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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.
23 ponses, i.e., degranulation, in single human mast cells (10-12 weeks old).
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
26                            Not surprisingly, mast cells act as sentinel cells that sense microbial at
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
30                                            A mast cell activation assay was used to determine whether
31 ed to determine whether an S8mAb can inhibit mast cell activation in human lung tissue ex vivo.
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
34 f COVID-19 in patients with mastocytosis and mast cell activation syndromes.
35                                       In the mast cell activation test, Ara h 2 induced significantly
36         ImmunoCAP inhibition experiments and mast cell activation tests in response to both Ara h 2 a
37                                     Systemic mast cell activation was determined by serum Mcpt1 ELISA
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
42 adapter molecule and promotes IgE/Ag-induced mast cell activation.
43  by augmenting Th2-mediated inflammation and mast cell activation.
44 onRI-mediated signals that are essential for mast cell activation.
45 is provides insights into how LysRS works in mast cell activation.
46 explained by epigenetic suppression of human mast cell activation.
47 d in diminished serum IgE titers and reduced mast cell activation.
48                                              Mast-cell activity may contribute to the pathogenesis of
49           Symptoms and duodenal eosinophils, mast cells (all, P < .0001), and paracellular passage (P
50         MrgprB2-mediated activation of local mast cells also clears cutaneous bacterial infection, pr
51                                              Mast cell and basophil activation by antigen cross-linki
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,
55 stric and mucosal biopsies were assessed for mast cell and eosinophil densities, respectively.
56 ibitor omeprazole can reduce both esophageal mast cell and eosinophil numbers and attenuate type 2 in
57 nt for treatment of diseases associated with mast cell and eosinophil-driven inflammation.
58 Ido1 in the cecum, and a complete absence of mast cell and IgE production.
59 erythema with increased epidermal thickness, mast cell and neutrophil infiltration, expression of inf
60 type 2 cytokines, and biochemical markers of mast cell and platelet activation.
61 he high-affinity IgE receptor FcepsilonRI on mast cells and basophils and drives allergic inflammatio
62                                              Mast cells and basophils are central to acquired resista
63                                              Mast cells and basophils are main drivers of allergic re
64 lobulin E (IgE) antibodies that are bound to mast cells and basophils, triggering the release of infl
65 gh-affinity IgE antibodies on the surface of mast cells and basophils.
66 ting degranulation of effector cells such as mast cells and basophils.
67  are required for IgE-mediated activation of mast cells and basophils.
68 e population of mature human tissue-resident mast cells and basophils.
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
72 s of PNA-specific IgE and intestinal mucosal mast cells and eosinophils over sham treatments.
73 ile some relationships between inflammation (mast cells and eosinophils) and depression have been rep
74         In conclusion, mucosal inflammation (mast cells and eosinophils) is associated with pain reli
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
79 E crosslinking in murine bone marrow-derived mast cells and human cord blood-derived mast cells.
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
82                      Codeine stimulates skin mast cells and is therefore used in skin tests and as an
83 avorable association between infiltration of mast cells and less aggressive tumor cell behavior.
84 TE synthesis, was predominantly expressed in mast cells and localized near 15-LO(+) epithelium in NPs
85             In several cell types, including mast cells and macrophages, exposure to extracellular AT
86                        Here, we propose that mast cells and nociceptors form a single regulatory unit
87 existence of unique functional links between mast cells and nociceptors in the skin.
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
90                Duodenal mucosal eosinophils, mast cells and permeability were quantified.
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
96        Abnormal synthesis of PGE2 by colonic mast cells appears to induce visceral hypersensitivity i
97 es CD4(+) T cells and innate lymphoid cells, mast cells are a source of GM-CSF in this model, and its
98                                          Yet mast cells are best known, in humans, as key sources of
99    We found that MALT1(-/-) and MALT1(PD/PD) mast cells are equally impaired in cytokine production f
100  novel effector itch mechanisms derived from mast cells are important.
101 m hematopoietic progenitors to basophils and mast cells are largely uncharted at the single-cell leve
102                                              Mast cells are multifunctional immune cells that are fou
103                                              Mast cells are tissue-resident immune cells that play pi
104 naling induced significant loss of choroidal mast cells, as well as an altered inflammatory response
105 es that also express KIT and colocalize with mast cells at barrier tissue sites.
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
108 bound to the alpha chain of FcepsilonRI, the mast cell/basophil high affinity IgE receptor.
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
111  in murine Th9 cells and bone marrow-derived mast cells (BMMC).
112                  Primary bone marrow-derived mast cells (BMMCs) and ECs from WT and Fn14(-/-) or TWEA
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
115 ently been identified, which is expressed on mast cells but not neutrophils and macrophages.
116 chored, and transmembrane (TM) probes in RBL mast cells by imaging fluorescence correlation spectrosc
117                                   In the RBL mast cell, Ca(2+) flux through the MCU but not NCLX is i
118                                              Mast cells (CD117(+) /CD45(+) ) are more abundant in the
119  Ang II were recorded, which originated from mast cell chymase activity.
120 vere reaction, serum tryptase elevation, and mast cell clonality.
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
124                                Basophils and mast cells contribute to the development of allergic rea
125 nd that AAMPhi polarized by IL-33-stimulated mast cells could suppress proliferation and IL-17 and IF
126 suggest a role for ILC2s and pathogenic ILC2-mast cell crosstalk in mastocytosis.
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
129 odel on both normal VA (VAN) and VAD feeding mast cell deficiency mice (ckit(w-sh/w-sh) ).
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
132                               Engraftment of mast cell-deficient mice with Tph1(-/-) mast cells or se
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
141                                              Mast cell degranulation, cytokine secretion, and early s
142 tructs to identify genes that regulate human mast cell degranulation.
143  factor ligand superfamily member 14; sparse mast cell degranulation; numerous forkhead box protein P
144  lymphocytic and neutrophil infiltration and mast cells degranulation (p < 0.05).
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
148 efined by antral and duodenal eosinophil and mast cell densities.
149                In IBS patients, rectosigmoid mast cell density was higher in those reporting pain rel
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.
153                                              Mast cell-derived IL-13 was required for induction of AA
154 ppressive responses by polarizing AAMPhi via mast cell-derived IL-6 and IL-13.
155 as required for induction of AAMPhi, whereas mast cell-derived IL-6 enhanced macrophage responsivenes
156 se activity in endothelial cells targeted by mast cell-derived vasoactive substances.
157 provided a detailed road map of basophil and mast cell development.
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
161                              Although clonal mast cell disease is the culprit in some individuals, it
162 yndrome coronavirus 2 may not be elevated in mast cell disease, certain conditions may increase the r
163  bone marrow evaluation to rule out a clonal mast cell disorder.
164                         Patients with clonal mast cell disorders (cMCD), systemic mastocytosis (SM) a
165                       Overall, patients with mast cell disorders should follow the general and local
166 c target for the treatment of eosinophil and mast cell disorders.
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
175 , NHERF1 rapidly localized to the nucleus of mast cells following FcepsilonRI stimulation.
176 an allergen in vivo and further primed human mast cells for degranulation in an antigen-independent f
177                           Differentiation of mast cells from bone marrow progenitors was also inhibit
178                                              Mast cells from infected mice had lower expression of th
179              We compared bone marrow-derived mast cells from MALT1 knockout (MALT1(-/-)) and MALT1 pr
180 RNA 155-3p and miRNA 155-5p, were altered in mast cells from NHERF1(+/-) mice.
181 sure to IgE/Ag were significantly reduced in mast cells from NHERF1(+/-) mice.
182 tokine signaling, skin barrier function, and mast cell function, as well as pathways that have not ye
183       However, the effects of SCFAs on human mast cell function, including the underlying mechanisms,
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
188                                              Mast cells have been shown to regulate wound healing in
189                                              Mast cells have existed long before the development of a
190                                      Because mast cells have the highest expression of ST2 relative t
191                   We also discuss aspects of mast cell heterogeneity and comment on how the plasticit
192 environment within granules is important for mast cell homeostasis, we sought to evaluate the effects
193                   We propose that harnessing mast cells' host defense and immunomodulatory properties
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.
196                             In mouse models, mast cell-ILC2 crosstalk can drive local inflammation.
197                                              Mast cells impact breast cancer outcome by directly affe
198 y cytokines after FcepsilonR1 stimulation in mast cells, implicating a role in allergy.
199 decrease sputum eosinophils and inhibit lung mast cells in asthma.
200 lec-8 is highly expressed on eosinophils and mast cells in asthmatic sputum and targeting Siglec-8 wi
201 h infiltration of eosinophils and IgE-coated mast cells in clinical specimens of BIA-ALCL.
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
205 ith asthma and inhibit FcepsilonR1-activated mast cells in lung tissues.
206 aused by wasp venom peptide degranulation of mast cells in mice by 51% (P < 0.05), which was comparab
207 localization of Staphylococcus aureus within mast cells in nasal polyps.
208 ources, predominantly from connective tissue mast cells in pig mucosa.
209  expressed on the surface of eosinophils and mast cells in sputum.
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
212 gulates Ca(2+) homeostasis and exocytosis in mast cells in vivo and ex vivo.
213                            Reconstitution of mast cells in W/W(V) mice restored the visceral hypersen
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
218 ed mast cell activation and markedly reduced mast cell infiltration into the small intestine.
219 inhibitory receptor CD33 (CD33L) to targeted mast cells inhibits antigen-induced, FcepsilonRI-depende
220                               Epithelial and mast cell interactions, leading to the synthesis of 15-O
221 e anaphylatoxins C3a and C5a, which activate mast cells leading to plasma extravasation, pain, and it
222                                    The human mast cell line (LUVA) was used to model MC(TC)s or MC(T)
223                                Patients with mast cell (MC) activation symptoms and elevated baseline
224                                Liver damage, mast cell (MC) activation, biliary H2HR, and histamine s
225                         Anaphylaxis includes mast cell (MC) activation, but less is known about downs
226 barrier defect on allergic sensitization and mast cell (MC) degranulation remains speculative.
227 sed: These are (a) A natural role of reduced mast cell (MC) reactivity in developing IgE-mediated rea
228                                              Mast cell (MC)-associated diseases, including allergy/an
229 ogic conditions, connective tissue phenotype mast cells (MC(TC)s) can be found in the lung parenchyma
230                          Because the role of mast cells (MC) in this process is poorly characterized
231 s determined in bone marrow-derived cultured mast cells (MCs) and human skin-derived MCs.
232                                              Mast cells (MCs) are central effector cells in allergic
233                                         Skin mast cells (MCs) are distinct from other MCs, and for ye
234                                              Mast cells (MCs) are part of tumor microenvironment, but
235                                              Mast cells (MCs) are the initial responders of innate im
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
239 h activation of effector cells, particularly mast cells (MCs).
240 ponses, promote colonic health, and suppress mast cell-mediated diseases.
241                                     Ex vivo, mast cell-mediated histamine release and degranulation w
242         In agreement with our in vitro data, mast cell-mediated passive cutaneous anaphylaxis and pas
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
245 ammatory mediators and by further augmenting mast cell mediator release.
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
249 ophil activation test) and in vitro (RBL-2H3 mast cell model).
250 -01 primarily altered the gene expression of mast cells, monocytes, and keratinocytes.
251                                  Among known mast cell MRGPRX2 agonists ciprofloxacin but not PMX-53
252                                          The mast cell-nerve unit classically has represented a funda
253 anding of the regulation and function of the mast cell-nerve unit in itch biology.
254 inst anaphylaxis, likely due to reduction in mast cell numbers and depletion of pre-formed inflammato
255 was augmented upon TPC1 inhibition, although mast cell numbers and size were diminished.
256                          However, peritoneal mast cell numbers were significantly lower in infected m
257 ation profiles of both edited and non-edited mast cells, offering a consistent internal control not f
258 rgic disease upon cross-linking allergens on mast cells or basophils.
259 t of mast cell-deficient mice with Tph1(-/-) mast cells or selective mast cell deletion of Tph1 enhan
260                                    In murine mast cells, phosphorylation of protein kinases, ERK and
261 ure experiments showed that IL-33-stimulated mast cells polarized AAMPhi through production of solubl
262                             IL-33-stimulated mast cells produced a range of cytokines, including IL-6
263 racterized population of peritoneal basophil-mast cell progenitors.
264 irculating levels of bacterial 16S DNA, IgE, mast cell protease 1 (Mcpt-1) and Mcpt-4, Th1 and Th2 cy
265 tic symptoms, as well as plasmatic levels of mast-cell proteases (mMCP)-1/7, were quantified.
266       This was associated with a decrease in mast-cell reactivity as attested by the reduction of mMC
267 t blaze a trail to develop new drugs against mast cell-related diseases, including allergic hypersens
268  represents the main opiate receptor of skin mast cells remains unknown.
269 f degranulation along with the percentage of mast cells responding.
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
275                                     Although mast cells share many features with other innate immune
276 turbation of gene expression using our human mast cell single-cell imaging system.
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
279 ng comparable to that achieved with systemic mast cell stabilization.
280          These increases were prevented by a mast cell stabilizer, COX2 inhibitor, or knockdown of EP
281      We developed an indole-carboxamide type mast cell stabilizer, MCS-01, which proved to be an effe
282            In addition, mechanoactivation of mast cells stimulated the synthesis and release of prost
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
290  captured by extracellular traps and entered mast cells through phagocytosis.
291 a suggest that therapies aimed at inhibiting mast cell Tph1 may represent a therapeutic approach for
292                             Murine and human mast cells treated with omeprazole exhibited diminished
293 icrobiota of 11 dogs affected by spontaneous mast cell tumor (MCT), using skin contralateral sites as
294 ion of skin surface and dermis is related to mast cell tumor.
295 ing to better define the interaction between mast cell tumors, microbiota and host immune response.
296                       Within the human lung, mast cells typically reside adjacent to the conducting a
297 mall-molecule peptide mimetics also activate mast cells via MRGPRX2/B2.
298                Treated human PBMCs and human mast cells were assessed by fluorescence-activated cell
299                              Human and mouse mast cells were co-cultured with SCFAs and assessed for
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

 
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