ライフサイエンスコーパス: mast cell

1 d IL-33-mediated cytokine release from human mast cells.

2 s by proteome analysis of primary human skin mast cells.

3 tes to KIT-dependent upregulation of CCL2 in mast cells.

4 comprised of CD11b(+) cells, monocytes, and mast cells.

5 he proangiogenic cytokine CCL2 in neoplastic mast cells.

6 could have an impact on epigenetic events in mast cells.

7 ially eliminating IgE-mediated activation of mast cells.

8 colon and lung parenchyma by eosinophils and mast cells.

9 ls and enhancing the responses of individual mast cells.

10 during differentiation for the formation of mast cells.

11 CCL7 also induced chemotaxis in mast cells.

12 , type 2 innate lymphoid cells, and probably mast cells.

13 ed in vivo because it concurrently activates mast cells.

14 se model that allows conditional ablation of mast cells.

15 ns were found to be selectively expressed in mast cells.

16 tosis, is pivotal for compound exocytosis in mast cells.

17 tes the development, number, and function of mast cells.

18 rovide broad inhibitory signals to activated mast cells.

19 pressed proteins previously not described in mast cells; 21 of these proteins were found to be select

20 data demonstrate the relevance of Nbeal2 in mast cells above and beyond granule biosynthesis.

21 n of omega-3 epoxides, leading to attenuated mast cell activation and anaphylaxis following Fcvarepsi

22 3-dependent ILC2 expansion, and IL-33-driven mast cell activation are necessary for induction of type

23 current knowledge about the various types of mast cell activation disorders, their treatment, and are

24 ular allergy is associated with IgE-mediated mast cell activation in conjunctival tissue leading to t

25 compared the capability of Fel d 1 to induce mast cell activation in its free form versus displayed o

26 However, exacerbated mast cell activation in Sucnr1(-/-) mice did not contrib

27 This observation correlated with increased mast cell activation in vitro and in vivo.

28 nt in vivo, and maximal FcepsilonRI-mediated mast cell activation in vitro.

29 Mast cell activation is common and possibly necessary fo

30 The mast cell activation is negatively regulated by an inhib

31 Disordered mast cell activation occurs when mast cells are patholog

32 th active FPIES suggest low-grade intestinal mast cell activation or increased mast cell load.

33 has been proposed to interpret acute MCT in mast cell activation syndrome (MCAS).

34 treatment in the last decade, many areas of mast cell activation syndrome are in need of research.

35 rlying clonal mast cell disorder (monoclonal mast cell activation syndrome or systemic mastocytosis)

36 Mast cell activation syndrome refers to a group of disor

37 ith systemic mastocytosis but not monoclonal mast cell activation syndrome.

38 zed that IVIG will attenuate the ICH-induced mast cell activation via FcgammaRIIB/SHIP1 pathway, resu

39 hallenge by 84% to 90%, as well as diarrhea, mast cell activation, and TH2 cytokine responses and ser

40 TGF-beta-dependent Treg-cell suppression of mast cell activation, in the absence of modulation of T-

41 is characterized by tissue eosinophilia and mast cell activation, including abundant production of p

42 d positive signaling modalities that control mast cell activation, with an emphasis on novel Fcepsilo

43 ed the effects of TGF-beta on IL-33-mediated mast cell activation.

44 ng the role of DNA methylation in regulating mast cell activation.

45 as Fel d 1 displayed on VLPs fails to induce mast cell activation.

46 lcium mobilization and to the attenuation of mast cell activation.

47 tion/degranulation, IVIG attenuated post-ICH mast cell activation.

48 y displayed allergen on VLPs failed to cause mast cell activation.

49 We demonstrated that while ICH induced mast cell activation/degranulation, IVIG attenuated post

50 educed levels of serum tryptase, a marker of mast-cell activation, to a greater extent than did place

51 Therefore, we explored the role of CCL7 in mast cell activity and motility in vitro and investigate

52 interaction between IgE and FcRI, preventing mast cell and basophil activation, and blocks IgE bindin

53 and cellular mechanisms of AIT include early mast cell and basophil desensitization effects, regulati

54 high-affinity IgE receptors (FcepsilonRI) on mast cells and basophils and low-affinity IgE receptors

55 Mast cells and basophils are developmentally related cel

56 receptor for IgE expressed on the surface of mast cells and basophils interacts with antigens, via bo

57 cterize the transcriptional heterogeneity of mast cells and basophils upon their activation, we perfo

58 nking of IgE-FcepsilonRI complexes activates mast cells and basophils, initiating the allergic respon

59 Degranulation of mast cells and basophils, with release of agents of the

60 tering demonstrated that bone marrow-derived mast cells and BMBs shared specific activation-associate

61 ve microarrays of murine bone marrow-derived mast cells and bone marrow-derived basophils (BMBs) at r

62 mmunoglobulins and allergic mediators, lower mast cells and eosinophil counts, lower protein expressi

63 membrane receptor (mCD48) on eosinophils and mast cells and exists in a soluble form (sCD48).

64 estigate whether MMP-1 could be activated by mast cells and increase asthma severity.

65 tion potently inhibited histamine release by mast cells and inhibited adipocyte UCP1 mRNA induction b

66 In this review, we document the biology of mast cells and introduce new concepts and opinions regar

67 mice exhibit increased numbers of activated mast cells and neutrophils in the perivascular area of a

68 lammation through activation of receptors on mast cells and sensory neurons.

69 Mast cells and TH2 cells might decrease epithelial barri

70 KIT and other relevant targets in neoplastic mast cells and will hopefully receive recognition by hea

71 nd inhibition of responses from eosinophils, mast cells, and basophils in the affected tissues.

72 expressed selectively on human eosinophils, mast cells, and basophils, making it an ideal target for

73 creased numbers of lamina propria TH2 cells, mast cells, and eosinophils, shock (hypothermia), mast c

74 iated with eosinophilic airway inflammation, mast cells, and group 3 innate lymphoid cells were more

75 inflammatory pathways involving eosinophils, mast cells, and group 3 innate lymphoid cells.

76 nd pro-angiogenic (VEGFA) genes expressed by mast cells, and mitigated neo-angiogenesis formation in

77 , the effect of activated TH1 and TH2 cells, mast cells, and neurons was tested in vitro.

78 a cooperative role of activated eosinophils, mast cells, and the cytokines IL-5 and IL-13, mediated b

79 ecular mechanisms were interrogated by using mast cell- and FcgammaRIIb-deficient mice.

80 CD4(+) T cells is of critical importance but mast cells, antibodies, and basophils have few or no non

81 Our laboratory previously determined that mast cells are activated via a non-FcepsilonRI mediated

82 In asthma, mast cells are associated with airway smooth muscle grow

83 l as reduced bleeding times, indicating that mast cells are more efficient in their ability to downre

84 Disordered mast cell activation occurs when mast cells are pathologically overproduced or if their a

85 Mast cells are powerful immune modulators of the tissue

86 We found that MRGPRX2-expressing mast cells are present in normal gingiva and that their

87 Mast cells are present in the airways of patients who ha

88 Mast cells are significantly involved in IgE-mediated al

89 Mast cells are unique tissue-resident immune cells that

90 performed in vitro by using human and mouse mast cells, as well as rat basophil leukemia cells, and

91 gE to IgG4 and regulation of dendritic cell, mast cell, basophil, innate lymphoid cell, T-cell, and B

92 response, B cell, platelet, neutrophil, and mast cell/basophil activity.

93 Modules of mast cell/basophil and neutrophil function show temporal

94 on histamine release and the contribution of mast cells, basophils, macrophages, and neutrophils.

95 IgG subclasses controls the contributions of mast cells, basophils, neutrophils, and macrophages to I

96 We illustrate the effect of IL-33 on mast cell biology at the single-cell level by showing th

97 rs in humans, the role of DNA methylation in mast cell biology is not understood.

98 Bone marrow-derived cultured mast cells (BMCMCs) and peritoneal cell-derived mast cel

99 Using bone marrow-derived mast cells (BMMCs), we tested the hypothesis that ENM ph

100 her serum tryptase levels, reflective of the mast cell burden.

101 ber of degranulating and chemokine-producing mast cells but also the magnitude of individual mast cel

102 compared with wild-type bone marrow-derived mast cells, but there was no difference in degranulation

103 In conclusion, mast cells can infiltrate and elicit a degenerate phenot

104 Mast cells, central to the innate immune response, are o

105 y inhibited adipocyte UCP1 mRNA induction by mast cell CM.

106 athogenesis of IA involves a hyperresponsive mast cell compartment.

107 lts suggest that KIT-dependent processes and mast cells contribute to the pathobiologic basis of seve

108 cerebral hemorrhage (ICH), the activation of mast cell contributes to brain inflammation and brain in

109 Airway mast-cell counts declined in both groups.

110 atinib decreased airway hyperresponsiveness, mast-cell counts, and tryptase release.

111 Mast cell deactivation resulted in reduced inflammation,

112 flects a hematopoietic defect in addition to mast cell deficiency.

113 Our findings in mast cell-deficient Kit(W-sh/W-sh) mice and two types of

114 Mast cell-deficient mice exhibited increased FXIIIA plas

115 ficient Kit(W-sh/W-sh) mice and two types of mast cell-deficient mice that have normal c-kit ("Hello

116 l sensitivity to IgG-mediated arthritis in 2 mast cell-deficient murine lines: KitWsh/Wsh, which deve

117 ated lungs of wild-type, PKCalpha-deficient, mast cell-deficient, or eNOS-deficient mice.

118 cells, and eosinophils, shock (hypothermia), mast cell degranulation (increased serum mouse mast cell

119 t cells but also the magnitude of individual mast cell degranulation and chemokine production.

120 more, differential regulation of HDP-induced mast cell degranulation by PgLPS1690 and PgLPS1435/1449

121 ate beta-glucan (a DECTIN-1 agonist) induced mast cell degranulation in mesenteric windows and HMC-1

122 We monitored mast cell degranulation in real time by exploiting the c

123 Pharmacological block of mast cell degranulation potently inhibited histamine rel

124 evealed a strong heterogeneity of individual mast cell degranulation responses.

125 caused substantial inhibition of HDP-induced mast cell degranulation, but PgLPS1435/1449 had no effec

126 distinct feature of CSU, which could enhance mast cell degranulation.

127 iation by mast cells was not correlated with mast cell degranulation.

128 l and that TRPV4 loss of function attenuates mast cell degranulation.

129 phil migration and survival, and suppressing mast cell degranulation.

130 r skin diseases associated with IgE-mediated mast cell degranulation.

131 whether TRPV4-mediated Ca(++)-influx evokes mast cell degranulation.

132 hat ENM physicochemical properties influence mast cell degranulation.

133 thermore, although not completely protected, mast cell-depleted mice displayed less organ atrophy and

134 xpression in cultured human LAD2 and primary mast cells derived from umbilical cord blood.

135 omega-3 (omega-3) fatty acid epoxides as new mast cell-derived lipid mediators and show that they are

136 s and seemed to be due to alterations during mast cell development as augmented mast cell responses c

137 A deficiency in succinate sensing during mast cell development confers these cells with a hyperac

138 and KIT signaling are dispensable for early mast cell development.

139 cell responses could be recapitulated in wt mast cells differentiated in the absence of succinate.

140 cycle inhibitor p27, which are essential for mast cell differentiation, proliferation, and cytokine p

141 Clonal mast cell disease was diagnosed in 14% of patients refer

142 nts more likely to have an underlying clonal mast cell disorder (monoclonal mast cell activation synd

143 has prompted the question of whether clonal mast cell disorders also occur in patients with idiopath

144 sought to determine the prevalence of clonal mast cell disorders among patients with IA, criteria to

145 Clonal mast cell disorders are known to occur in a subset of pa

146 atients may present with unrecognized clonal mast cell disorders with KIT mutations may present as Hy

147 Chronic spontaneous urticaria (CSU) is a mast cell-driven skin disease characterized by the recur

148 s, our results suggest a deleterious role of mast cells during the acute inflammatory phase of IRI pr

149 nhanced skin infiltration of eosinophils and mast cells, elevation of T helper type 2 cytokines/chemo

150 sought to explore the role played by PDH in mast cell exocytosis and to determine whether MITF is lo

151 OVA-specific IgE production, and intestinal mast cell expansion in offspring.

152 ly, neither BM, blood, lung neutrophils, nor mast cells expressed C3aR.

153 cells, macrophages, dermal dendritic cells, mast cells, fibroblasts, and lymphatic endothelium, but

154 nts are temporary reflects rapid recovery of mast cells from a desensitized state.

155 However, the role of PDH in mast cell function has not been described.

156 The effect of PDH inhibition on mast cell function was examined.

157 ion-mediated ATP production is essential for mast cell function.

158 e differentially required for the control of mast cell function.

159 ith PDH emerges as an important regulator of mast cell function.

160 E-mediated allergic reactions, whereas other mast cell functions are poorly defined.

161 pportunities for therapeutic intervention of mast cell functions in inflammatory diseases.

162 mast cell research, including regulation of mast cell functions, differentiation, survival, and nove

163 ognized role for copper in the regulation of mast cell gene expression and maturation.

164 CD4(+) T cells/ILC2 cells, IgG, and FcRgamma>mast cells>IgE and FcepsilonRI>basophils.

165 rized by abnormal accumulation of neoplastic mast cells harboring the activating KIT mutation D816V i

166 The function of skin mast cells has been well documented in IgE-mediated alle

167 tion on the development of immune responses, mast cell homeostasis, and anaphylactic food allergy was

168 Mice bearing Kit defects lack mast cells; however, strains bearing different Kit allel

169 docytosed in human eosinophils and malignant mast cells, identify mechanisms underlying its endocytos

170 MS mice showed an increased number of mast cells in both adipose tissue and the brain.

171 In this study, we investigated the role of mast cells in both the early and late phases of the infl

172 Our studies reveal a novel role of mast cells in defense against bacterial infections.

173 lls that are relevant to the contribution of mast cells in diseases.

174 dyl peptidase 4 was found to be expressed in mast cells in normal, psoriasis, and mastocytosis skin a

175 L1 was found to be highly expressed in mast cells in normal, psoriasis, and mastocytosis skin.

176 mastocytosis skin as well as in bone marrow mast cells in patients with systemic mastocytosis.

177 dentified a central role for IgE/FcepsilonRI/mast cells in promoting IgE-mediated anaphylaxis.

178 port that TRPV4 expression is upregulated in mast cells in response to the proteolytic cathelicidin f

179 ddition to lower numbers of chymase-positive mast cells in the submucosa compared to patients with no

180 critical role for immune cells, specifically mast cells in their pathophysiology, eluding to a potent

181 activation of hematopoietic progenitors over mast cells in vitro and in vivo.

182 We differentiated human mast cells in vitro from blood-derived stem cell progeni

183 nt prevents progenitors from developing into mast cells in vitro.

184 creased fibrosis, increased vascularity, and mast cell infiltration.

185 agents that antagonize mediators released by mast cells, inhibit mediator secretion, or modulate mast

186 r findings suggest that airway smooth muscle/mast cell interactions contribute to asthma severity by

187 finity receptor FcepsilonRI on basophils and mast cells is a central event in the development of alle

188 demonstrate that this inability to activate mast cells is based on a biophysical as well as a bioche

189 e responses, but the impact of this metal on mast cells is poorly understood.

190 of mast cells within the IVD, specifically, mast cell-IVD cell interactions using immunohistochemist

191 By using mast cells lacking Dnmt3a, we found that this enzyme is

192 sive cell death in eosinophils and the human mast cell leukemia cell line HMC-1.2.

193 cluding aggressive systemic mastocytosis and mast cell leukemia.

194 Studies in mast cell-like RBL-2H3 cells provide direct evidence tha

195 re, HDPs stimulated degranulation in a human mast cell line (LAD2) and in RBL-2H3 cells stably expres

196 human basophil cell line KU812 and the human mast cell line HMC-1.

197 h mesenteric windows (ex vivo) and the human mast cell line HMC-1.

198 th a profound upregulation of markers of non-mast cell lineages, loss of proliferative control, chrom

199 intestinal mast cell activation or increased mast cell load.

200 otein fibronectin by peritoneal cell-derived mast cell lysates diminished GBS adherence.

201 Interleukin (IL)-4 and, unexpectedly, the mast cell marker CPA3 predicted UCP1 gene expression.

202 Importantly, we demonstrate that skin mast cell (MC) activation and local sphingosine-1-phosph

203 While allergic mast cell (MC) degranulation occurs by FcepsilonRI aggre

204 h systemic mastocytosis (SM) may suffer from mast cell (MC) mediator-related symptoms insufficiently

205 Mast cell (MC) progenitors leave the bone marrow, enter

206 levels of which are altered in patients with mast cell (MC)-related disorders.

207 Mast cells (MCs) and dendritic cells (DCs) are essential

208 olonic epithelium, and determine the role of mast cells (MCs) and vasoactive intestinal polypeptide (

209 The mechanism by which mast cells (MCs) are activated in T cell-mediated inflam

210 Mast cells (MCs) are innate immune cells that are a majo

211 Mast cells (MCs) are involved in host defenses against p

212 Mast cells (MCs) contribute to the pathogenesis of a mul

213 We sought to determine the role of mast cells (MCs) in DVT initiation and validate MCs as a

214 Mast cells (MCs) play a key role in asthma where their n

215 us cell types, including responding T cells, mast cells (MCs), and infected monocytes, can contribute

216 Mast cells (MCs), the primary effector cell of the atopi

217 enterally challenged with PN, they exhibited mast-cell-mediated systemic anaphylaxis, as indicated by

218 It will be of use when guideline-recommended mast cell mediator antagonists fail to control symptoms

219 ith characteristic skin lesions, episodes of mast cell mediator release, and disturbances of hematopo

220 isodic multisystem symptoms as the result of mast cell mediator release.

221 Dermal mast cell migration from the skin to the draining lymph

222 Activated mast cell MPs (CD137(+) FcepsilonRI(+)c-kit(+)MPs) were

223 n-like hormone receptor-like 1[EMR1](+)MPs), mast cell MPs (high-affinity IgE receptor [FcepsilonRI](

224 We found that in mast cells, Nbeal2 regulates the activation of the Shp1-

225 e pathogenesis, evolution, and complexity of mast cell neoplasms.

226 pulation, and an increase in intraepithelial mast cell numbers in the lung.

227 Mast cell numbers were associated with airway smooth mus

228 arker of severe asthma, as well as on airway mast-cell numbers and activation in patients with severe

229 d Kit(W-sh) mice were injected with cultured mast cells or 1x phosphate-buffered saline (PBS) before

230 Mast cells perform important barrier functions and help

231 There was no evidence of a hyperresponsive mast cell phenotype in patients with IA.

232 Based on released MPs, mast cells, platelets, and basophils were more highly ac

233 Mast cells play an important role in periodontitis, but

234 work in Kit(W/W-v) mice that suggested that mast cells play an important role in S. venezuelensis eg

235 Depletion of mast cells prior to IRI resulted in improved renal funct

236 Here, we demonstrate that circulating mast cell progenitors are present in patients undergoing

237 In addition, we show that mast cell progenitors from peripheral blood survive, mat

238 However, these observations do not mean that mast cell progenitors require SCF and KIT signaling thro

239 lls, inhibit mediator secretion, or modulate mast cell proliferation.

240 terns and mutations in DNMT3A correlate with mast cell proliferative disorders in humans, the role of

241 d genetic approaches using mice deficient in mast cell protease (MCPT) 4, the mouse functional homolo

242 st cell degranulation (increased serum mouse mast cell protease 1), increased serum IgG1 anti-EW and

243 Our study indicates that the mast cell protease content can shape its releasate prote

244 This study aimed at identifying novel mast cell proteins by proteome analysis of primary human

245 proteomics approach we identified two novel mast cell proteins potentially relevant to skin homeosta

246 Within the mast cell proteome, we identified 49 highly expressed pr

247 Human lung mast cells readily recover from a desensitized state fol

248 for maximal OVA-induced ocular anaphylaxis, mast cell recruitment in vivo, and maximal FcepsilonRI-m

249 ntial mechanisms in CIU/CSU include reducing mast cell releasability, reversing basopenia and improvi

250 We aimed to define the proteome contained in mast cell releasates on activation to better understand

251 Our studies show that mast cells release a protease with chymotrypsin-like cle

252 Conversely, basophils (but not mast cells) released histamine and marked levels of IL-4

253 light recent discoveries and developments in mast cell research, including regulation of mast cell fu

254 urrogates" for mucosal and connective tissue mast cells, respectively, and their releasate proteomes

255 TIB64 mast cells responded to cold by releasing histamine and

256 ember of the IL-1 family capable of inducing mast cell responses and enhancing IgE-mediated activatio

257 showing that IL-33 potentiates IgE-mediated mast cell responses by both increasing the number of res

258 ns during mast cell development as augmented mast cell responses could be recapitulated in wt mast ce

259 The exacerbated mast cell responses observed in the absence of Dnmt3a we

260 that this enzyme is involved in restraining mast cell responses to acute and chronic stimuli, both i

261 Desensitization of mast cell responses was readily induced with concentrati

262 LC2s), which promote tissue eosinophilia and mast cell responses, undergo chemotaxis and cytokine pro

263 aling pathways, and adaptor proteins governs mast cell responsiveness to stimuli.

264 nds from their secretory granules, including mast cell-restricted proteases such as tryptase.

265 Furthermore, knockdown of CCL2 in neoplastic mast cells resulted in reduced microvessel density and r

266 Together, these data show that mast cells sense colder temperatures, release factors th

267 showed IL-24 to release histamine from human mast cells sensitized with purified IgE of patients with

268 CCL7-deficient bone marrow-derived mast cells showed decreased degranulation following IgE

269 This work advances our understanding of mast cell signaling and represents a generalizable appro

270 Airway smooth muscle treated with activated mast cell supernatants produced extracellular matrix, wh

271 ndogenous cysLTs was assessed by using human mast cell supernatants.

272 s, complete with tissue engraftment by human mast cells that are competent to mount specific IgE-medi

273 to better understand the factors secreted by mast cells that are relevant to the contribution of mast

274 ystemic mastocytosis is a clonal disorder of mast cells that may variably present with characteristic

275 recruitment of macrophages, neutrophils, and mast cells, the recruitment and activation of fibroblast

276 auses FcepsilonRI receptors on basophils and mast cells to be downregulated.

277 However, the response of individual mast cells to cumulative stimuli remains poorly understo

278 The sensitivity of mast cells to fungi was tested with mesenteric windows (

279 For mast cells treated with IgE and Ag, the presence of CCL7

280 MMP-1 is activated by mast cell tryptase resulting in a proproliferative extra

281 P3, CD20, CD138, CD68, CD1a, CD15, CD23, and mast cell tryptase were performed.

282 MP-1, which was proteolytically activated by mast cell tryptase.

283 ytosis, systemic mastocytosis, and localized mast cell tumors.

284 RIalpha transgenic mouse bone marrow-derived mast cells via driving internalization of the IgE/Fcepsi

285 7 and human beta-defensin-3), which activate mast cells via Mas-related G protein-coupled receptor X2

286 The proteome of skin mast cells was compared to other cell types and analyzed

287 E-mediated histamine release from human lung mast cells was explored by methods that partially replic

288 In addition, CCL2 secreted by KIT D816V(+) mast cells was found to promote the migration of human e

289 isingly, minimal ENM cellular association by mast cells was not correlated with mast cell degranulati

290 Mast cells were cultured from peripheral blood CD34(+) c

291 nctional human T and B lymphocytes and human mast cells were found in significant numbers in their ti

292 lergic response, the numbers of conjunctival mast cells were lower in CCL7-deficient mice than in wil

293 stry, we found that numbers of basophils and mast cells were markedly increased in the jejunal mucosa

294 Mast cells were upregulated in painful human IVD tissue

295 t cells (BMCMCs) and peritoneal cell-derived mast cells were used as "surrogates" for mucosal and con

296 location, can be found within the nuclei of mast cells where it truncates core histones at their N-t

297 d 1 induces degranulation of IgE-sensitized mast cells whereas Fel d 1 displayed on VLPs fails to in

298 ng finding was decreased tryptase content in mast cells with copper overload, whereas copper starvati

299 a and in the proinflammatory interactions of mast cells with eosinophils via its ligand CD244.

300 ght to characterize the presence and role of mast cells within the IVD, specifically, mast cell-IVD c