/beta1 (TPSAB1) copy num

95 This anti-tryptase antibody potently blocks tryptase enzymatic activity in a humanized mouse model,

96 disulfide bond (Cys(220)-Cys(248) in betaII-tryptase) exists in oxidized and reduced states in the e

97 The degree to which alpha-tryptase expression may be associated with asthma has no

98 a transcription factor critical for driving tryptase expression.

99 ha- and 2beta-tryptase protomers (alpha/beta-tryptase) form naturally in individuals who express alph

100 DNA methylation changes in tryptase gamma 1 (TPSG1), schlafen 12 (SLFN12), and MUC4

101 ry alpha-tryptasemia, due to increased alpha-tryptase gene copies and protein expression, presents wi

102 We have investigated the alpha-tryptase gene copy number variation and its potential as

103 mRNA levels, suggesting that copper affects tryptase gene regulation.

104 ecreted by activated mast cells (chymase and tryptase) generate mature forms of IL-33 with potent act

105 ur consistent melting patterns for the alpha-tryptase genotype were identified with alleles carrying

106 mine the prevalence and associated impact of tryptase genotypes on anaphylaxis in humans.

107 , Slovenia, and the United States, underwent tryptase genotyping by droplet digital PCR.

108 total of 10 patients who were available for tryptase genotyping were all confirmed to have HalphaT.

109 A subgroup of patients was available for tryptase genotyping.

110 month 6, reduction of KIT D816V EAB >/=25%, tryptase >/=50%, and alkaline phosphatase >/=50% were si

111 oring alleles encoding three copies of alpha-tryptase had higher basal serum levels of tryptase and w

112 absence of cytotoxic agent, suggesting that tryptase has a homeostatic impact on nuclear events.

113 The transient increase in serum tryptase has been proposed since 1989 as a diagnostic to

114 zole acetic acid, plasma histamine and serum tryptase have been reported, consistent with mast cell a

115 d samples were taken for assays of mast cell tryptase, histamine, anaphylatoxins (C3a, C4a, C5a), cyt

116 oled mature tryptases but not alpha- or beta-tryptase homotetramers.

117 Here we report an inhibitory anti-tryptase IgG antibody with a bivalency-driven mechanism

118 Serum tryptase levels and tryptase immunohistochemical staining in skin biopsies w

119 ed systemic anaphylaxis, and inhibits airway tryptase in Ascaris-sensitized cynomolgus monkeys with f

120 umab also enhanced secretory IgA and reduced tryptase in BAL fluid.

121 m(2), MIMA has a greater value compared with tryptase in estimating the need for bone marrow biopsy.

122 mong the inflammatory infiltrate, c-kit, and tryptase in individuals both with and without HIV.

123 The roles of macrophages and MC tryptase in pathogenesis were evaluated by using depleti

124 sputum eosinophilia and with lower levels of tryptase in sputum and lower plasma levels of interleuki

125 ignificant increases in PGE2, histamine, and tryptase in the colonic mucosa.

126 and bronchial function may reflect roles for tryptases in regulating IgE production and other process

127 In a previous study, we showed that tryptase, in addition to its intragranular location, can

128 authors showed that recombinant chymase and tryptase increased endothelial permeability in a dose-de

129 her cases of potential MMR in the absence of tryptase increments.

130 ntial therapeutic prevented and reversed the tryptase-induced vascular permeability.

131 We find that mast cell-derived tryptase induces inflammation, chondrocyte apoptosis, an

132 lated proteases, good target engagement, and tryptase inhibition in HMC1 xenograft models.

133 They went on to evaluate the tryptase inhibitor nafamostat mesylate in a mouse model

134 is also cleaved by mast cell tryptase, and a tryptase inhibitor reduced IL-33-dependent allergic airw

135 A potent tryptase inhibitor, nafamostat mesylate, blocked DENV-in

136 These heterodimeric tryptase inhibitors demonstrate superior activity compar

137 These heterodimeric tryptase inhibitors demonstrate the power of target-driv

138 We show that mast cell tryptase is elevated in severe asthma patients independe

139 y human mast cells, but the purpose of alpha-tryptase is enigmatic, because its tetramers lack protea

140 Fibrocyte potentiation by thrombin and tryptase is mediated by protease-activated receptors 1 a

141 ation associated with higher basal mast cell tryptase is possibly one of the commonest autosomal domi

142 Genetic variation in the tryptases is extensive, and alpha-tryptase, an allelic v

143 single agreed definition of positive serial tryptases is needed to enable robust evaluation of diagn

144 variant of the more extensively studied beta-tryptase, is absent in substantial numbers of the genera

145 e, we identified that a MC-derived protease, tryptase, is consequential for promoting vascular permea

146 No significant changes in s-tryptase/KIT D816V allele burden were observed.

147 from patients with IBS had higher levels of tryptase, larger numbers of MCs, and a higher percentage

148 ylaxis and to examine predictors of elevated tryptase level (defined as >/=11.4 mug/L during reaction

149 ivation symptoms and elevated baseline serum tryptase level (MCAS-T) may not necessarily have a clona

150 diseases or with an elevated baseline serum tryptase level and in untreated patients with a history

151 tients with mastocytosis and/or elevated sBT tryptase level and systemic reactions to hymenoptera ven

152 aphylaxis was correlated with baseline serum tryptase level and was associated with an increased risk

153 related or other typical symptoms, the basal tryptase level is an important parameter.

154 An elevated basal serum tryptase level is associated with severe systemic anaphy

155 816V is detected and/or (ii) the basal serum tryptase level is clearly increased (>25-30 ng/ml) and/o

156 igation is usually not required, even if the tryptase level is increased.

157 Currently, measurement of serum tryptase level is the most commonly used test to estimat

158 A detectable acute mature tryptase level showed lower sensitivity, particularly in

159 ogic changes are associated with an elevated tryptase level that has been confirmed to be caused by H

160 es in bone marrow mast-cell burden and serum tryptase level were -59% and -58%, respectively.

161 A baseline serum tryptase level within the upper normal range (8-11.5 ng/

162 shold level of 2 ng/mL + 1.2 x (postreaction tryptase level) detected most of the anaphylactic reacti

163 In those with a slightly increased tryptase level, additional investigations, including a s

164 tration of the bone marrow and lowered serum tryptase level.

165 el of at least 2 ng/mL + 1.2 x [postreaction tryptase level]).

166 nd significantly lower median serum baseline tryptase levels (22.4 vs 28.7 and 45.8 mug/L; P </= .009

167 at patients with intermediate baseline serum tryptase levels (8-11 ng/mL) and without skin involvemen

168 s were more likely associated with increased tryptase levels (beta-adjusted, 4.0; 95% CI, 0.95-7.0, a

169 al resolution and the percentage decrease in tryptase levels (P = .0014).

170 years (P < 0.001) as well as elevated basal tryptase levels (P = 0.001) as risk factors.

171 0.07, area under the curve) and early-phase tryptase levels (P = 0.06).

172 sis and is more severe in patients with high tryptase levels and advanced disease.

173 Baseline tryptase levels and at least 1 subsequent tryptase measu

174 iatric mastocytosis in relationship to serum tryptase levels and bone marrow pathology to provide pra

175 FMD inversely correlated with age and serum tryptase levels and directly with median arterial pressu

176 ere used to evaluate the association between tryptase levels and risk factors.

177 In patients with high tryptase levels and severe mediator symptoms, all with o

178 Tryptase levels and symptoms decreased over time in most

179 Serum tryptase levels and tryptase immunohistochemical stainin

180 ion is required, but the clinical course and tryptase levels are monitored in the follow-up.

181 Tryptase levels are particularly useful for the diagnosi

182 Elevated basal serum tryptase levels are present in 4-6% of the general popul

183 Tryptase levels are seldom increased because of infant a

184 th dominantly inherited elevated basal serum tryptase levels associated with multisystem complaints i

185 use of infant anaphylaxis, although baseline tryptase levels can be increased in the first few months

186 ms decreased over time in most patients, and tryptase levels correlated with bone marrow mast cell bu

187 ly, in two independent human dengue cohorts, tryptase levels correlated with the grade of DHF severit

188 Serum tryptase levels decreased (P = .01).

189 Serum tryptase levels differed significantly between patients

190 Yet tryptase levels do not solely reflect the mast cell load

191 vels; and did not display increases in serum tryptase levels during aspirin reactions on the placebo

192 Serum tryptase levels furthered classification and reflected c

193 gate with inherited increases in basal serum tryptase levels in 35 families presenting with associate

194 We aimed to evaluate tryptase levels in children with anaphylaxis and to exam

195 ve longitudinal monitoring of baseline serum tryptase levels in healthy and atopic infants during the

196 and there was no correlation between DAO and tryptase levels in mastocytosis patients.

197 Elevated baseline serum tryptase levels in patients with active FPIES suggest lo

198 Total tryptase levels in serum discriminated between nonanaphy

199 Determination of basal serum tryptase levels is an established diagnostic tool for ri

200 y, particularly in patients with acute total tryptase levels lower than 16 mug/L.

201 difference between reaction and postreaction tryptase levels may improve diagnostic sensitivity.

202 Over a 4-year period, 203 children had serum tryptase levels measured.

203 anaphylaxis, without skin lesions, and with tryptase levels of less than 11.4 ng/mL underwent bone m

204 nsus recommendation of 2012 that acute total tryptase levels should be greater than ([1.2xbaseline tr

205 Acute tryptase levels varied as a function of the clinical sev

206 Correspondingly elevated tryptase levels were detected in IPF lung tissue samples

207 (172 individuals) that elevated basal serum tryptase levels were exclusively associated with duplica

208 er baseline serum levels of IL-10 and higher tryptase levels were found in active CM-FPIES versus res

209 While serum tryptase levels were higher in patients with SM as compa

210 Serum cytokine and tryptase levels were measured before and after a positiv

211 Serum tryptase levels were measured by immunofluorescence.

212 Mature and total serum tryptase levels were measured.

213 Significant differences in serum tryptase levels were observed between 2 and 24 h in the

214 Tryptase levels were only increased in NAPTs with Pru p

215 Tryptase levels were positive in 3 challenges.

216 bone marrow mast cell infiltration and serum tryptase levels) with molecular data (serial monitoring

217 -tryptase allele count correlates with blood tryptase levels, and asthma patients carrying more activ

218 er prevalence in males, lower serum baseline tryptase levels, and KIT mutation more frequently restri

219 ine relationships between clinical findings, tryptase levels, and marrow histopathology.

220 r specific IgE to alpha-gal and higher serum tryptase levels, reflective of the mast cell burden.

221 s, were characterized by significantly lower tryptase levels, shorter disease duration, and earlier d

222 cated by hypothermia and increases in plasma tryptase levels.

223 atients with symptoms, AOPPs correlated with tryptase levels.

224 with mastocytosis, regardless of their serum tryptase levels.

225 s, which was independent from atopy or serum tryptase levels.

226 orrelated with clinical parameters and serum tryptase levels.

227 hylaxis, no skin lesions, and baseline serum tryptase </=20 ng/mL.

228 Also, only alpha/beta-tryptase makes mast cells susceptible to vibration-trigg

229 yl histamine correlated with levels of serum tryptase, mast cell burden in the bone marrow, the prese

230 possibility that inhibitors of this membrane tryptase may provide additional therapeutic benefit in t

231 MCP-4 and the tryptase MCP-6 emerge to be protective in central nervou

232 d method for assessing serum total mast cell tryptase (MCT) in anaphylaxis.

233 ne tryptase levels and at least 1 subsequent tryptase measurement was available in 84 and 37 of these

234 diagnosis is often missed, with underuse of tryptase measurement; its treatment is delayed, with lit

235 clinicopathologic findings, while sequential tryptase measurements were useful in supplementing clini

236 idney function on the diagnostic accuracy of tryptase, MH, and MIMA to select the most optimal test i

237 study population, the diagnostic accuracy of tryptase, MH, and MIMA were comparable (area under the c

238 e of high clinical suspicion and/or elevated tryptase, MH, or MIMA.

239 ulling the tetramer apart into inactive beta-tryptase monomers, and may provide an alternative strate

240 were associated with corresponding shifts in tryptase mRNA levels, suggesting that copper affects try

241 tor 2 agonist and antagonist peptides, and a tryptase-neutralizing mAb on human umbilical vein endoth

242 Mast cells were cultured from wild-type and tryptase null mice, followed by an assessment of their p

243 cell phenotype in terms of protease content (tryptase-only [MCT], tryptase + chymase [MCTC]) and tumo

244 ave a significant correlation with the serum tryptase or mast cell burden in the bone marrow.

245 ase, exhaled nitric oxide (P < 0.05), plasma tryptase (P < 0.01), and blood eosinophil (P < 0.01) and

246 ith PAR-2 overexpression and higher alveolar tryptase (P </= .02) and KLK14 (P </= .03) levels.

247 echanisms, with elevated mast cell mediators tryptase (p<0.0001), chymase (p=0.02), and carboxypeptid

248 s were constructed by cloning alpha-and beta-tryptase PCR products to generate artificial templates.

249 n lung function, urinary eicosanoids, plasma tryptase, platelet-leukocyte aggregates, and platelet ac

250 uding pruritis and dermatitis, the number of tryptase-positive mast cells is increased.

251 OPD, most IL-17A(+) cells were identified as tryptase-positive mast cells.

252 The constitutive presence of tryptase-positive MCs was reduced in affected lungs from

253 d on hypoxic zones of melanoma tumors (where tryptase-positive MCs were also found).

254 PAR-4 was found to be coexpressed in 32% of tryptase-positive skin mast cells, and AYP caused a 2-fo

255 llular traps comprising of DNA, histones and tryptase probably to ensnare these pathogens.

256 The effects of pooled and recombinant human tryptases, protease activated receptor 2 agonist and ant

257 eterotetramers composed of 2alpha- and 2beta-tryptase protomers (alpha/beta-tryptase) form naturally

258 alpha-tryptase protomers on neighboring beta-tryptase protomers likely result in the novel substrate

259 Allosteric effects of alpha-tryptase protomers on neighboring beta-tryptase protomer

260 KIT D816V burden also correlated with serum tryptase (R = 0.5, P < 0.005) but not with mast cell inf

261 Standards for the possible alpha-/beta-tryptase ratios were constructed by cloning alpha-and be

262 (HLFs) induced MC activation, as evinced by tryptase release, and stimulated HLF proliferation; IPF

263 y hyperresponsiveness, mast-cell counts, and tryptase release.

264 Proteolysis of CCL26 by chymase and tryptase, respectively, released distinct fragments of t

265 MMP-1 is activated by mast cell tryptase resulting in a proproliferative extracellular m

266 thms with tightly controlled time frames for tryptase sampling, their robustness with inadequate samp

267 Patients with elevated basal tryptase (sBT) >15 mug/l and anaphylaxis may have an und

268 associated with elevation of baseline serum tryptase (sBT) and/or mastocytosis in about 5% of patien

269 A relationship between serum basal tryptase (sBT) levels, anaphylactic reactions, and clona

270 Hymenoptera stings and increased serum basal tryptase (SBT) levels.

271 ometric mean immunostained area by mast cell tryptase staining in ETR samples (0.018%) than in TP (0.

272 pear to have been traversed by prosemins and tryptases, suggesting that mutational tail loss is an im

273 ultaneously occupy four exosites on the beta-tryptase tetramer, inducing allosteric changes at the sm

274 tramers lack protease activity, whereas beta-tryptase tetramers are active proteases.

275 the novel substrate repertoire of alpha/beta-tryptase tetramers that in turn cause some of the clinic

276 plications in the TPSAB1 gene encoding alpha-tryptase that segregate with inherited increases in basa

277 For tryptase, the proportion of elevated values increased mo

278 MMR in an additional 14% of cases with peak tryptase (Tp) between 5 and 14 mug/L and a further 15% w

279 athepsin S (CTSS), mast cell chymase (CMA1), tryptase (TPS1) and mastin, neuromedin-B (NMB), nerve gr

280 We show that tryptase truncates nucleosomal histone 3 and histone 2B

281 tors, including the PAR-2 ligands, mast cell tryptase, trypsin, tissue factor, and kallikrein (KLK) 5

282 ase serine member S31 (Prss31)/transmembrane tryptase/tryptase-gamma is a mast cell (MC)-restricted p

283 Tryptase, UMH and clinical details were analysed.

284 operative anaesthetic reactions using serial tryptase, urinary methylhistamine (UMH) and clinical inf

285 localization of antigen, HLA molecules, and tryptase was analyzed by using structured illumination m

286 ucleus, and it was found that the absence of tryptase was associated with a pronounced accumulation o

287 Nasal fluid tryptase was elevated at 5 min after challenge (P < 0.05

288 Tryptase was elevated by age and body weight in non-ISM

289 Indeed, tryptase was found in the nucleus of viable cells and wa

290 During the cell death process, tryptase was found to relocalize from granules into the

291 ls with nonatopic disease were recruited and tryptase was genotyped by droplet digital PCR and in sil

292 MC-specific tryptase was identified to regulate PKA activity in card

293 gment to NH2 -terminal fragment generated by tryptase was obtained after incubation with supernatants

294 Possessing one copy of alpha-tryptase was significantly associated with lower serum l

295 Levels of VIP and tryptase were measured in plasma and biopsy lysates.

296 CD138, CD68, CD1a, CD15, CD23, and mast cell tryptase were performed.

297 itive inhibitory antibody against human beta-tryptase, which dissociates active tetramers into inacti

298 inF2alpha and N-methyl histamine, with serum tryptase, whole blood serotonin, and bone marrow finding

299 We recorded serum tryptase, whole blood serotonin, levels of urinary mast

300 totifen fumarate or inhibition of MC-derived tryptase with APC 366 prevented all of GA-like phenotype