ライフサイエンスコーパス: pyroptosis

1 ytokine release and inflammatory cell death (pyroptosis).

2 ed increased IL-1beta production but reduced pyroptosis.

3 afenib-treated MPhi revealed an induction of pyroptosis.

4 nd HIV-1 induced indistinguishable levels of pyroptosis.

5 terleukin-1beta (IL-1beta) and cell death by pyroptosis.

6 key role in the induction of bystander cell pyroptosis.

7 ch activate inflammatory caspases and induce pyroptosis.

8 f Vpx into HIV-1 virions also did not reduce pyroptosis.

9 d inducing an inflammatory cell death called pyroptosis.

10 tion as a trigger for blood clotting through pyroptosis.

11 ith reduced IL-1beta secretion and inhibited pyroptosis.

12 ammasome activation, ASC speck formation and pyroptosis.

13 talk and caspase-driven gasdermin D-induced pyroptosis.

14 ng pro-inflammatory cytokines and triggering pyroptosis.

15 nella leading to its enhanced activation and pyroptosis.

16 omain binds the N-terminal domain to inhibit pyroptosis.

17 lease of interleukin-1beta (IL-1beta) and to pyroptosis.

18 to promote interleukin-1beta production and pyroptosis.

19 cells caused less IL-1beta release and more pyroptosis.

20 mmatory caspases for cytokine maturation and pyroptosis.

21 identify genes required for NLRP1B-mediated pyroptosis.

22 plasma membrane to induce secondary necrosis/pyroptosis.

23 ion, followed by activation of caspase-4 and pyroptosis.

24 erminal fragment disrupted for inducing cell pyroptosis.

25 allmark of a novel form of cell death termed pyroptosis.

26 eased from GSDMD acts as an effector in cell pyroptosis.

27 1beta causing inflammation and cell death by pyroptosis.

28 on of human airway epithelia can also induce pyroptosis.

29 to more recently discovered pathways such as pyroptosis.

30 duced IL-1 release occurred independently of pyroptosis.

31 orms membrane-disrupting pores, and executes pyroptosis.

32 ns, signifying the inflammatory potential of pyroptosis.

33 tokines interleukin (IL)-1beta and IL-18 and pyroptosis.

34 at robustly activate necrosis, apoptosis, or pyroptosis.

35 proteins that suppress apoptosis and promote pyroptosis.

36 that suppress apoptosis and thereby promote pyroptosis.

37 ukin (Il)-18 and gasdermin D (Gsdmd)-induced pyroptosis.

38 y cytokines IL-1beta and IL-18 and promoting pyroptosis.

39 s an activator of the NLRP3 inflammasome and pyroptosis.

40 turation of interleukin 1beta (IL-1beta) and pyroptosis.

41 sdermin D (GSDMD), an essential component of pyroptosis.

42 endocytosis, phagocytosis, inflammation, and pyroptosis.

43 ion receptor driving HBoV1 infection-induced pyroptosis.

44 interleukin-1beta (IL-1beta) and macrophage pyroptosis.

45 avage of pro-IL-1beta to active IL-1beta and pyroptosis.

46 such as necrosis, apoptosis, necroptosis and pyroptosis.

47 uboptimal inflammatory milieu in the case of pyroptosis.

48 mediated inflammatory cytokine secretion and pyroptosis.

49 mbrane, resulting in lytic cell death called pyroptosis.

50 IL-18 and an inflammatory cell death called pyroptosis.

51 and induction of proinflammatory cell death pyroptosis.

52 interleukin-1 release, but only LPS induces pyroptosis.

53 a and IL-18, and a form of cell death termed pyroptosis.

54 of an inflammatory form of cell death called pyroptosis.

55 virus infection-apoptosis, necroptosis, and pyroptosis.

56 ll as a special type of cell death, known as pyroptosis.

57 o secretion of proinflammatory cytokines and pyroptosis.

58 uced inflammatory cell death, referred to as pyroptosis.

59 ry responses and a form of cell death termed pyroptosis.

60 zation, membrane binding, pore formation and pyroptosis.

61 ts in proinflammatory cytokine signaling and pyroptosis.

62 ronic inflammatory response generated during pyroptosis.

63 g mammalian cells when it is released during pyroptosis.

64 y pathogens have evolved to avoid or subvert pyroptosis.

65 ammasome assembly, caspase-1 activation, and pyroptosis.

66 erovar Typhimurium reduced flagellin-induced pyroptosis.

67 ent agonists and act independently to induce pyroptosis.

68 aspase-1-mediated production of IL-1beta and pyroptosis.

69 ependent on ASC but independent of NLRP3 and pyroptosis.

70 of an inflammatory cell death pathway termed pyroptosis.

71 ion of proinflammatory cytokines and induces pyroptosis.

72 l blood-derived CD4 T cells naturally resist pyroptosis.

73 ytokines IL-1beta and IL-18 and induction of pyroptosis.

74 key regulatory role of Ca2+ in EPEC-induced pyroptosis.

75 eath, including necroptosis, ferroptosis and pyroptosis.

76 forms pores on the cell membrane and induces pyroptosis.

77 ion, thereby preventing IL-1beta release and pyroptosis.

78 ation, membrane vesiculation, autophagy, and pyroptosis.

79 s, and induction of inflammatory cell death, pyroptosis.

80 me and increases Gasdermin D, an effector of pyroptosis.

81 death, suggesting that it does not activate pyroptosis.

82 ize to the PM or increase PM permeability or pyroptosis.

83 mmasome complexes or caspase-4 which trigger pyroptosis.

84 ive GSDMD transcription for the execution of pyroptosis.

85 e assembly, and death by caspase-1-dependent pyroptosis.

86 of interleukin-1beta and interleukin-18, and pyroptosis.

87 ermin-D-mediated form of cell death known as pyroptosis(1-4).

88 al fragments causes inflammatory cell death (pyroptosis)(1).

89 with flow cytometry to detect apoptosis and pyroptosis; 26% were pyroptotic (Caspase-1-positive).

90 elds an N-terminal p30 fragment that induces pyroptosis, a death program important for the eliminatio

91 Some recent studies suggested that pyroptosis, a form of programmed cell death triggered du

92 Sensing of these DNA fragments results in pyroptosis, a highly inflammatory form of programmed cel

93 spase-1 or caspase-11 inflammasomes triggers pyroptosis, a lytic form of cell death protective agains

94 ptosome formation, which in turn leads to AM pyroptosis, a type of caspase-1-dependent inflammatory c

95 Pyroptosis, a unique form of programmed cell death (PCD)

96 1beta and IL-18 and drives cell fate towards pyroptosis-a form of programmed inflammatory cell death

97 5, and 11 are essential steps in initiating pyroptosis after inflammasome activation.

98 forming protein, gasdermin D, which triggers pyroptosis, an inflammatory form of cell death.

99 ), has been identified as the executioner of pyroptosis, an inflammatory form of lytic cell death tha

100 Also, AgNP15 induced pyroptosis and activation of the NLRP-3 inflammasome as

101 es mediate two distinct forms of cell death: pyroptosis and apoptosis, respectively.

102 oss-talk between initiators and effectors of pyroptosis and apoptosis, where initiator caspases-1 and

103 vity-independent cell death complex to drive pyroptosis and apoptosis.

104 1beta-IL-1RI signaling is responsible for AM pyroptosis and augmented lung injury in response to LPS.

105 release of proinflammatory cytokines through pyroptosis and caspase-1 activation.

106 , activation of NLRC4 by flagellin initiates pyroptosis and concomitant release of lysophospholipids

107 n an inflammasome complex, caspase-1 induces pyroptosis and converts pro-IL-1beta and pro-IL-18 into

108 Disulfiram blocks pyroptosis and cytokine release in cells and lipopolysac

109 melioidosis is primarily due to induction of pyroptosis and direct killing of bacteria rather than pr

110 nt proteins within GSDMD that support native pyroptosis and facilitate live-cell imaging of pyroptoti

111 this inflammasome induces pore formation and pyroptosis and facilitates the restriction of bacterial

112 mmasome activation, IRGM/Irgm1 protects from pyroptosis and gut inflammation in a Crohn's disease exp

113 yperinflammation associated with M1-mediated pyroptosis and IL-1beta release could aggravate tissue i

114 trate required for efficient NLRP3-triggered pyroptosis and IL-1beta release, was not essential for M

115 t increase membrane permeability, leading to pyroptosis and IL-1beta release.

116 rmin D is essential for caspase-11-dependent pyroptosis and interleukin-1beta maturation.

117 ial emphasis on lytic cell death pathways of pyroptosis and necroptosis and their implications in inf

118 though other types of necrotic death such as pyroptosis and necroptosis are mediated by active mechan

119 nding the molecular cascades regulating both pyroptosis and necroptosis will yield even more targets

120 a membrane pores, similarly to cell lysis in pyroptosis and necroptosis(3,4).

121 ive forms of regulated cell death, including pyroptosis and necroptosis, have been described.

122 gulated forms of necrotic cell death, termed pyroptosis and necroptosis, respectively.

123 In this review, we focus on how pyroptosis and necroptosis, which release potent immune

124 d potassium efflux contribute to HIV-induced pyroptosis and NLRP3 inflammasome activation in podocyte

125 ulting amino-terminal fragment promotes both pyroptosis and NLRP3-dependent activation of caspase-1 i

126 or of NLRC4 inflammasome-mediated macrophage pyroptosis and pathogen eradication.

127 is essential to induce gasdermin-D-dependent pyroptosis and processing of interleukin-18, thereby des

128 monella enterica serovar Typhimurium-induced pyroptosis and proinflammatory cytokine secretion in mac

129 ant functions beyond the direct induction of pyroptosis and proinflammatory cytokine secretion in the

130 nical inflammasome activation and suppressed pyroptosis and secretion of IL-1alpha and IL-1beta induc

131 s completely blocked the effect of AgNP15 on pyroptosis and secretion of IL-1beta, indicating that AT

132 ch recognizes intracellular LPS and promotes pyroptosis and secretion of proinflammatory cytokines.

133 ytoskeleton components were disrupted during pyroptosis and that sensitivity to rupture was calpain-d

134 Pyroptosis and the resultant IL-1beta production were de

135 latory mechanism of sorafenib involving MPhi pyroptosis and unleashing of an NK-cell response that se

136 These specks were not associated with pyroptosis and were controlled by transient receptor pot

137 (GSDMD-NT) that triggers inflammatory death (pyroptosis) and release of inflammatory cytokines such a

138 that induce interferon responses instead of pyroptosis, and a SMOC-like nanomachine that induces int

139 induces inflammasome activation, macrophage pyroptosis, and accompanying tissue factor release, dire

140 have been identified, including necroptosis, pyroptosis, and autophagic cell death.

141 on of interleukin-1 (IL-1) family cytokines, pyroptosis, and control of pathogen replication.

142 f active cell death (apoptosis, necroptosis, pyroptosis, and ferroptosis) mainly in mammals, this Per

143 ndeed, RNA and DNA sensors induce apoptosis, pyroptosis, and necroptosis.

144 cluding immunogenic cell death, necroptosis, pyroptosis, and netosis that interweave different cell d

145 me activation, signaling leading to cellular pyroptosis, and the downstream cytokines as a promising

146 aberration, drives activation of caspase-1, pyroptosis, and the release of the pro-inflammatory cyto

147 IP(L) promotes complex II formation, driving pyroptosis, and the secretion of IL-1beta in response to

148 of programmed cell death pathways including pyroptosis, apoptosis, and necroptosis (PANoptosis) and

149 vity-independent inflammasome activation and pyroptosis, apoptosis, and necroptosis (PANoptosis) that

150 infection induces cell death in the form of pyroptosis, apoptosis, and necroptosis (PANoptosis).

151 mmatory programmed cell death in the form of pyroptosis, apoptosis, and necroptosis (PANoptosis).

152 ty has been shown to be essential to driving pyroptosis, apoptosis, and necroptosis.

153 responsible for activating the inflammasome/pyroptosis, apoptosis, and necroptosis.

154 ZBP1 triggers NLRP3 inflammasome activation/pyroptosis, apoptosis, and necroptosis; the specific lig

155 nnate immune-mediated programmed cell death (pyroptosis, apoptosis, necroptosis) is an integral part

156 Inflammasome activation and subsequent pyroptosis are critical defense mechanisms against micro

157 induced secondary necrosis and GSDMD-induced pyroptosis are dependent on caspase activation, we propo

158 fected cells underwent apoptosis rather than pyroptosis, as indicated by increased cleaved caspase-3

159 r1Delta and stp2Delta strains did not induce pyroptosis, as measured by caspase-1-dependent interleuk

160 of proinflammatory cytokines, apoptosis, and pyroptosis, as well as resistance to chronic microglial

161 , which has been shown to prevent macrophage pyroptosis, attenuated both cell killing by p30 in a 293

162 nt progress in the field of nanomedicines in pyroptosis-based cancer therapy has not yet been present

163 following various cell death processes, with pyroptosis being a common mechanism.

164 t only expand the molecular understanding of pyroptosis but also enable its direct visualization.

165 ed through PYD, whose overexpression induced pyroptosis but only after substantial delay.

166 cella-infected macrophages exhibited minimal pyroptosis but secreted IL-1beta, which was suppressed b

167 e roles of human GBPs in regulating not only pyroptosis, but also apoptosis.

168 caspase-1 inhibitor, a key enzyme promoting pyroptosis, but not by a caspase-3 inhibitor, an importa

169 ation, interleukin (IL)-1beta secretion, and pyroptosis, but not Nlrc4 phosphorylation by cytosolic f

170 igm that inflammasome signaling necessitates pyroptosis by demonstrating that ESCRTIII-dependent memb

171 liberates the GSDME-N domain, which mediates pyroptosis by forming pores in the plasma membrane.

172 Induction of pyroptosis by the AIM2 inflammasome was a major componen

173 that impaired NLRP3 inflammasome function or pyroptosis can lead to negative consequences for the hos

174 Loss of pyroptosis, caspase-8-driven apoptosis, or necroptosis h

175 -1beta production, caspase-1 activation, and pyroptosis caused by several inflammasome-activating sig

176 Our results demonstrated that pyroptosis contributes to the CD4(+) T cell death in viv

177 Thus, blocking CD4(+) T cell pyroptosis could be a complementary treatment to antiret

178 Interestingly, HIV-induced podocyte pyroptosis could be partially inhibited by Tempol (a sup

179 ndiscovered cellular events occurring during pyroptosis, define the mechanisms driving pyroptotic rup

180 dermin D (GSDMD) is an effector molecule for pyroptosis downstream of canonical and noncanonical infl

181 hat HIV-2 infection produces lower levels of pyroptosis due to the action of its Vpx gene product.

182 nstrate that DNA damage drives AIM2-mediated pyroptosis during normal brain development, preventing a

183 All inflammatory caspases activate the pyroptosis effector protein gasdermin D, but caspase-1 m

184 en by CD4 T cell depletion, mostly involving pyroptosis elicited by abortive HIV infection of CD4 T c

185 ME acts as a tumour suppressor by activating pyroptosis, enhancing anti-tumour immunity.

186 , we discuss molecular mechanisms that drive pyroptosis, evidence for pyroptosis within the CNS, and

187 We further showed that AM pyroptosis exaggerates lung inflammation.

188 tion of NLRP3-dependent IL-1beta release and pyroptosis, facilitating the spread of bacteria to neigh

189 n overview of recent developments within the pyroptosis field, beginning with the discovery of Gasder

190 Pyroptosis ('fiery death') is an inflammatory type of re

191 cent studies have uncovered the mechanism of pyroptosis following inflammasome activation, how pyropt

192 ous strategies have been developed to induce pyroptosis for cancer therapy, including ions, small-mol

193 on distinguishes NLRP3 activators that cause pyroptosis from those that do not, and SARM modulation r

194 [PARP] and caspase-3 [CASP-3] cleavage) and pyroptosis (gasdermin D [GSDMD] cleavage) in livers, and

195 During pyroptosis, GSDMD (gasdermin D), the pore-forming effect

196 Precisely how GsdmD p30 triggers pyroptosis has not been established.

197 es, which are canonically formed upstream of pyroptosis, have been characterized as key mediators of

198 Because pyroptosis (ie, cell death resulting from inflammasome a

199 and inflammatory environments attenuates EC pyroptosis, improves EC survival mediated by vascular en

200 -1beta and the programmed cell death pathway pyroptosis in a caspase-1-dependent manner.

201 HIV induced pyroptosis in a dose- and time-dependent manner within p

202 This is the first report of pyroptosis in airway epithelia infected by a respiratory

203 Antibiotic chemotherapy drugs induce pyroptosis in breast cancer.

204 n abortive infection and caspase-1-dependent pyroptosis in bystander CD4 T cells.IMPORTANCE CD4 T cel

205 PD-L1 switches TNFalpha-induced apoptosis to pyroptosis in cancer cells, resulting in tumour necrosis

206 reby converting noninflammatory apoptosis to pyroptosis in GSDME-expressing cells(3-5).

207 We show that EPEC induces pyroptosis in IECs in a Tir-dependent but actin polymeri

208 tion with an extracellular pathogen leads to pyroptosis in IECs.

209 stimulus triggered speck formation and rapid pyroptosis in keratinocytes in vivo.

210 Recent reports have shown caspase-8-mediated pyroptosis in LPS-activated macrophages but have provide

211 release of interleukin-1beta (IL-1beta), and pyroptosis in LPS-activated macrophages infected with wi

212 previous reports showing that NLRP1 enhances pyroptosis in macrophages, NLRP1 in melanoma behaved dif

213 he central role of inflammatory caspases and pyroptosis in mediating immunity to infection and cleara

214 gest that NMII induces a caspase-1-dependent pyroptosis in murine peritoneal B1a cells.

215 nown for inducing inflammasome formation and pyroptosis in myeloid cells, increasing evidence highlig

216 lammatory signaling, IL-1beta production and pyroptosis in primed murine bone marrow-derived macropha

217 Caspase-11-mediated pyroptosis in response to cytosolic LPS is critical for

218 tory cytokines and danger signals as well as pyroptosis in response to infections and cellular stress

219 t activate inflammatory cytokines and induce pyroptosis in response to intracellular danger-associate

220 ranzyme B also activates caspase-independent pyroptosis in target cells by directly cleaving GSDME at

221 ve eosinophilia, and we were able to confirm pyroptosis in the infiltrating eosinophils.

222 ally, our study demonstrates CIRP-induced EC pyroptosis in the lungs of C57BL/6 mice for the first ti

223 Recent investigations implicate pyroptosis in the pathogenesis of multiple neurological

224 ome-wide CRISPR screen with compound induced pyroptosis in THP-1 cells, we identified that inflammaso

225 However, aberrant, systemic activation of pyroptosis in vivo may contribute to sepsis.

226 o induce a new type of programed cell death, pyroptosis, in T lymphocytes through induction of Nod-li

227 and caspase-1 activation, thereby preventing pyroptosis independent of GSDMD targeting.

228 recent progress in cancer treatment based on pyroptosis induced by nanoparticles will be described in

229 breast cancer by recruiting MDSC in part by pyroptosis-induced IL-1beta generation and downstream CC

230 -5/-11, release of the cytokine IL-1beta and pyroptosis, inducing elevated inflammation after non-hyg

231 Pyroptosis-inducing, but not hyperactivating, NLRP3 stim

232 By inducing pyroptosis, inflammasomes can also drive the release of

233 This demonstrated that pyroptosis is a cellular pathway used by eosinophils in

234 Pyroptosis is a form of cell death important in defenses

235 Pyroptosis is a form of cell death that occurs in a rest

236 Pyroptosis is a form of inflammatory programmed cell dea

237 Pyroptosis is an inflammatory cell death response initia

238 Pyroptosis is an inflammatory form of cell death that no

239 Pyroptosis is an inflammatory form of programmed cell de

240 Although pyroptosis is critical for macrophages against pathogen

241 from host immune cells; instead, macrophage pyroptosis is driven by fungal cell-wall remodelling and

242 The pyroptosis is executed by the pore-forming protein GSDMD

243 Pyroptosis is mediated directly by the recently identifi

244 Pyroptosis is the caspase-dependent inflammatory cell de

245 Mechanistically, pyroptosis is triggered by the alarmin S100A9 that is fo

246 ng a type of inflammatory cell death termed "pyroptosis." Leukotriene B(4) (LTB(4)) is a lipid mediat

247 -8 can cleave gasdermin D (GSDMD) leading to pyroptosis-like cell death and IL-1beta release in murin

248 inflammasome activation is closely linked to pyroptosis, lytic cell death did not occur following C.

249 showed that chronic inflammation induced by pyroptosis may facilitate persistence of the HIV latent

250 We propose that IL-1beta release without pyroptosis may occur in early-recruited monocytes to reg

251 in early SIV infection, which suggests that pyroptosis may play a pivotal role in the pathogenesis o

252 uggest that NMII-induced caspase-1-dependent pyroptosis may require its T4SS and activation of the TL

253 the use of caspase-1 inhibitors that inhibit pyroptosis, may maintain the CD4+ T cell population and

254 ews about the close relationship between the pyroptosis mechanism and the occurrence of various cance

255 ZBP1 activation triggers inflammation and pyroptosis, necroptosis, and apoptosis (PANoptosis) by a

256 To investigate the relative importance of pyroptosis, necroptosis, and apoptosis during Salmonella

257 h of wild type (WT) BMDC via NLRP3-dependent pyroptosis, nigericin-stimulated Casp1/11(-/-) BMDC exhi

258 SIV, and by extension, that of HIV-1, since pyroptosis not only induces CD4(+) T cell death but also

259 Pyroptosis occurs via two pathways: the canonical pathwa

260 causes caspase-1/NLRP3/gasdermin D-mediated pyroptosis of human monocytes and macrophages.

261 Finally, we provide evidence that pyroptosis of in vitro infected macrophages is directly

262 P2X7 stimulation promotes caspase-mediated pyroptosis of Tfh cells and controls the development of

263 ammasomes which are subsequently involved in pyroptosis of the cell and pathogen clearance.

264 ving these cells with a LF and/or inhibiting pyroptosis of the cells can be a new therapeutic approac

265 n and subsequent proinflammatory cell death (pyroptosis) of the infected phagocyte.

266 Pyroptosis operates to remove the replication niche of i

267 This is correlated with the lack of pyroptosis or inhibition of viral replication.

268 of latently infected cells brought about by pyroptosis, or to a lesser extent by superinfection, mig

269 otic or necrotic pathway; involvement of the pyroptosis pathway has not been reported previously.

270 hat GSDMC/caspase-8 mediates a non-canonical pyroptosis pathway in cancer cells, causing tumour necro

271 terleukin 1beta [IL-1beta]) in the canonical pyroptosis pathway were significantly upregulated in exp

272 tions did not affect gasdermin D function or pyroptosis, polymorphisms disrupting sites predicted to

273 Apoptosis, pyroptosis, pyronecrosis, necroptosis, ferroptosis, and

274 Herein, we report that the pyroptosis regulator gasdermin D (GSDMD) was necessary f

275 We had previously assumed that pyroptosis releases intracellular bacteria to the extrac

276 Pyroptosis requires cleavage and activation of the pore-

277 Thus, caspase-1-driven pyroptosis requires induction of initial prelytic pores

278 acologic inhibition of NLRP3 or NOX suppress pyroptosis, ROS generation, and nuclear beta-catenin in

279 Consistent with a role for SARM in pyroptosis, Sarm1(-/-) mice were protected from lipopoly

280 L-1beta but also provided protection against pyroptosis, suggesting that HIV-induced podocyte injury

281 aspase-1 maturation, IL-1beta secretion, and pyroptosis, suggesting that it retained Nlrc4 Ser533 pho

282 els of latency that do not take into account pyroptosis, superinfection, or other potential complexit

283 D (Gsdmd)-dependent lytic cell death called pyroptosis that promotes antimicrobial host defense but

284 nflammatory, lytic form of cell death termed pyroptosis that underlies many of the hallmark features

285 C. muridarum infections induce GBP-dependent pyroptosis through both caspase-11-dependent noncanonica

286 s, such as Salmonella, must prevent or delay pyroptosis to avoid being trapped in the PIT and subsequ

287 hock can directly activate ECs and induce EC pyroptosis to cause lung injury.

288 polysaccharide elicits gasdermin D-dependent pyroptosis to enable passive SQSTM1 release from macroph

289 that most T cells in the tissue die through pyroptosis triggered by abortive infection, i.e., infect

290 rstanding of intracellular LPS detection and pyroptosis via noncanonical inflammasome and discuss the

291 Gasdermin D (GSDMD) induces pyroptosis via the pore-forming activity of its N-termin

292 -18 and induces the inflammatory cell death, pyroptosis, via gasdermin D.

293 ein (MLKL) in necroptosis and gasdermin-D in pyroptosis] were recently discovered, bringing us closer

294 the intramolecular domain interface enhanced pyroptosis, whereas mutations at the predicted lipid-bin

295 inflammasome-dependent cytokine release and pyroptosis, whereby cells displayed increased IL-1beta p

296 lar LPS elicits the lytic cell death called 'pyroptosis', which occurs in multiple cell types.

297 bial infection of immune cells often induces pyroptosis, which is mediated by a cytosolic protein com

298 ghly inflammatory cell death reaction termed pyroptosis, which plays a key role in mammalian innate i

299 A dynamic interplay of pyroptosis with ESCRT-mediated plasma membrane repair al

300 chanisms that drive pyroptosis, evidence for pyroptosis within the CNS, and emerging therapeutic stra