ライフサイエンスコーパス: tryptase

1 uding mast cell-restricted proteases such as tryptase.

2 relates with mast cell burden as assessed by tryptase.

3 pression, storage, and enzymatic activity of tryptase.

4 eficial and adverse functional roles for the tryptase.

5 a nonpulmonary cause was stained for MCs and tryptase.

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

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

8 a potential inhibitor of the serine protease tryptase.

9 s, this was not true for either histamine or tryptase.

10 CD34 and Ano1, but not with mast cell marker tryptase.

11 responsible for the antiapoptotic effects of tryptase.

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

13 h was proteolytically activated by mast cell tryptase.

14 detection of potentially relevant changes in tryptases.

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

16 y investigating the antiapoptotic effects of tryptase, a major product of mast cells, on RA synovial

17 Tryptase, a major secretory product of human mast cells

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

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

20 Mast cells, bearing both c-Kit and tryptase, accumulated in the sublining area of prolifera

21 These observations indicate that betaII-tryptase activity is post-translationally regulated by a

22 propose that TSG-6 can promote inhibition of tryptase activity via a mechanism similar to inhibition

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

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

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

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

27 age by serine proteases, including mast cell tryptase and activated coagulation factors.

28 NPs were characterized by the expression of tryptase and carboxypeptidase A3 but not chymase.

29 Tryptase and carboxypeptidase A3 expression in epithelia

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

31 that MCs containing either tryptase only or tryptase and chymase have long been considered to be the

32 Tryptase and cysteinyl leukotriene (cysLT) levels were m

33 onse with release of inflammatory mediators (tryptase and eosinophil cationic protein).

34 bar spine and femoral neck was measured, and tryptase and histamine metabolites were analysed.

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

36 nd to investigate the association with serum tryptase and the urinary histamine metabolites, methylhi

37 Tryptase and thrombin are upregulated in wound healing a

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

39 We report that tryptase and thrombin potentiate human fibrocyte differe

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

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

42 otease inhibitor that rapidly inactivates MC tryptases and why mammals have two genes that encode tet

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

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

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

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

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

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

49 n tree using clinical characteristics, serum tryptase, and the urinary histamine metabolites methylim

50 a dose-dependent manner, by the addition of tryptase, and this effect correlated with increased acti

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

52 uggest that human and mouse tetramer-forming tryptases are MMP convertases that mediate cartilage dam

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

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

55 In vivo TSG-6-tryptase association could also be detected in arthritic

56 -UA and controls with the highest release of tryptase at 60 min (P < 0.05).

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

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

59 rimary proteolytic targets for the serglycin-tryptase axis.

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

61 isease (IBD) have increased numbers of human tryptase-beta (hTryptase-beta)-positive mast cells (MCs)

62 Increased basal serum tryptase (bsT) levels are a well-described risk factor f

63 actors including elevation of baseline serum tryptase (BST), older age, concomitant diseases, and con

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

65 Thus, we propose that the release of tryptase by mast cells leads to the binding of tryptase

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

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

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

69 of a single population of MCs with a uniform tryptase(+), chymase(+), CPA3(+), cathepsin G(+), and gr

70 We analyzed mRNA for the mast cell proteases tryptase, chymase, and carboxypeptidase A3 by using real

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

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

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

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

75 verload, whereas copper starvation increased tryptase content.

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

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

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

79 phosphorylation of Lyn kinase and release of tryptase, decreased accumulation and degranulation of ma

80 Mechanistic studies demonstrated that tryptase deficiency affected endothelial cell (EC) chemo

81 Intriguingly, tryptase deficiency resulted in defective proteolytic mo

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

83 covery that mouse and human tetramer-forming tryptases destroy fibrinogen before this circulating pro

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

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

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

89 Macrophages and tryptase-expressing MCs were required for the developmen

90 nd we show a requirement for macrophages and tryptase-expressing MCs.

91 IL-33 is the first factor shown to modulate tryptase expression in MCs at the mRNA and protein level

92 esults revealed strong increase in PAR-2 and tryptase expression in the lungs of idiopathic pulmonary

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

94 a transcription factor critical for driving tryptase expression.

95 inhibitors substantially reduced mature beta-tryptase formation.

96 ed tryptase tetramer formation and protected tryptase from degradation by CTSB and CTSL.

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

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

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

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

101 of cartilage explants with tetramer-forming tryptases generated aggrecan fragments that contained C-

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

103 e <10 mug/l, in 45 of 98 (46%) patients with tryptase >/=10 mug/l and in 18 of 52 patients (35%) with

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

105 10 mug/l and in 18 of 52 patients (35%) with tryptase >20 mug/l.

106 ostic World Health Organization criterion of tryptase >20 mug/l.

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

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

109 These results demonstrate that tryptase has a strong antiapoptotic effect on RASFs thro

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

111 ciated with severity, and 1 group (mast cell tryptase, histamine, IL-6, IL-10, and tumor necrosis fac

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

113 mental AAAs, we proved a direct role of this tryptase in AAA pathogenesis.

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

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

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

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

118 ed receptor (PAR)-2 and its ligand mast cell tryptase in the development of PH.

119 y establishes the direct participation of MC tryptase in the pathogenesis of experimental AAAs, and s

120 targets for attenuating production of mature tryptase in vivo.

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

122 highest level of TSG-6 was co-localized with tryptases in the heparin-containing secretory granules o

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

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

125 phosphorylation of Lyn kinase and release of tryptase, indicating mast cell activation.

126 Tryptase induced PASMC proliferation and migration as we

127 Recombinant MC tryptase induced proinflammatory responses from cultured

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

129 If tryptase is >/=10 mug/l, this risk depends on MIMA and M

130 ISM risk is very low (if present at all) if tryptase is <10 mug/l.

131 inations in suspected patients without UP if tryptase is <10 mug/l.

132 Mast cell betaII-tryptase is a S1A protease that is associated with patho

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

134 lates with severity relative to histamine or tryptase is not known.

135 Human beta-tryptase is stored in secretory granules of human mast c

136 Tryptase is the most abundant MC granule protein and par

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

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

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

140 veral MC differentiation antigens, including tryptase, Kit, and a functional IgE receptor.

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

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

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

144 ented by a substantial increase in the serum tryptase level above baseline.

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

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

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

148 816V is detected and/or (ii) the basal serum tryptase level is clearly increased (>25-30 ng/ml) and/o

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

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

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

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

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

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

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

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

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

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

159 0.07, area under the curve) and early-phase tryptase levels (P = 0.06).

160 Baseline tryptase levels and at least 1 subsequent tryptase measu

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

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

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

164 Tryptase levels and symptoms decreased over time in most

165 Serum tryptase levels and tryptase immunohistochemical stainin

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

167 Tryptase levels are particularly useful for the diagnosi

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

169 Tryptase levels are seldom increased because of infant a

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

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

172 Serum tryptase levels correlated significantly with the annual

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

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

175 Serum tryptase levels differed significantly between patients

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

177 Serum tryptase levels furthered classification and reflected c

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

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

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

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

182 Similar reductions of tryptase levels in primary skin-derived mast cells were

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

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

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

186 Elevated tryptase levels were also detected in plasma samples fro

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

188 Serum basal tryptase levels were estimated by UniCAP (Pharmacia & Up

189 (172 individuals) that elevated basal serum tryptase levels were exclusively associated with duplica

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

191 Tryptase levels were higher in AERD compared with MNSAID

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

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

194 Serum tryptase levels were measured by immunofluorescence.

195 PAF, histamine, and tryptase levels were measured in blood samples collected

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

197 Tryptase levels were only increased in NAPTs with Pru p

198 Tryptase levels were positive in 3 challenges.

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

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

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

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

203 Levels of NGF-beta and NT-4 correlated with tryptase levels, suggesting a link between MC load and b

204 macologic inhibitor of CTSC markedly reduced tryptase levels, suggesting an off-target effect.

205 with markers of M2 macrophages but not with tryptase levels, suggesting that M2 macrophages are majo

206 cated by hypothermia and increases in plasma tryptase levels.

207 atients with symptoms, AOPPs correlated with tryptase levels.

208 with mastocytosis, regardless of their serum tryptase levels.

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

210 SM was absent in all 44 patients with tryptase <10 mug/l, in 45 of 98 (46%) patients with tryp

211 be drawn between the densities of c-kit and tryptase mast cells and the density of inflammatory infi

212 ls with HIV had higher densities of c-kit or tryptase mast cells than those without HIV, both groups

213 staining was performed to identify c-kit and tryptase mast cells.

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

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

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

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

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

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

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

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

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

223 ect venom anaphylaxis as presenting symptom, tryptase, MIMA, and MH were independent ISM predictors.

224 hypothesized that this mMCP, or the related tryptase mMCP-7, might have a prominent proinflammatory

225 burn, whereas mice lacking the MC-restricted tryptases, mMCP-6 and mMCP-7, or MC-specific carboxypept

226 t the ectopic expression of a mouse-specific tryptase mMCP11 does not lead to gp96 cleavage in human

227 the chymase mouse mast cell protease-4, the tryptase mouse mast cell protease-6, and carboxypeptidas

228 a large number of serine proteases including tryptases, mouse mast cell protease (mMCP)-6 and -7; chy

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

230 Tryptase mRNA was significantly increased in nasal polyp

231 In vitro, TSG-6 formed complexes with the tryptases murine mast cell protease-6 and -7 via either

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

233 hibitor, reduced the antiapoptotic effect of tryptase on RASFs, suggesting that Rho was responsible f

234 mited by the fact that MCs containing either tryptase only or tryptase and chymase have long been con

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

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

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

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

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

240 ine-aspirin challenge were analyzed for ECP, tryptase, PGE2 , PGD2 , LTD4 , and LTE4 .

241 Since tryptase plays a crucial role in the development of alle

242 ting that this mast cell (MC)-specific mouse tryptase plays prominent roles in articular cartilage ca

243 mannose receptor-positive M2 macrophages and tryptase-positive mast cells in NPs.

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

245 s used to assess the numbers of eosinophils, tryptase-positive mast cells, IL-9(+) cells, and mast ce

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

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

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

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

250 beta-Tryptase processing activity(ies) distinct from CTSC wer

251 Tryptase protein was also elevated in NPs and in nasal l

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

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

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

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

256 FBM) was measured by beta-hexosaminidase and tryptase release.

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

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

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

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

261 Serum baseline total tryptase (sbT) levels in 111 children with MIS - 80 macu

262 The importance of serum basal tryptase (sBT) levels on patients with venom allergy is

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

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

265 Neither histamine nor tryptase showed as good correlations with severity score

266 completely suppressed trypsin and mast cell tryptase signaling through PAR2 in neutrophils and colon

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

268 Immunohistochemistry demonstrated enhanced tryptase staining in media and adventitia of human and m

269 Tryptase stimulated HLF growth in a PAR-2/PKC-alpha/Raf-

270 y, mast cell-derived interleukin (IL)-13 and tryptase stimulated PSC proliferation.

271 Thrombin or tryptase stimulation of WT lung endothelial cells result

272 SB2 and TPSAB1 genes encode tetramer-forming tryptases stored in the secretory granules of mast cells

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

274 Heparin promoted tryptase tetramer formation and protected tryptase from

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

276 For tryptase, the proportion of elevated values increased mo

277 O) and wild type (WT) mice with thrombin and tryptase to determine the role of iPLA(2)beta in endothe

278 yptase by mast cells leads to the binding of tryptase to PAR-2 on RASFs and inhibits the apoptosis of

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

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

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

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

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

284 Tryptase, UMH and clinical details were analysed.

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

286 If tryptase was >/=10 mug/l, the diagnostic accuracy of MIM

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

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

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

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

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

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

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

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

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

296 Proproliferative properties of tryptase were attenuated by knockdown or pharmacological

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

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

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

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