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1 deed the dominant codeine receptor of dermal mast cells.
2 mice that have large numbers of activated hu mast cells.
3 t(W-sh/W-sh) mice engrafted with NHERF1(+/-) mast cells.
4 sophagitis have increased numbers of mucosal mast cells.
5 but acts as an "alarmin" via stimulation of mast cells.
6 to promote internalization of S aureus into mast cells.
7 oloBLG, which also impaired degranulation of mast cells.
8 human cytokines, and develop numerous human mast cells.
9 produced by additional cell types, including mast cells.
10 mbers of the lineage known in vertebrates as mast cells.
11 lease of proinflammatory mediators from skin mast cells.
12 1 (NHERF1) promotes C3aR functions in human mast cells.
13 e-formed inflammatory mediators in remaining mast cells.
14 llular signal-regulated kinase activation in mast cells.
15 tes with gene expression for eosinophils and mast cells.
16 I(CRAC) ) under a range of conditions in RBL mast cells.
17 The majority of c-Kit(+) cells were mast cells.
18 ived mast cells and human cord blood-derived mast cells.
19 antigen dependent-FcepsilonRI activation in mast cells.
20 2+) stores, thereby regulating exocytosis in mast cells.
21 hemistry showed that most of the COX2 was in mast cells.
22 Most c-Kit(+) cells in the renal pelvis are mast cells.
24 is a hematological disease in which aberrant mast cells accumulate because of gain-of-function mutati
25 roup, VAD mice manifested significantly more mast cells accumulation in the skin lesions, more severe
27 nd IL-13, cytokines known for their roles in mast cell activation and growth-enhancing activity as we
28 ed the expression of factors associated with mast cell activation and malaria-associated bacteremia i
29 Protection was associated with suppressed mast cell activation and markedly reduced mast cell infi
32 was allergen-induced mast cell expansion and mast cell activation in the intestine in a model of food
33 ), systemic mastocytosis (SM) and monoclonal mast cell activation syndrome (MMAS), represent an incre
38 E, IL-9, and IL-13 that maintain and enhance mast cell activation while disrupting the protease/antip
39 uppress rat paw inflammation, macrophage and mast cell activation, and histopathology induced by intr
40 e) on mast cell-mediated pathology and human mast cell activation, including the molecular mechanisms
41 These factors include certain comorbidities, mast cell activation-related events affecting the cardio
52 s using human IgE to selectively evoke human mast cell and basophil activation, and response severity
53 t mAbs are to induce anaphylaxis and deplete mast cell and basophil IgE, but mv mAbs still strongly s
54 viduals, results from the production of IgE, mast cell and basophil sensitisation and degranulation,
56 ibitor omeprazole can reduce both esophageal mast cell and eosinophil numbers and attenuate type 2 in
59 erythema with increased epidermal thickness, mast cell and neutrophil infiltration, expression of inf
61 he high-affinity IgE receptor FcepsilonRI on mast cells and basophils and drives allergic inflammatio
64 lobulin E (IgE) antibodies that are bound to mast cells and basophils, triggering the release of infl
69 ion and cytokine production in primary human mast cells and blocked allergen-induced contraction of i
70 s safely removed >98% of IgE from peritoneal mast cells and completely suppressed IgE-mediated anaphy
71 production of early cytokines that activate mast cells and drive IgE production, followed by elevate
73 ile some relationships between inflammation (mast cells and eosinophils) and depression have been rep
75 bulin-like lectin (Siglec)-8 is expressed on mast cells and eosinophils, but information about Siglec
76 histology and immunofluorescence to quantify mast cells and expression of advanced glycosylation end-
77 the differentiation and activation of murine mast cells and for the manifestations of food allergy an
78 protease that is predominantly expressed by mast cells and has key roles in immune defense and the c
80 olving eosinophil and basophil granulocytes, mast cells and humoral factors such as IgE are key drive
81 as used to characterize S aureus uptake into mast cells and investigate the effects of SEB on this pr
84 TE synthesis, was predominantly expressed in mast cells and localized near 15-LO(+) epithelium in NPs
88 e cells equally well as biopsies, except for mast cells and nonmigratory CD163+ macrophages that were
89 w, we briefly describe the origins of tissue mast cells and outline evidence that these cells can hav
91 zed patients presented a reduced activity of mast cells and phagocytes as an effect of the treatment.
92 ibody that depletes eosinophils and inhibits mast cells and that has shown potential in animal models
93 There was a correlation between submucosal mast cells and the early-phase clinical response (r = 0.
94 arrow-derived cells, such as eosinophils and mast cells and the intriguing innate lymphoid cells, whi
95 other hand, increased MRGPRX2 expression on mast cells and their inappropriate activation may contri
97 es CD4(+) T cells and innate lymphoid cells, mast cells are a source of GM-CSF in this model, and its
99 We found that MALT1(-/-) and MALT1(PD/PD) mast cells are equally impaired in cytokine production f
101 m hematopoietic progenitors to basophils and mast cells are largely uncharted at the single-cell leve
104 naling induced significant loss of choroidal mast cells, as well as an altered inflammatory response
106 ow that AAMPhi polarized by IL-33-stimulated mast cells attenuated the encephalitogenic function of T
107 ding endothelial cells, smooth muscle cells, mast cells, B cells, myeloid cells, and T cells and iden
109 ec-8 on the surface of human eosinophils and mast cells binds to sialic acid-containing ligands in th
110 review, we present an overview of classical mast cell biology and put these concepts into the contex
113 both the specific antigen recognized by the mast cell-bound IgE and a high-affinity glycan ligand of
114 e hypothesize that a high cutaneous D816V(+) mast cell burden alters the skin microenvironment to ind
116 chored, and transmembrane (TM) probes in RBL mast cells by imaging fluorescence correlation spectrosc
121 ed distinctively low expression of ZNF263 in mast cells compared with other (non-heparin-producing) i
122 se features included basophils and increased mast cell contents; increased immunostaining for tumor n
123 In addition to their role in host defense, mast cells contribute to a number of chronic inflammator
125 nd that AAMPhi polarized by IL-33-stimulated mast cells could suppress proliferation and IL-17 and IF
127 lls has been hampered by low yields of human mast cell cultures and their poor transfection efficienc
128 llergic response, mediating 1) IgE-dependent mast cell cytokine production, and 2) histamine-induced
130 F substitution in Ptgs2 (Ptgs2(Y385F) mice), mast cell-deficient (W/W(V)) mice, and W/W(V) mice given
131 hylaxis were reduced in NHERF1(+/-) mice and mast cell-deficient Kit(W-sh/W-sh) mice engrafted with N
133 dase secretion (IC(50) 8 nM) from human LAD2 mast cells degranulated by 100 nM C3a, and (c) selectivi
134 adducts in re-challenge reactions leading to mast cell degranulation and anaphylaxis is unclear.
135 We developed an imaging system in which mast cell degranulation can be visualized in single cell
136 ted IgE- and non-IgE-mediated human or mouse mast cell degranulation in a concentration-dependent man
137 zer, MCS-01, which proved to be an effective mast cell degranulation inhibitor in vitro and can be de
138 In addition to cytokine production, acute mast cell degranulation is a critical component of aller
139 lting in eosinophil apoptosis, inhibition of mast cell degranulation, and suppression of inflammation
140 creases in circulating IgE, which can induce mast cell degranulation, as well as Mcpt-1 and Mcpt-4, w
143 factor ligand superfamily member 14; sparse mast cell degranulation; numerous forkhead box protein P
145 mice with Tph1(-/-) mast cells or selective mast cell deletion of Tph1 enhances uncoupling protein 1
146 vs. 17.5) and peak (26.2 vs. 22.9) duodenal mast cell densities as compared those without nausea.
147 In the descending colon, eosinophil and mast cell densities both correlated with depression scor
150 Nausea is associated with increased mucosal mast cell density, non-gastrointestinal somatic symptoms
151 onses were investigated as was its impact on mast cell-dependent anaphylaxis and food allergy phenoty
152 )) mice, and W/W(V) mice given injections of mast cells derived from wild-type or Ptgs2(Y385F) mice.
155 as required for induction of AAMPhi, whereas mast cell-derived IL-6 enhanced macrophage responsivenes
158 , and cell fate assays to chart basophil and mast cell differentiation at single-cell resolution in m
159 reconstructed a detailed map of basophil and mast cell differentiation, including a bifurcation of pr
160 is how to integrate conventional markers of mast cell disease burden (percentage of bone marrow mast
162 yndrome coronavirus 2 may not be elevated in mast cell disease, certain conditions may increase the r
167 ment of new therapeutic strategies to target mast cells during anaphylaxis or other allergic diseases
168 udy were to: (1) assess densities of colonic mast cells, eosinophils, and TH17 cells in youth with IB
169 ending and rectosigmoid colons, densities of mast cells, eosinophils, and TH17 cells were higher in I
170 igmoid colons, densities were determined for mast cells, eosinophils, and TH17 cells, respectively, i
171 vantage that it may give time to desensitize mast cells, even in already sensitized individuals.
172 etween the aberrant LysRS-P542R function and mast cell-exacerbated activation with increase in proinf
173 ated with omeprazole as was allergen-induced mast cell expansion and mast cell activation in the inte
174 s elicited by mechanical activation in human mast cells expressing p.C492Y-ADGRE2 and attached to der
176 an allergen in vivo and further primed human mast cells for degranulation in an antigen-independent f
182 tokine signaling, skin barrier function, and mast cell function, as well as pathways that have not ye
184 X2 signaling is a primary mechanism by which mast cells functionally interact with nociceptors to for
185 ght to evaluate the effects of omeprazole on mast cell functions including development, IgE:Fcepsilon
186 iption factor, which is involved in critical mast cell functions such as synthesis of mediators and g
187 lication to gene expression studies in human mast cells has been hampered by low yields of human mast
192 environment within granules is important for mast cell homeostasis, we sought to evaluate the effects
194 these patients, friction of the skin induces mast cell hyper-degranulation through p.C492Y-ADGRE2, ca
195 ilonRIalpha mAbs also safely removed ~98% of mast cell IgE and prevented IgE-mediated anaphylaxis.
200 lec-8 is highly expressed on eosinophils and mast cells in asthmatic sputum and targeting Siglec-8 wi
202 tivity, associated with increased numbers of mast cells in colon and expression of AGER; these can be
203 ntrols, associated with increased numbers of mast cells in colon and expression of the receptor for A
204 els of spontaneous release of molecules from mast cells in colonic mucosa from patients with IBS with
206 aused by wasp venom peptide degranulation of mast cells in mice by 51% (P < 0.05), which was comparab
210 revealed overexpression of genes related to mast cells in the TME of SCMs, and a predominance of exh
211 aracterize interactions between S aureus and mast cells in this setting and elucidate potential inter
214 e investigated the role of COX2, produced by mast cells, in mediation of visceral hypersensitivity us
215 tributed global histone acetylation in human mast cells, including significantly decreased acetylatio
216 s into the interactions between S aureus and mast cells, including the internalization process, and d
217 ll disease burden (percentage of bone marrow mast cell infiltration and serum tryptase levels) with m
219 inhibitory receptor CD33 (CD33L) to targeted mast cells inhibits antigen-induced, FcepsilonRI-depende
221 e anaphylatoxins C3a and C5a, which activate mast cells leading to plasma extravasation, pain, and it
227 sed: These are (a) A natural role of reduced mast cell (MC) reactivity in developing IgE-mediated rea
229 ogic conditions, connective tissue phenotype mast cells (MC(TC)s) can be found in the lung parenchyma
236 e and evolution of the complement system and mast cells (MCs) can be traced back to sea urchins and t
237 on and pathologic accumulation of neoplastic mast cells (MCs) in various tissues, leading to severe s
238 s mice with selective deficiency of IL-13 in mast cells (MCs) were studied; in addition, dendritic ce
243 SCFAs (acetate, propionate, and butyrate) on mast cell-mediated pathology and human mast cell activat
244 t, following skin transplantation, the donor mast cell-mediated senescence in FRCs was associated wit
246 6 potential items tested in 97 patients with mast cell mediator-induced (n = 49) or bradykinin-mediat
247 problem in the context of chronic urticaria (mast cell mediator-induced), ACE-inhibitor intake and he
248 previously identified IL-9-producing mucosal mast cell (MMC9) as the primary source of IL-9 to drive
254 inst anaphylaxis, likely due to reduction in mast cell numbers and depletion of pre-formed inflammato
257 ation profiles of both edited and non-edited mast cells, offering a consistent internal control not f
259 t of mast cell-deficient mice with Tph1(-/-) mast cells or selective mast cell deletion of Tph1 enhan
261 ure experiments showed that IL-33-stimulated mast cells polarized AAMPhi through production of solubl
264 irculating levels of bacterial 16S DNA, IgE, mast cell protease 1 (Mcpt-1) and Mcpt-4, Th1 and Th2 cy
267 t blaze a trail to develop new drugs against mast cell-related diseases, including allergic hypersens
270 current study, we show that NHERF1 regulates mast cell response following FcepsilonRI stimulation.
271 he mechanisms through which NHERF1 modulates mast cell responses will lend insights into the developm
272 e levels of microRNAs (miRNAs) that regulate mast cell responses, miRNA 155-3p and miRNA 155-5p, were
273 led to the expansion and eventual rupture of mast cells, resulting in release of viable S aureus into
274 o cell-culture model was used to investigate mast cell-S aureus interactions by using a combination o
277 upled receptor X2 (MRGPRX2) is regarded as a mast cell-specific receptor mediating non-IgE-dependent
278 f diabetic wound healing and suggest topical mast cell stabilization as a potentially successful trea
281 We developed an indole-carboxamide type mast cell stabilizer, MCS-01, which proved to be an effe
283 GS mice, which are immune-deficient, produce mast cell-stimulating human cytokines, and develop numer
284 etter understanding of factors that regulate mast cell subtype and their different effector functions
285 diated activation controlled by eosinophils, mast cells, T(H)2 cells, group 2 innate lymphoid cells,
286 f the IL-33R complex, expressed primarily on mast cells, Th2 cells, group 2 innate lymphoid cells and
287 he infiltration of white adipose tissue with mast cells that are highly enriched with tryptophan hydr
288 order assemblies on the nuclear envelope of mast cells; these assemblies were linked to leukotriene
289 Collectively, codeine degranulates skin mast cells through MRGPRX2, at which it acts as a balanc
291 a suggest that therapies aimed at inhibiting mast cell Tph1 may represent a therapeutic approach for
293 icrobiota of 11 dogs affected by spontaneous mast cell tumor (MCT), using skin contralateral sites as
295 ing to better define the interaction between mast cell tumors, microbiota and host immune response.
300 ation of anaphylaxis revealed that FcER1 and mast cells were required for hypothermia and elevated se
301 he synthesis of prostaglandin E(2) (PGE2) by mast cells, which activates the receptor PTGER2 (also ca