ライフサイエンスコーパス: alarmin

1 duction of Th2 responses and functions as an alarmin.

2 hypothesized that GNLY might function as an alarmin.

3 IL-33 to produce a super-active form of the alarmin.

4 erminal centers, and increased expression of alarmins.

5 ells that were drawn to injured cartilage by alarmins.

6 sidered as endogenous multifunctional immune alarmins.

7 in response to two hallmark ILC2-activating alarmins.

8 act to host-derived molecules referred to as alarmins.

9 rmin D inhibited the secretion of these S100 alarmins.

10 cytokine producing capability in response to alarmins.

11 vel therapeutic targets including epithelial alarmins.

12 innate mediators of inflammation such as the alarmins.

13 ion of CVB3 led to a downregulation of these alarmins.

14 lled damage associated molecular patterns or alarmins.

15 ersely, a lack of biologically active S100A8 alarmin, achieved by antibody neutralization or by using

16 and immune responses through production of "alarmins." Alarmins are endogenous molecules secreted fr

17 g liver injury; however, a link between this alarmin and ALD has not been established.

18 oup nucleosome-binding protein 1) as a novel alarmin and demonstrate that it contributes to the induc

19 secreted upon acute epithelial injury as an alarmin and induces type 2 immune responses.

20 In particular, GRHL3 suppressed a number of alarmin and other proinflammatory genes after immune inj

21 helium leading to the aberrant production of alarmins and activation of T(H)2-type allergic inflammat

22 on, MIS-C patients had elevated S100A-family alarmins and decreased antigen presentation signatures,

23 o-inflammatory cytokines IL-1beta and IL-18, alarmins and endogenous danger-associated molecular patt

24 Thus, alarmins and founder gene mutations in MDSs license a co

25 dly, we reveal a lymphoneogenic function for alarmins and ILC2s.

26 rden, PMN infiltration, the presence of S100 alarmins and inflammatory cytokines and chemokines.

27 ed type 1 immunity, including reduced type 1 alarmins and intraepithelial lymphocytes.

28 its involved in COPD, including neutrophils, alarmins and kinases, are also in clinical development.

29 r that shapes innate lymphocyte responses to alarmins and neuropeptides during type 2 innate immune r

30 n activated state in the absence of multiple alarmins and supported mucosal resilience while avoiding

31 cell population that interfaces with tissue alarmins and the circulating immune system for timely ho

32 f interleukin (IL)-33, an epithelial-derived alarmin, and IL-33/ST2 pathway activation are linked wit

33 Liver-derived HRG, similar to alarmins, appears to be an endogenous molecular factor p

34 Alarmins are a group of structurally diverse host defens

35 Alarmins are classified by their release from damaged or

36 Alarmins are endogenous mediators capable of promoting t

37 Alarmins are endogenous mediators that can induce recrui

38 responses through production of "alarmins." Alarmins are endogenous molecules secreted from cells un

39 Alarmins are endogenous molecules that are constitutivel

40 These alarmins are ligands of Toll-like receptor 4 and amplifi

41 derived PAMPs and that endogenously produced alarmins are not sufficient.

42 ion and tissue damage, virulence factors and alarmins are pro-inflammatory and induce activation of v

43 or lipoteichoic acid as would be expected if alarmins are sufficient to activate the TLRs.

44 oxin-free" particles as would be expected if alarmins are sufficient to activate the TLRs.

45 ction of lipid mediators of inflammation and alarmins, are just some examples of how advances in immu

46 emodelling signature and identify endogenous alarmins as amplifiers of the inflammatory response that

47 ly cleaved IL-18 and IL-33, two IL-1-related alarmins, as well as the cytokine IL-15, which is import

48 the presence of microbial danger signals or alarmins associated with cytopathic damage.

49 uce release of IL-33, an epithelial-derived "alarmin." Astegolimab, a human IgG(2) mAb, selectively i

50 urine epidermis, IL-33 behaved similar to an alarmin, being constitutively expressed in keratinocyte

51 These alarmins bind to the Toll-like receptor 4 and prime the

52 ad trauma, released galectin-3 may act as an alarmin, binding, among other proteins, to TLR-4 and pro

53 iew, we discuss our current understanding of alarmin biology with a primary focus on allergic airway

54 Cleavage of the alarmins by HC and hCG suggests a function in regulating

55 generation and release of immunostimulatory alarmins by stressed mitochondria remains nebulous.

56 e-associated molecular pattern molecules (or alarmins) by engaging the receptor for advanced glycatio

57 s presumably driven by release of endogenous alarmins called danger-associated molecular patterns (DA

58 pression and subcellular localization of the alarmins calreticulin and HMGB-1 and the induction of an

59 nger hypothesis," it was recently shown that alarmins can also directly sense and report damage by si

60 Y is the first identified lymphocyte-derived alarmin capable of promoting APC recruitment, activation

61 TNF-like protein 1A (TL1A) as an epithelial alarmin constitutively expressed by a subset of lung epi

62 t TNF-like ligand 1A (TL1A) is an epithelial alarmin, constitutively expressed in alveolar epithelium

63 s that uncontrolled and excessive release of alarmins contributes to the dysregulated processes seen

64 Thus, extracellular HMGN1 acts as a novel alarmin critical for LPS-induced development of innate a

65 Interleukin-33 (IL-33) acts as an alarmin cytokine by alerting the system of potential env

66 Interleukin-33 (IL-33) is an alarmin cytokine from the IL-1 family.

67 The alarmin cytokine IL-33 stimulates the formation of immun

68 e pre-malignant pancreatic epithelium is the alarmin cytokine interleukin 33, which recapitulates the

69 nd adherens junctions, triggering epithelial alarmin cytokine responses such as IL-25, IL-33, and thy

70 Interleukin (IL)-33 is a broad-acting alarmin cytokine that can drive inflammatory responses f

71 l expression of IL-33, an epithelium-derived alarmin cytokine, in patients with EoE.

72 ease of IL-33, a pro-atopy, innate immunity, alarmin cytokine.

73 state and after in vivo stimulation with the alarmin cytokines IL-25 and IL-33.

74 The alarmin cytokines thymic stromal lymphopoietin (TSLP), i

75 on, the intestinal epithelial cells secrete "alarmin" cytokines, such as interleukin-25 (IL-25) and I

76 Innate cells respond to 'alarmin' cytokines (IL-25, IL-33, TSLP) by producing IL-

77 The alarmin, cytotoxicity, TCR repertoire, and plasmablast s

78 utrophils, T cells, reactive oxygen species, alarmins, danger-associated molecular patterns, purinerg

79 recently been attributed to the epithelial "alarmin" defense system.

80 products that interfere with epithelial cell alarmins, dendritic cell activation, macrophage function

81 The term alarmin denotes a broad class of molecules rapidly relea

82 ting a potential pathophysiological role for alarmin/DNA complexes in contributing to inflammation.

83 In PDAC, the alarmin domain of IL-33 activates group 2 innate lymphoi

84 cells exposed to environmental triggers, the alarmins drive airway inflammation through the release o

85 involvement of MCs in fibrosis (COPD/PF), T1/alarmin-driven inflammation (COVID-19) and mixed T1/T2 i

86 n programs in vivo and in vitro, attenuating alarmin-driven proliferative and effector responses.

87 CGRP potently inhibited alarmin-driven type 2 cytokine production and proliferat

88 is a nuclear protein and may function as an "alarmin" during cell death, a process that is uncommon i

89 ng history; complement products function as "alarmins" during innate responses.

90 to alloSCT induces the release of endogenous alarmins (eg, HMGB-1, ATP, IL-1alpha, IL-33) from recipi

91 (eg, IFN-gamma) and sources of inflammatory alarmins (eg, S100A8/9).

92 ssue-resident lymphocytes sense antigens and alarmins elicited by infectious microbes and abiotic str

93 recognize Ag, instead, they are sensitive to alarmin engagement, upon which they produce type 2 cytok

94 We conclude that IL-1alpha acts as an alarmin essential for leukocyte recruitment and protecti

95 y, proinflammatory cytokines, and epithelial alarmins even when stable on mepolizumab.

96 TL1A is now considered a novel alarmin expressed by human and mouse bronchial and intes

97 Alarmin expression is additionally enhanced by the up-re

98 aracterized by a high level of chemokine and alarmin expression, along with unique combinations of st

99 The alarmin family has been expanding in terms of both numbe

100 um had increased expression of chemokine and alarmin genes including IL33.

101 subsets had increased expression of S100A8/9 alarmin genes involved in NLRP3 inflammasome activation.

102 established in host immune responses, termed alarmins, has been largely overlooked in cancer biology.

103 Conversely, alarmins have also been found to play a major role in th

104 Many alarmins have been found to increase vascular tone and o

105 r-associated molecular pattern molecules, or alarmins, have been recognized as signaling mediators of

106 lial-derived cytokines, often referred to as alarmins, have been studied in large randomized trials,

107 The alarmin high mobility group box 1 (HMGB1) can be release

108 Here, we investigated whether the alarmin high mobility group box 1 (HMGB1) mediates age-a

109 The alarmin high mobility group box 1 (HMGB1) was released b

110 The causal role of the prototype alarmin high mobility group box 1 protein in systemic in

111 omers, but not monomers and fibrils, and the alarmin high-mobility group box-1 protein (HMGB-1) could

112 D8(+) Treg cell-surface Tim-3 binding to the alarmin, high-mobility group box 1 (HMGB-1).

113 Here, we provide an update and overview on alarmins, highlighting the areas that may benefit from t

114 LR-5 signalling mediates upregulation of the alarmin HMGB1 (High Mobility Group Box 1) in wound-induc

115 The alarmin HMGB1 and the chemokine CXCL12, both released in

116 We demonstrate that HS/R through the alarmin HMGB1 induces IL-23 secretion from macrophages i

117 The secreted alarmin HMGB1 is a proinflammatory partner, inducer, and

118 erate effector CD8(+) T cells by binding the alarmin HMGB1 via CD24 and presenting it to RAGE(+) T ce

119 without anticoagulant function inhibited the alarmin HMGB1-lipopolysaccharide (LPS) interaction and p

120 formation, and elevated concentration of the alarmins HMGB1 and histone 3 in the lungs.

121 h Ifngamma-Ifngammar-mediated release of the alarmin, Hmgb1, which disrupts the bone marrow endotheli

122 icle, we present a novel role for two potent alarmins, human beta-defensin 2 and 3 (HBD2 and 3), in p

123 s passed since the conceptualization of the "alarmin" hypothesis.

124 se, but not MC tryptase, also degraded other alarmins, i.e. biglycan, HMGB1, and IL-33, a degradation

125 es the release of mature IL-1beta and of the alarmin IL-1alpha Dying cells release IL-1alpha also, in

126 acts extracellularly as an antagonist of the alarmin IL-1alpha to immediately counteract its inflamma

127 gondii infection, microglia can release the alarmin IL-1alpha, promoting neuroinflammation and paras

128 lammasomes can also drive the release of the alarmin IL-1alpha.

129 ression by B cells is induced by the mucosal alarmin IL-33 (ref.

130 The alarmin IL-33 and its receptor STimulation-2 (ST2) promo

131 Objectives: The potent alarmin IL-33 has emerged as a critical regulator of typ

132 The alarmin IL-33 plays a role in a wide range of pathologie

133 l checkpoint linked to the nuclear-localized alarmin IL-33 that was independent of IL-33 receptor sig

134 ) show that injured spinal cord releases the alarmin IL-33 to drive chemokines that recruit monocytes

135 Whether T(reg) cells also respond to the alarmin IL-33 to regulate specific aspects of the immune

136 monstrated that tumor-cell expression of the alarmin IL-33 was necessary and sufficient for eosinophi

137 n response to inflammatory mediator IL-18 or alarmin IL-33, but not by TCR signaling that is required

138 ST2, the receptor for the alarmin IL-33, is expressed by a subset of regulatory T

139 shortly after infection, upregulation of the alarmin IL-33, which drives type 2 immunity, and activat

140 MTMs expressed the receptor for the alarmin IL-33, which induced both MTM activation and eos

141 its pathogenic production is promoted by the alarmin IL-33.

142 ion of pro-resolving AAMs in response to the alarmin IL-33.

143 in the context of diseases triggered by the alarmin IL-33.

144 ression by B cells is induced by the mucosal alarmin IL-33.

145 nity, and their activation by the epithelial alarmins IL-25 and IL-33 is a defining trait.

146 ice was dependent on TSLP, but not the other alarmins IL-25 and IL-33.

147 Rationale: The alarmins IL-33 and HMGB1 (high mobility group box 1) con

148 Y(13)-R as a novel gatekeeper of the nuclear alarmins IL-33 and HMGB1 and demonstrate that the target

149 nriched IL-1 family cytokines, including the alarmins IL-33 and thymic stromal lymphopoietin, orchest

150 Among them, the alarmins Il-33 and TSLP, IL-4 and IL-13, eosinophil-rela

151 Here, we provide evidence that the "alarmin" IL-33, a nuclear cytokine that activates type 2

152 en together, we report that the IL-1 family "alarmins" IL-18 and IL-33 in addition to amplifying both

153 enomewide association studies implicate the 'alarmin' IL-33 in asthma, but its role in mast cell-ASM

154 mice along with reduction in epithelial cell alarmins, IL-25 and IL-33, suggests an overall change in

155 inophils, type 2 innate-like lymphoid cells, alarmins, IL-4, IL-5, IL-9, IL-13 and IL-17).

156 ure induced thymic stromal lymphopoietin, an alarmin implicated in epicutaneous allergen sensitizatio

157 Overproduction of the UA alarmin in the local microenvironment plays a critical r

158 on exhibited elevated levels of vaginal S100 alarmins in both vaginal epithelia and secretions in the

159 wledge of type 2 inflammation and epithelial alarmins in COPD, explore potential biomarkers of type 2

160 targeting type 2 inflammation and epithelial alarmins in COPD.

161 -products (RAGE) revealed the involvement of alarmins in inflammatory gene expression, which was foun

162 oduction as well as exaggerated responses to alarmins in mice lacking the CGRP receptor.

163 matory condition of VVC is initiated by S100 alarmins in response to C. albicans, which stimulate pol

164 ovide a general view on the participation of alarmins in the induction of innate and adaptive immune

165 secretion by ILC2s, with additive effects to alarmins in vitro.

166 ities by grouping them under the novel term 'alarmins', in recognition of their role in mobilizing th

167 functions as an endogenous danger signal, or alarmin, in response to tissue damage.

168 AGEs and other alarmins inadvertently prime innate signaling through mu

169 integrity, triggering local inflammation via alarmins including IL-25, IL-33, and TSLP, which activat

170 ing of epithelium-derived cytokines known as alarmins, including thymic stromal lymphopoietin, IL-25,

171 The function of several alarmins-including the defensins, LL-37, and HMGB1-in tu

172 In CVB3-infected RAW macrophages, both alarmins increased MIP-2 (macrophage inflammatory protei

173 Activation of local ILC2s by tissue-specific alarmins induced their proliferation, lymph node migrati

174 birth occur in the context of microbial- or alarmin-induced inflammation.

175 ponse in mucosal candidiasis as well as S100 alarmin induction, this study aimed to determine whether

176 r in vivo in the presence or absence of S100 alarmins initiated by several approaches.

177 mediary of the citric acid cycle, acts as an alarmin, initiating and propagating danger signals resul

178 Here, we show the alarmin interleukin (IL) 33 is a product of Sca1(+) thym

179 icroglia at sites of SCI rapidly express the alarmin interleukin (IL)-1alpha, and that infiltrating n

180 dy, we identify a cell-intrinsic role of the alarmin interleukin (IL)-33 in the functional stability

181 nts, the respiratory epithelium releases the alarmin interleukin (IL)-33 to elicit a rapid immune res

182 sis are selectively targeted by the cytokine/alarmin interleukin (IL)-33.

183 The alarmin interleukin-1a (IL-1a) is expressed in a variety

184 ular mechanisms that drive expression of the alarmin interleukin-33 (IL-33) in endothelial cells are

185 the recipient microbiome, the impact of the alarmin interleukin-33 on alloreactivity, and the role o

186 new monoclonal antibody against the upstream alarmin interleukin-33.

187 Here we identify the nuclear alarmin, interleukin (IL)-33, as an important regulator

188 le of ILC2 in translating epithelial-derived alarmins into downstream adaptive type-2 responses via d

189 These results suggest that S100A8 alarmin is sufficient, but not necessary, to induce PMN

190 The upstream positioning of the alarmins is an attractive pharmacological target to bloc

191 find that oligodendrocyte-derived IL-33, an alarmin, is key for locally regulating the pathogenicity

192 cytokine interleukin-1alpha (IL-1alpha), an alarmin, is necessary and sufficient to trigger rapid he

193 he expression of fibroblast-derived IL33, an alarmin known to induce invasion, was repressed upon MNK

194 kedly increased epithelial expression of the alarmin-like cytokine IL-33 in nasal polyps, as compared

195 er-1 prevented the upregulation of IL-33, an alarmin linked to necroptosis, and other chemokines and

196 from distinct tissues that are dependent on alarmins matched to the receptor profile of the specific

197 Clinical evidence suggests that red cell alarmins may cause AKI in SCD, however, the sterile infl

198 pecific degradation of virulence factors and alarmins may depend on the presence of accessible extend

199 vestigations highlighting tendinopathy as an alarmin mediated pathology we sought evidence of S100A8

200 er the Th17 pathway plays a role in the S100 alarmin-mediated acute inflammation during VVC using the

201 h-mobility group box 1 (HMGB1), a prototypic alarmin, mediates the systemic inflammatory response syn

202 neuroinflammation and, while the release of alarmin mediators aggravates disease at late stages, ear

203 Parkin ubiquitinates the alarmin molecule HMGB1 to enable its regulated release i

204 study, we showed that PRKN ubiquitinates the alarmin molecule, high-mobility group box-1 (HMGB1) on L

205 also with C3a, CpG DNA oligonucleotides, and alarmin molecules such as HMGB1 to initiate a proinflamm

206 The alarmins myeloid-related protein (MRP)8 and MRP14 are th

207 ered by endogenous TLR4 ligands, such as the alarmins myeloid-related protein 8 (MRP8, S100A8) and MR

208 ge-associated molecular patterns, so-called "alarmins," orchestrates the immune response.

209 Thus, the preferential activation of a key alarmin pathway facilitates early discrimination of micr

210 IL-33/ST2 alarmin pathway regulates inflammation, fibrosis, and re

211 It has recently become clear that alarmins play important roles as initiators and particip

212 known as "calprotectin" or "MRP8/14," is an alarmin primarily secreted by activated myeloid cells wi

213 lls are activated by interleukin (IL)-33, an alarmin produced by the tumor epithelium in response to

214 is mediated by chemotactic S100A8 and S100A9 alarmins produced by vaginal epithelial cells in respons

215 pithelium-derived type 2 initiator cytokines/alarmins, producing type 2 effector cytokines such as IL

216 Enhanced chemokine and alarmin production, and seeding of the skin with antigen

217 -presenting cells and impaired chemokine and alarmin production.

218 ly releases a transcriptional brake, fueling alarmin production.

219 lear decoy RNA, keeping PU.1 from binding to alarmin promoters and promoting its binding to pseudogen

220 , released during infections, is a bona fide alarmin promoting myeloid cell activation [M.

221 with inflammatory responses (S100 proteins, alarmins, protease inhibitors); and glycolysis and antio

222 such activation is important for release of alarmins, pyroptosis, and early IFN-gamma production by

223 Here, we identify H. polygyrus Binds Alarmin Receptor and Inhibits (HpBARI) and HpBARI_Hom2,

224 his stress response was triggered in part by alarmin recognition and was blunted in CD24 sensor- and

225 immunostimulatory bactericidal proteins and alarmins, relative to lupus and control neutrophils.

226 as primary sensors for aeroallergen-induced alarmin release by airway epithelial cells.

227 Here, we identified H. polygyrus Alarmin Release Inhibitor (HpARI), an IL-33-suppressive

228 eligmosomoides polygyrus bakeri secretes the Alarmin Release Inhibitor HpARI2, an effector protein th

229 ertain inflammatory conditions, such as with alarmin release or gut dysbiosis.

230 celerated execution of necroptosis, limiting alarmin release, and thereby preventing inflammation and

231 n damaged areas where they degraded IL33, an alarmin released by epithelial cells during tissue damag

232 ere we show that interleukin-33 (IL-33), the alarmin released by inflamed tissues(2), induces TLSs.

233 HMGB1 is an alarmin released by stressed cells.

234 We hypothesized that IL33, an alarmin released early after tissue injury and a known r

235 Alarmins represent epithelial-derived cytokines that ini

236 Taken together, these studies indicate that alarmins represent potential new targets for manipulatio

237 These data suggest that the vaginal S100 alarmin response to Candida does not require the cells o

238 as C-reactive protein, myeloperoxidase, and alarmin S100-A9.

239 ence of T. gondii infection by detecting the alarmin S100A11 protein, which is released from parasite

240 o data and determine the requirement for the alarmin S100A8 in the PMN response and to evaluate patte

241 these reservoirs in vitro are induced by the alarmin S100A8, an endogenous factor produced by M4-macr

242 The alarmin S100A8/A9 has been implicated in the induction o

243 The alarmin S100A8/A9 is implicated in sterile inflammation-

244 f TB, our new data provide evidence that the alarmin S100A8/A9 mediates neutrophil accumulation durin

245 In conclusion, the alarmin S100A8/S100A9 is a valuable and sensitive molecu

246 l molecular imaging, we demonstrate that the alarmin S100A8/S100A9 serves as a sensitive local and sy

247 The proinflammatory alarmins S100A8 and S100A9 are among the most abundant p

248 The alarmins S100A8 and S100A9 are damage-associated molecul

249 Alarmins S100A8 and S100A9 are endogenous molecules rele

250 ne expression of filaggrin and antimicrobial alarmins S100A8 and S100A9 was measured in keratinocyte

251 genes, including a multifold upregulation of alarmins S100A8/A9, as a top hit in ponatinib-treated he

252 n monocytes, governing the production of the alarmins S100A8/A9, key drivers of COVID-19 pathogenesis

253 e for the primary role of neutrophil-derived alarmins (S100A8/A9) in dictating the nature of the ensu

254 to the infarct, where they release specific alarmins, S100A8 and S100A9.

255 The alarmin S100A9 hampers osteoclast differentiation from h

256 hanistically, pyroptosis is triggered by the alarmin S100A9 that is found in excess in MDS HSPCs and

257 S100A8/A9 is an endogenous alarmin secreted by myeloid cells during many acute and

258 drive epithelial remodeling and orchestrate alarmin secretion.

259 acidic ribonuclease, recently proposed as an alarmin signal associated with inflammatory responses.

260 y function as an endogenous danger signal or alarmin, similar to IL-1alpha or high-mobility group box

261 a CGRP-specific gene signature after in vivo alarmin stimulation, suggesting CGRP regulated this resp

262 tly were found to be activated by endogenous alarmins such as fragmented extracellular matrix protein

263 mage-associated molecular patterns including alarmins such as HMGB1 and IL-1beta, Toll-like receptors

264 n this article, we review the involvement of alarmins such as IL-1alpha, IL-33, IL-16, and high-mobil

265 ng the target and source of adipocytokines, 'alarmins' such as interleukin-9 (IL-9) and interleukin-3

266 Alarmins, such as ATP, likely play a pivotal role in the

267 y associated with the presence of endogenous alarmins, such as extracellular ATP (an indicator of cyt

268 c proteins, cytokines, chemokines, or immune alarmins, such as granulysin (GNLY), leading to the exte

269 Epithelium-derived cytokines or alarmins, such as interleukin-33 (IL-33) and thymic stro

270 ll level, as well as upstream cytokines, or "alarmins," such as thymic stromal lymphopoietin, IL-25,

271 Alarmins, T2- and pro-inflammatory cytokines, IFNbeta IF

272 EDN to have the properties of an endogenous alarmin that alerts the adaptive immune system for prefe

273 High molecular group S (HMGB1) is a major alarmin that binds to the receptor for advanced glycatio

274 herapeutic vaccination that free ISG15 is an alarmin that induces tissue alert, characterized by extr

275 Extracellular DNA (eDNA) is also an alarmin that intensifies inflammation in cystic fibrosis

276 Therefore, we conclude that HRF is a novel alarmin that promotes allergic airway inflammation.

277 servations suggest that IL-36gamma may be an alarmin that signals the cause, e.g., viral infection, o

278 The damaged epithelium is a source of alarmins that activate the innate immune system, yet the

279 d persistent overexpression of extracellular alarmins that can trigger inflammation via pattern recog

280 Often characterized as "alarmins" that are released by the barrier epithelium in

281 -1beta, IL-6, and soluble IL-6R), epithelial alarmins (thymic stromal lymphopoietin [TSLP] and IL-33)

282 IL-5, and IL-13 preceded by induction of the alarmins (thymic stromal lymphopoietin, IL-33, and IL-25

283 ibility that IL-33 may function as a nuclear alarmin to alert the innate immune system after injury o

284 mune cells secrete HMGB1 as an extracellular Alarmin to signal tissue damage.

285 the airway epithelium, which functions as an alarmin to stimulate type 2 immunity.

286 However, the relevance of alarmins to the induction of adaptive immune responses r

287 the lncRNA PIRAT (PU.1-induced regulator of alarmin transcription) as a major PU.1 feedback-regulato

288 unclear, although IL-33 might function as an alarmin triggered by damage-associated molecular pattern

289 essed in lung ILCs and is further induced by alarmins TSLP and IL-33.

290 type 2 immunity, comprising increased type 2 alarmins, tuft cells and activated group 2 innate lympho

291 terleukin-1alpha and interleukin-33 exhibit 'alarmin'-type properties that can signal tissue or cell

292 Specific targeting of alarmins, type 2 cytokines and IgE has shown varying deg

293 Coculturing with alarmins upregulated NMUR1 in ILC2s, which was attenuate

294 of Th2-associated cytokines but acts as an "alarmin" via stimulation of mast cells.

295 -to-cytoplasmic translocation and release of alarmins was measured by using immunohistochemistry and

296 and, is an IL-1 family member and acts as an alarmin, we explored the ST2 pathway in human and mouse

297 Two epithelial alarmins were measured longitudinally in bronchoalveolar

298 Alarmins, which are locally released during cellular str

299 The effects of these alarmins, which can act upstream of immune cells, involv

300 S100A8 and S100A9 are cytosolic alarmins with autocrine functions that facilitate neutro