ライフサイエンスコーパス: autoinflammatory

1 n of the somatosensory system to autoimmune, autoinflammatory, allergic, and infectious processes in

2 ic for NLRP3-associated syndromes, including autoinflammatory and autoimmune diseases, and a tool for

3 e increased by stress and infections, and in autoinflammatory and autoimmune diseases.

4 ammasome has also been linked to a number of autoinflammatory and autoimmune disorders.

5 with previously genetically uncharacterized autoinflammatory and immunodeficiency syndrome.

6 tory responses that are associated with both autoinflammatory and metabolic diseases.

7 NLRs have known roles in autoimmune, autoinflammatory, and infectious diseases.

8 association with (usually) viral infections, autoinflammatory/autoimmune diseases, malignant diseases

9 rome (SchS) is a rare disease with suspected autoinflammatory background that shares several clinical

10 of complex multifactorial conditions with an autoinflammatory basis.

11 H oxidase activity is a key factor promoting autoinflammatory bone damage in Pstpip2(cmo) mice.

12 urrent multifocal osteomyelitis (CRMO) is an autoinflammatory bone disease mediated by the inflammato

13 Cherubism is a rare autoinflammatory bone disorder that is associated with p

14 ate on the genetics and immunologic basis of autoinflammatory bone disorders including chronic recurr

15 and IL1RN have been identified in monogenic autoinflammatory bone disorders that have allowed more d

16 ed on what has been learned in the monogenic autoinflammatory bone disorders, IL-1 is emerging as an

17 r protein PSTPIP2, these animals suffer from autoinflammatory chronic multifocal osteomyelitis simila

18 Here, we identify a novel hematological/autoinflammatory condition (NOCARH syndrome) in four unr

19 ic syndrome (TRAPS) is an autosomal-dominant autoinflammatory condition caused by mutations in the TN

20 n in human OTULIN causes a potentially fatal autoinflammatory condition termed OTULIN-related autoinf

21 ical adenitis (PFAPA) is a relatively common autoinflammatory condition that primarily affects childr

22 Pseudogout is an autoinflammatory condition triggered by calcium pyrophos

23 CD4 T cells from the target site in a human autoinflammatory condition.

24 nflammasome has been associated with several autoinflammatory conditions including gout.

25 3 activation and type I IFN production cause autoinflammatory conditions such as Aicardi-Goutieres sy

26 1) demonstrate that not all IL-1beta-driven autoinflammatory conditions will benefit from the therap

27 seen in type I interferonopathies and other autoinflammatory conditions.

28 oval of IL-1-blocking agents for a number of autoinflammatory conditions.

29 as well as their role in the pathogenesis of autoinflammatory Crohn's disease.

30 at in contrast to related IL-1beta-dependent autoinflammatory cryopyrinopathies, Blau syndrome is not

31 Autoinflammatory disease and hyperinflammatory syndromes

32 ells affects inflammatory responses in human autoinflammatory disease and in mouse models of inflamma

33 iated alterations in patients with monogenic autoinflammatory disease and opens up possibilities for

34 EFV or pyrin) are associated with hereditary autoinflammatory disease and severe IBD.

35 of interferon genes (STING) lead to a severe autoinflammatory disease called STING-associated vasculo

36 Autoinflammatory disease can result from monogenic error

37 sum, and Acne Syndrome (PAPA syndrome) is an autoinflammatory disease caused by aberrant production o

38 culopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by gain-of-function muta

39 Familial Mediterranean fever (FMF) is an autoinflammatory disease caused by homozygous or compoun

40 Here, we report an autoinflammatory disease caused by loss-of-function muta

41 or DIRA, to denote this autosomal recessive autoinflammatory disease caused by mutations affecting I

42 rranean fever (FMF) is an IL-1beta-dependent autoinflammatory disease caused by mutations of Mediterr

43 promote activation of RIPK1, and lead to an autoinflammatory disease characterized by hypersensitivi

44 onset in infancy (SAVI), a severe pediatric autoinflammatory disease characterized by pulmonary fibr

45 Schnitzler syndrome is an adult-onset autoinflammatory disease characterized by urticarial exa

46 adaptor protein PSTPIP2 are the cause of the autoinflammatory disease chronic multifocal osteomyeliti

47 nction mutations in MEFV responsible for the autoinflammatory disease Familial Mediterranean Fever (F

48 utations in its B30.2/SPRY domain causes the autoinflammatory disease familial Mediterranean fever by

49 components HOIP and HOIL-1 yield a systemic autoinflammatory disease in humans, whereas their geneti

50 We have now identified an autoinflammatory disease in mice driven by IL-18, but no

51 N153S knock-in mice may develop more severe autoinflammatory disease in response to a virus challeng

52 We describe a patient with an autoinflammatory disease in which the main clinical feat

53 ase-interacting protein 2 (PSTPIP2), lead to autoinflammatory disease involving extramedullary hemato

54 tor antagonist (IL-1Ra) deficiency is a rare autoinflammatory disease involving neonatal onset of pus

55 Our understanding of the etiology of autoinflammatory disease is growing rapidly.

56 The autoinflammatory disease mevalonate kinase deficiency (M

57 mic juvenile idiopathic arthritis (sJIA), an autoinflammatory disease of unknown etiology, this appro

58 tible to environmental mycobacteria and have autoinflammatory disease presentations.

59 questions that are expected to be central in autoinflammatory disease research in the coming decade.

60 ponsible for the development of a persistent autoinflammatory disease resembling chronic recurrent mu

61 Blau syndrome is an autoinflammatory disease resulting from mutations in the

62 t that the definition of what constitutes an autoinflammatory disease should be reassessed.

63 This new phenotype encompasses an autoinflammatory disease showing similarities to many as

64 Mutations in the NLRP3 gene cause the autoinflammatory disease spectrum cryopyrin-associated p

65 irst recognized just over 2 decades ago, the autoinflammatory disease spectrum has expanded rapidly t

66 flammasome defect that expands the monogenic autoinflammatory disease spectrum to include MAS and sug

67 e, and cause the autosomal dominant systemic autoinflammatory disease spectrum, termed cryopyrin-asso

68 tolerance, antiviral signaling, and complex autoinflammatory disease states.

69 Recognizing autoinflammatory disease symptom patterns, performing ap

70 Rheumatoid arthritis is a chronic autoinflammatory disease that affects 1-2% of the world'

71 His case highlights IL-1Ra deficiency as an autoinflammatory disease that is distinct from neonatal-

72 well established genetic model of autoimmune/autoinflammatory disease that resembles systemic lupus e

73 he cause of a life-threatening but treatable autoinflammatory disease that underscores the divergent

74 ppropriate TLR9 responses can drive a severe autoinflammatory disease under homeostatic conditions an

75 We describe a novel autoinflammatory disease with defective neutrophil funct

76 ean fever (FMF) is the most common monogenic autoinflammatory disease worldwide.

77 Inactivating mutations cause rhabdomyolysis, autoinflammatory disease, and aberrant fat storage.

78 One such autoinflammatory disease, called STING-associated vascul

79 ncy in patients that suffer from a pediatric autoinflammatory disease, chronic recurrent multifocal o

80 ivation in patients with an NLRP3-associated autoinflammatory disease, cryopyrin-associated periodic

81 ulation in adult mice causes a mild systemic autoinflammatory disease, dysregulation of TLR9 early in

82 ary inflammasome-driven, IL-1beta-dependent, autoinflammatory disease, making it an attractive therap

83 itin-related genes, previously implicated in autoinflammatory disease, may define new disorders.

84 nd F-BAR protein that has been implicated in autoinflammatory disease, most notably in the PAPA syndr

85 Ndfip1 deletion in Treg cells results in autoinflammatory disease.

86 tivation by NEMO, and its absence results in autoinflammatory disease.

87 ies in patients with Schnitzler syndrome, an autoinflammatory disease.

88 host-regulated actin-dependent processes and autoinflammatory disease.

89 identify IFN-gamma as a mediator of systemic autoinflammatory disease.

90 filamentous bacteria, and an extraintestinal autoinflammatory disease.

91 ional target for therapeutic intervention in autoinflammatory disease.

92 which gain-of-function pyrin mutations cause autoinflammatory disease.

93 anean fever (FMF), the most common Mendelian autoinflammatory disease.

94 nd humans, to a propensity for infection and autoinflammatory disease.

95 hat is associated with a macrophage-mediated autoinflammatory disease.

96 aggerated and sustained responses leading to autoinflammatory disease.

97 We define six categories of autoinflammatory disease: IL-1beta activation disorders

98 NLRP3-associated autoinflammatory diseases (NLRP3-AIDs) include condition

99 th other inborn errors of immunity including autoinflammatory diseases and C1 inhibitor deficiency, a

100 onal avenues for treatment of infectious and autoinflammatory diseases and cancer.

101 Hereditary autoinflammatory diseases are caused by gene mutations o

102 Systemic autoinflammatory diseases are caused by mutations in gen

103 Autoinflammatory diseases are characterized by dysregula

104 The autoinflammatory diseases are characterized by seemingly

105 Autoinflammatory diseases are conditions in which pathog

106 Autoinflammatory diseases are disorders of the innate im

107 Systemic autoinflammatory diseases are driven by abnormal activat

108 Although some autoinflammatory diseases are due to gain-of-function mu

109 Autoinflammatory diseases are monogenic and polygenic di

110 The newly recognized group of autoinflammatory diseases are often accompanied by repet

111 Autoinflammatory diseases are often associated with a di

112 cell death implicated in the pathogenesis of autoinflammatory diseases as well as in disorders charac

113 deployment of anti-IL-1 therapies to control autoinflammatory diseases associated with aberrant infla

114 the innate immune system can cause systemic autoinflammatory diseases associated with increased IL-1

115 tients with COVID-19 or other infectious and autoinflammatory diseases by limiting tissue damage/infl

116 fication of disease alleles underlying human autoinflammatory diseases can provide important insights

117 and perhaps treat, lupus nephritis and other autoinflammatory diseases caused by the decreased abilit

118 ense mutations in NLRP3 result in a group of autoinflammatory diseases collectively known as the cryo

119 cterization of a growing number of monogenic autoinflammatory diseases has provided important insight

120 The study of autoinflammatory diseases has uncovered mechanisms under

121 le, the role of IL-1, novel entities such as autoinflammatory diseases have been described.

122 Unlike other autoinflammatory diseases in which anti-TNF therapy is l

123 e association of mutations in NLR genes with autoinflammatory diseases indicates an important functio

124 ption of a systems-based concept of systemic autoinflammatory diseases is anticipated to have implica

125 the gene encoding NLRP3 cause a spectrum of autoinflammatory diseases known as cryopyrin-associated

126 ted periodic syndromes (CAPS) are a group of autoinflammatory diseases linked to gain-of-function mut

127 Autoinflammatory diseases manifest inflammation without

128 Patients with autoinflammatory diseases present with noninfectious fev

129 matoses are a group of complex heterogeneous autoinflammatory diseases that all demonstrate excessive

130 iated with autoimmunity and a broad array of autoinflammatory diseases that include the interferonopa

131 Autoinflammatory diseases were first recognized nearly 2

132 ely activate these pathways underlie several autoinflammatory diseases with diverse clinical features

133 gulate these TLRs can lead to autoimmune and autoinflammatory diseases(2-6).

134 immunodeficiencies, inherited autoimmune and autoinflammatory diseases, and hematologic and oncologic

135 ddition, they are elevated in autoimmune and autoinflammatory diseases, and in these settings they ar

136 tory processes, including infection, sepsis, autoinflammatory diseases, and metabolic diseases.

137 genetic basis of both mendelian and complex autoinflammatory diseases, and with the recognition that

138 against secondary infections, its impact on autoinflammatory diseases, associated with inflammasome

139 active mutant (NLRC4-V341A) associated with autoinflammatory diseases, but not FCAS, showed neither

140 evelopment of novel biological therapies for autoinflammatory diseases, including IBD.

141 erlie familial Mediterranean fever and other autoinflammatory diseases, may predispose to vasculitis.

142 Here we review these monogenic autoinflammatory diseases, ranging from periodic fever s

143 ations in NFKB1 and suggest that a subset of autoinflammatory diseases, such as Behcet disease, can b

144 w, we describe the genetically characterized autoinflammatory diseases, we summarize our understandin

145 for promoting inflammation, particularly in autoinflammatory diseases, whereas IL-1alpha and the IL-

146 Finally, we analyse key features of autoinflammatory diseases, which are helpful to distingu

147 disease, which attacks specific tissues, to autoinflammatory diseases, which cause low-grade systemi

148 age, but its aberrant activation can lead to autoinflammatory diseases.

149 e damaged by genotoxic agents and in certain autoinflammatory diseases.

150 entral to the pathogenesis of many monogenic autoinflammatory diseases.

151 and contributes to the pathology of various autoinflammatory diseases.

152 that LDHA may be targeted therapeutically in autoinflammatory diseases.

153 at contribute to a variety of autoimmune and autoinflammatory diseases.

154 o new treatments for cytosolic DNA-triggered autoinflammatory diseases.

155 nd modulation of exaggerated inflammation in autoinflammatory diseases.

156 rapy of RA and possibly other autoimmune and autoinflammatory diseases.

157 ot in cells of patients afflicted with other autoinflammatory diseases.

158 mutations are associated with autoimmune and autoinflammatory diseases.

159 et juvenile idiopathic arthritis and related autoinflammatory diseases.

160 not in that of patients with other inherited autoinflammatory diseases.

161 tools to address infectious, autoimmune, and autoinflammatory diseases.

162 tial therapeutic target in uveitis and other autoinflammatory diseases.

163 ated genes shared by multiple autoimmune and autoinflammatory diseases.

164 to understand human systemic autoimmune and autoinflammatory diseases.

165 immunomodulatory cytokines in autoimmune and autoinflammatory diseases.

166 hology associated with several autoimmune or autoinflammatory diseases.

167 mic and local inflammatory conditions called autoinflammatory diseases.

168 lead to the development of autoimmune and/or autoinflammatory diseases.

169 receptor signaling, exhibiting a feature of autoinflammatory diseases.

170 IL-1 family because of its role in mediating autoinflammatory diseases.

171 ght into IFN dysregulation in autoimmune and autoinflammatory diseases.

172 is linked to the pathology of autoimmune and autoinflammatory diseases.

173 for innate immune sensors in autoimmune and autoinflammatory diseases.

174 unction of dominant STING mutants that cause autoinflammatory diseases.

175 ne, encoding MDA5, lead to interferon-driven autoinflammatory diseases.

176 ion induced by NALP3 mutants associated with autoinflammatory diseases.

177 stinct interleukin-1beta (IL-1beta)-mediated autoinflammatory diseases: familial Mediterranean fever

178 1R1, is broadly used to treat autoimmune and autoinflammatory diseases; however, blocking IL-1 increa

179 immunological reclassification of SJIA as an autoinflammatory disorder as well as detailing the drama

180 e, and many features of FMF overlap with the autoinflammatory disorder associated with TNF receptor s

181 ase 1 (ERAP1), Hap10, is associated with the autoinflammatory disorder Behcet's disease (BD) in epist

182 tor-associated periodic syndrome (TRAPS), an autoinflammatory disorder caused by missense mutations i

183 Blau syndrome is a rare, autosomal-dominant, autoinflammatory disorder characterized by granulomatous

184 TRAPS, OMIM 142680) is an autosomal dominant autoinflammatory disorder characterized by prolonged att

185 al Mediterranean Fever (FMF) is an inherited autoinflammatory disorder characterized by unprovoked ep

186 the gene encoding pyrin are associated with autoinflammatory disorder Familial Mediterranean Fever (

187 ing pyrin in humans, are associated with the autoinflammatory disorder familial Mediterranean fever.

188 SJIA is an autoinflammatory disorder in which defects of innate imm

189 th FMF mutation (MefvV726A/V726A) exhibit an autoinflammatory disorder mediated by autoactivation of

190 function are the most frequent cause of this autoinflammatory disorder of childhood and are also asso

191 This mouse strain shows an autoinflammatory disorder that is prevented by genetic d

192 t multifocal osteomyelitis (CRMO) is a human autoinflammatory disorder that primarily affects bone.

193 me, 6 (6.4%) a phagocyte defect, 7 (7.4%) an autoinflammatory disorder, 14 (15%) a combined immunodef

194 Familial Mediterranean fever (FMF), an autoinflammatory disorder, is associated with mutations

195 The autoinflammatory disorder, Neonatal-onset Multisystem In

196 nderstood, but PG is generally considered an autoinflammatory disorder.

197 nsor of double-stranded DNA, is activated in autoinflammatory disorders and by DNA damage.

198 nition of self RNAs by RLRs is implicated in autoinflammatory disorders and cancer.

199 in patients with underlying rheumatologic or autoinflammatory disorders and is usually designated mac

200 the boundaries of what are considered to be autoinflammatory disorders are constantly evolving and c

201 involvement is a defining characteristic of autoinflammatory disorders caused by abnormal IL-1 signa

202 the gene encoding NLRP3 are associated with autoinflammatory disorders characterized with excessive

203 cal clues and tips that can help to identify autoinflammatory disorders in patients presenting with c

204 and introduce major categories of monogenic autoinflammatory disorders recognized to date, including

205 This pathway is dysregulated in autoinflammatory disorders such as hyper-IgD syndrome, i

206 Though a complex set of autoinflammatory disorders that can be precipitated by d

207 thogenesis of pustular psoriasis, a model of autoinflammatory disorders with predominant cutaneous ma

208 n and features prominently in autoimmune and autoinflammatory disorders, allergy, acute and chronic i

209 g the distinguishing features of the classic autoinflammatory disorders, and appreciating the treatme

210 CARD9 has been associated with autoinflammatory disorders, and loss-of-function mutatio

211 opoietic stem cell transplantation (HSCT) in autoinflammatory disorders, including PAMI syndrome, has

212 ulated, disruption of which triggers various autoinflammatory disorders, including TNF receptor-assoc

213 ment of precise therapeutic targets to treat autoinflammatory disorders, infectious diseases, and can

214 ed, inflammation may result in autoimmune or autoinflammatory disorders, neurodegenerative disease, o

215 s and treatment of rare, genetically defined autoinflammatory disorders, physicians are challenged by

216 urther underscored by their association with autoinflammatory disorders, wherein localized inflammati

217 ar connection between two seemingly distinct autoinflammatory disorders.

218 disrupt nucleic acid metabolism can lead to autoinflammatory disorders.

219 infections, malignancies, or autoimmune and autoinflammatory disorders.

220 erleukin-1 receptor antagonist used to treat autoinflammatory disorders.

221 implicated in the pathogenesis of hereditary autoinflammatory disorders.

222 ts of systemic inflammation in patients with autoinflammatory disorders.

223 ction and predispose individuals to specific autoinflammatory disorders.

224 rial rash, such as urticarial vasculitis and autoinflammatory disorders.

225 que IFN signaling signature, unlike in other autoinflammatory disorders.

226 nism of older-onset PsJIA appears to involve autoinflammatory dysregulation centered at the synovial-

227 However, autoinflammatory episodes continued unabated until hemat

228 tion had antibody deficiency and experienced autoinflammatory episodes, including aphthae, gastrointe

229 sponsible for instigating self-DNA triggered autoinflammatory events in the cell.

230 ons in MEFV (encoding human PYRIN) result in autoinflammatory familial Mediterranean fever syndrome.

231 pathways and cell types that drive cutaneous autoinflammatory features remain poorly understood.

232 der (XLPDR), a primary immunodeficiency with autoinflammatory features.

233 reover, we designed a panel consisting of 32 autoinflammatory genes to explore genetic susceptibility

234 Rheumatic heart disease (RHD), an autoinflammatory heart disease, was recently declared a

235 ing, and inherited ISG15 deficiency leads to autoinflammatory IFNopathies, in which individuals exhib

236 nduce immune-related adverse events that are autoinflammatory in nature.

237 /beta immunity, reminiscent of the Mendelian autoinflammatory interferonopathies Aicardi-Goutieres sy

238 and Elevated temperature (CANDLE) is a rare autoinflammatory interferonopathy caused by additive los

239 tigen receptors in B cells (BCR), promote an autoinflammatory loop in systemic lupus erythematosus (S

240 nd inflammasome activities contribute to the autoinflammatory manifestations of WAS, thereby identify

241 report on 4 PNH patients who also had marked autoinflammatory manifestations, including aseptic menin

242 cess IL-18 promotes hyperinflammation via an autoinflammatory mechanism distinct from, and synergisti

243 T1-IFN) are known to be a constituent of the autoinflammatory milieu within the pancreas of patients

244 However, evidence from an autoinflammatory murine model indicates that IL-18, the

245 ients with GPP are viewed as evidence for an autoinflammatory pathogenesis.

246 e findings identify pustular psoriasis as an autoinflammatory phenotype caused by defects in vesicula

247 Both autoimmune and autoinflammatory phenotypes are suppressed when spin hom

248 In this study, we characterize the autoinflammatory phenotypes in the skin of both autoimmu

249 mice did not affect IL-1beta levels, and the autoinflammatory process was initiated with similar kine

250 ith many different cellular functions in the autoinflammatory process.

251 and interferon activation, contribute to the autoinflammatory process.

252 mmasome complex with ASC after engagement by autoinflammatory PSTPIP1 mutants.

253 gin; these cells may support the destructive autoinflammatory response by the innate immune system.

254 EGCG administration blunted self DNA-induced autoinflammatory responses in an Aicardi-Goutieres syndr

255 gest that LINE-1s may drive physiological or autoinflammatory responses through dsRNA sensing and gen

256 we review the basic concepts underlying the "autoinflammatory revolution" in the understanding of imm

257 ding constitutive MDA5 activation, they lack autoinflammatory sequelae.

258 amily LMG446, hearing loss is accompanied by autoinflammatory signs and symptoms without serologic ev

259 Psoriasis is an autoinflammatory skin disease of unknown etiology.

260 ritical role in the pathogenesis of chronic, autoinflammatory skin diseases such as psoriasis.

261 C, in 15 unrelated individuals with a severe autoinflammatory skin disorder known as pustular psorias

262 mice (cpdm), is a major contributor to their autoinflammatory skin phenotype, as genetic coablation o

263 er the VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome.

264 tation, H443P in NLRC4, causes familial cold autoinflammatory syndrome (FCAS) characterized by cold-i

265 inflammatory condition termed OTULIN-related autoinflammatory syndrome (ORAS).

266 ich is classified as a proteasome-associated autoinflammatory syndrome (PRAAS).

267 me, also known as "cryopyrin," "cold-induced autoinflammatory syndrome 1" (CIAS1), or nacht domain-,

268 such as Muckle-Wells syndrome, familial cold autoinflammatory syndrome and urate crystal-induced peri

269 tugal and Mexico with an autosomal-recessive autoinflammatory syndrome characterized by joint contrac

270 4416) is a rare autosomal dominant inherited autoinflammatory syndrome characterized by pyogenic ster

271 ic juvenile idiopathic arthritis (JIA) is an autoinflammatory syndrome in which the myelomonocytic li

272 elevated temperature (CANDLE syndrome) is an autoinflammatory syndrome recently described in children

273 in cholesterol metabolism result in a severe autoinflammatory syndrome termed mevalonate kinase defic

274 et disease is a chronic, relapsing-remitting autoinflammatory syndrome with a strong HLA-B*51 associa

275 on we term 'cleavage-resistant RIPK1-induced autoinflammatory syndrome'.

276 cal and pathogenic description of this novel autoinflammatory syndrome, thereby expanding the clinica

277 onocytes expressing familial cold-associated autoinflammatory syndrome-associated Cryopyrin mutations

278 Here, we show that one of the autoinflammatory syndrome-causing mutants of NLRC4, H443

279 n healthy control subjects and patients with autoinflammatory syndrome.

280 some-related genes might be involved in this autoinflammatory syndrome.

281 tivation of inflammasomes is associated with autoinflammatory syndromes and other pathologies.

282 d inflammasome activation is associated with autoinflammatory syndromes and several common diseases.

283 These include rare diseases such as autoinflammatory syndromes and urticarial vasculitis in

284 and clinical characterizations of monogenic autoinflammatory syndromes have led to ground breaking i

285 mation and thus novel therapeutic targets in autoinflammatory syndromes including other IL-1beta medi

286 IRA have encouraged their wider use in other autoinflammatory syndromes including the classic heredit

287 Monogenic autoinflammatory syndromes present with excessive system

288 witched B cells and 'IgD-armed' basophils in autoinflammatory syndromes with periodic fever, our data

289 ations in inflammasome-related genes lead to autoinflammatory syndromes, and review the contribution

290 and IL1RN, cause two severe and early-onset autoinflammatory syndromes, CAPS (cryopyrin associated p

291 l of diseases presenting with fever includes autoinflammatory syndromes, infections associated with i

292 cial role of IL-1beta in the pathogenesis of autoinflammatory syndromes, we hypothesized that IL-1bet

293 Point mutations in NLRC4 cause autoinflammatory syndromes.

294 une system activation owing to infections or autoinflammatory syndromes.

295 from gene mutations is related to monogenic autoinflammatory syndromes.

296 the adaptive immune system in patients with autoinflammatory syndromes.

297 in NLRP3 are associated with recurrent fever/autoinflammatory syndromes.

298 lease is central to the pathogenesis of many autoinflammatory syndromes.

299 le dermatomyositis, juvenile scleroderma and autoinflammatory syndromes.

300 editerranean fever, 2 archetypical monogenic autoinflammatory syndromes.