ライフサイエンスコーパス: autoimmune

1 ese receptors in myeloid cells during B cell autoimmune activation remain less clear.

2 Tregs suppress both autoimmune and alloimmune responses and are particularly

3 ation may lead to the development of chronic autoimmune and degenerative diseases and cancer.

4 The mechanisms leading to autoimmune and inflammatory diseases in the CNS have not

5 mmatory T helper 17 cell responses linked to autoimmune and inflammatory diseases.

6 ngolipid involved in the development of many autoimmune and inflammatory diseases.

7 owed large overlaps in genetic variants with autoimmune and inflammatory diseases.

8 e potential to become pathogenic and promote autoimmune and inflammatory diseases.

9 isease-associated variants, particularly for autoimmune and inflammatory disorders, indicating that d

10 ediated pathways to benefit the treatment of autoimmune and inflammatory disorders.

11 is extensively used for the immunotherapy of autoimmune and inflammatory disorders.

12 l kinase (JNK), and an important mediator of autoimmune and inflammatory responses.

13 of regulatory B cells (Bregs) that suppress autoimmune and inflammatory responses.

14 of inflammation and have been implicated in autoimmune and metabolic diseases.

15 ion and cancer, as well as susceptibility to autoimmune and neurodegenerative disorders.

16 at are heavily implicated in human allergic, autoimmune, and malignant diseases.

17 and to investigate the presence and role of autoimmune antibodies in 25 cases of acute zonal occult

18 Using the K/BxN autoimmune arthritis model, we elucidate a novel mechani

19 Using an autoimmune arthritis model, we show that a constituent o

20 re used to study the importance of LAIR-1 in autoimmune arthritis.

21 ifferentiative cues, yields B cells with the autoimmune-associated T-bet+ phenotype.

22 mechanisms responsible for the disease, the autoimmune attack on the CNS that leads to chronic infla

23 e self-proteins that are most susceptible to autoimmune attack, and we suggest that this link could b

24 lar environment protects ocular tissues from autoimmune attack.

25 by likely increasing the risk for seeding of autoimmune B cell responses.

26 Dermatitis herpetiformis (DH) is an autoimmune blistering condition seen in the context of c

27 k of bullous pemphigoid (BP), a subepidermal autoimmune blistering disease characterized by autoantib

28 assess the incidence of PCP in patients with autoimmune blistering diseases receiving no routine prop

29 A total of 801 patients with autoimmune blistering diseases were included in this stu

30 Bullous pemphigoid (BP) is an autoimmune bullous disease of the skin characterized by

31 w-titer GAD65-Ab, Abs strongly suggesting an autoimmune cause of epilepsy were seen in 23 patients (2

32 nd are generally considered reflective of an autoimmune cholangitis.

33 Patients with CD have extra-intestinal autoimmune comorbid conditions more frequently than expe

34 aimed at mitigating the risk of post-stroke autoimmune complications driven by adaptive immune syste

35 ells in patients with cDGS but with frequent autoimmune complications in survivors.

36 ned in immune cell subsets in the absence of autoimmune complications.

37 ANCA-associated vasculitis is an autoimmune condition characterized by vascular inflammat

38 mice could have been influenced by emerging autoimmune conditions that are characteristic of the mic

39 arkers have limited specificity for a single autoimmune connective tissue disease.

40 ker domain of STAT1 who had life-threatening autoimmune cytopenias and chronic mucocutaneous candidia

41 Type 1 diabetes (T1D) results from the autoimmune destruction of insulin-producing beta-cells i

42 ype 1 diabetes (T1D) is characterized by the autoimmune destruction of pancreatic beta cells.

43 on in the pancreas facilitate progression to autoimmune destruction of pancreatic beta-cells.

44 The autoimmune destruction was also diminished in mice admin

45 The persistent protection from autoimmune destruction was paralleled by an increase in

46 e islet graft, thereby playing a role in the autoimmune destruction.

47 uppressed immunopathology in mouse models of autoimmune diabetes and airway inflammation, and increas

48 s in innate immunity influence the course of autoimmune diabetes and support the use of targeted stra

49 ice treated with AZD1480 were protected from autoimmune diabetes, and diabetes was reversed in newly

50 Using a transgenic model of autoimmune diabetes, here we show that ablation of TGF-b

51 a-cell line were implanted subcutaneously in autoimmune diabetes-prone NOD mice, beta-cell-reactive T

52 nzyme A deficiency in the NOD mouse model of autoimmune diabetes.

53 to block the JAK-STAT pathway would prevent autoimmune diabetes.

54 ife-threatening consequence of treatment for autoimmune disease (AID) and an emerging clinical phenom

55 ravis (MG) is a prototypical B cell-mediated autoimmune disease affecting 20-50 people per 100,000.

56 that recapitulate causative mutations in the autoimmune disease Aicardi-Goutieres syndrome demonstrat

57 better understanding the molecular basis for autoimmune disease and cancer.

58 lymphocytes that protect against infection, autoimmune disease and cancer.

59 y for viral RNA, with major implications for autoimmune disease and cancer.

60 iated with positive and negative outcomes in autoimmune disease and infection.

61 l-specific ablation of murine Gclc prevented autoimmune disease but blocked antiviral defense.

62 ic lupus erythematosus (SLE) is an incurable autoimmune disease characterized by autoantibody deposit

63 Systemic sclerosis is an autoimmune disease characterized by fibrosis of skin and

64 allmark of Sjogren's syndrome (SS), a common autoimmune disease characterized by lymphocytic infiltra

65 Sjogren's syndrome (SS) is a common chronic autoimmune disease characterized by lymphocytic infiltra

66 Systemic sclerosis is an autoimmune disease characterized by T-cell infiltration

67 ental pollutants have been shown to modulate autoimmune disease development.

68 us DNA and play a role in tumor immunity and autoimmune disease development.

69 cells and the establishment of a lupus-like autoimmune disease in mice.

70 The occurrence of autoimmune disease is a negative prognostic factor for s

71 Type 1 diabetes (T1D) is an autoimmune disease leading to beta-cell destruction.

72 Primary membranous nephropathy (MN) is an autoimmune disease mainly caused by autoantibodies again

73 In the autoimmune disease multiple sclerosis and its animal mod

74 Multiple sclerosis (MS) is an autoimmune disease of the central nervous system.

75 Vitiligo is an autoimmune disease of the skin that results in the destr

76 sulin-reactive CD4(+) T cell development and autoimmune disease outcome.

77 responses to DNA vaccines, gene therapy, and autoimmune disease pathogenesis.

78 autoantibodies in myasthenia gravis (MG), an autoimmune disease that causes neuromuscular transmissio

79 Type 1 diabetes (T1D) is a chronic autoimmune disease that causes severe loss of pancreatic

80 Type 1 diabetes is a T cell-mediated autoimmune disease that is characterized by Ag-specific

81 Type 1 diabetes (T1D) is an autoimmune disease that results from the destruction of

82 Multiple sclerosis (MS) is a common autoimmune disease that targets myelin in the central ne

83 l superantigens may precipitate a lupus-like autoimmune disease through activation of DNT cells.

84 The rampant autoimmune disease was associated with enhanced T cell p

85 lupus erythematosus (SLE) is a heterogeneous autoimmune disease with a strong genetic component chara

86 Systemic sclerosis is an orphan, systemic autoimmune disease with no FDA-approved treatments.

87 ignaling is associated with immunopathology, autoimmune disease, and cancer progression.

88 D) is primarily perceived as a T cell-driven autoimmune disease, islet autoantibodies are the best cu

89 its antiviral activity and association with autoimmune disease, leading to aberrant activation of in

90 ex, previous venous thromboembolism, cancer, autoimmune disease, thrombosis of non-varicose veins).

91 r the dominantly protective effect of HLA in autoimmune disease, whereby HLA polymorphism shapes the

92 Autoimmune disease-associated variants are preferentiall

93 f-recognition, conferring heightened risk of autoimmune disease.

94 w therapeutic horizons in patients with this autoimmune disease.

95 ling for age, sex, race, smoking status, and autoimmune disease.

96 hes for limiting the effects of IgG-mediated autoimmune disease.

97 lity to migrate into inflamed tissues during autoimmune disease.

98 vaccines and immunotherapies for cancer and autoimmune disease.

99 a mouse model with genetic susceptibility to autoimmune disease.

100 is essential to prevent immunopathology and autoimmune disease.

101 dent NKp46(+) ILCs in the development of CNS autoimmune disease.

102 Autoimmune diseases affect 7.5% of the US population, an

103 zed GWAS data from a selection of archetypal autoimmune diseases among 138511 individuals of European

104 Th17 cells are major players in multiple autoimmune diseases and are developmentally contingent o

105 ulatory drugs are increasingly used to treat autoimmune diseases and cancer.

106 d attenuates the progression and severity of autoimmune diseases and experimental colitis.

107 t is a target of therapeutic intervention in autoimmune diseases and lymphoma.

108 Growing insight into the pathogenesis of autoimmune diseases and numerous studies in preclinical

109 factors contributing to the pathogenesis of autoimmune diseases and the mechanisms involved is still

110 Finally, the role of the laminins in autoimmune diseases and transplantation will be discusse

111 logy in multiple sclerosis and perhaps other autoimmune diseases as well.

112 s that was also represented in patients with autoimmune diseases but not those with other diseases.

113 ently been implicated in the pathogenesis of autoimmune diseases by various mechanisms, including for

114 ls of IL-15 expression with inflammatory and autoimmune diseases has led to the development of variou

115 s and establishment of clinical tolerance in autoimmune diseases have proven to be challenging.

116 cription factor Prdm1 has been implicated in autoimmune diseases in humans through genome-wide associ

117 in, is one of the most common organ-specific autoimmune diseases in humans.

118 improvement of clinical symptoms of certain autoimmune diseases including autoimmune hepatitis (AIH)

119 A notable feature of many autoimmune diseases is their greater prevalence in femal

120 IL-27 exerts protective effects in autoimmune diseases like experimental autoimmune encepha

121 represent a potential avenue for combatting autoimmune diseases mediated by T reg cell dysfunction.

122 epilepsy and in an array of degenerative and autoimmune diseases of the central nervous system.

123 Current therapies for autoimmune diseases rely on traditional immunosuppressiv

124 ing their key effector functions in specific autoimmune diseases remains challenging.

125 ers with variants previously associated with autoimmune diseases such as Crohn disease, multiple scle

126 istently, mutations in TREX1 are linked with autoimmune diseases such as systemic lupus erythematosus

127 therapeutic application of NRF2 inducers in autoimmune diseases that are accompanied by Treg dysfunc

128 in the pathogenesis of several diseases, the autoimmune diseases that represent a relevant burden for

129 ontribute to the etiology of T-cell-mediated autoimmune diseases through the upregulation of type 2 a

130 enetic loci and pathways between allergy and autoimmune diseases to elucidate shared disease mechanis

131 ment of an array of diseases from cancer and autoimmune diseases to infectious diseases.

132 IL-35 suppresses autoimmune diseases while preventing host defense to inf

133 argeted tolerance induction and treatment of autoimmune diseases, allergic disorders, and graft rejec

134 rograms operating during acute inflammation, autoimmune diseases, allergic inflammation, pregnancy, c

135 cytes in various diseases including cancers, autoimmune diseases, and virus infections.

136 the BACH2 locus are associated with several autoimmune diseases, but BACH2 mutations that cause Mend

137 IL-23/IL-17 pathway is important in multiple autoimmune diseases, but its effect on lupus pathology r

138 CD40-CD40L pathway is implicated in various autoimmune diseases, but the activity status of this pat

139 Autoimmune diseases, including Aicardi-Goutieres syndrom

140 Th17 cells play a critical role in autoimmune diseases, including multiple sclerosis and it

141 s, OR = 2.02 in African Americans) and other autoimmune diseases, including primary Sjogren's syndrom

142 implied the association of IRF5 with several autoimmune diseases, including systemic lupus erythemato

143 seases, including inflammatory rheumatic and autoimmune diseases, infections, and malignancies can mi

144 ommonalities in pathways between allergy and autoimmune diseases, suggesting shared disease mechanism

145 crucial to identify the occurrence of other autoimmune diseases, to control relapses, and to evaluat

146 Among 290 loci previously associated with 16 autoimmune diseases, we found a significant enrichment o

147 Hi-C data with genetic associations for five autoimmune diseases, we prioritised 245 candidate genes

148 lay an important role in the pathogenesis of autoimmune diseases.

149 novel therapies for transplant rejection and autoimmune diseases.

150 ficiency causes lethal, CD4(+) T cell-driven autoimmune diseases.

151 of utilizing naive T cells for understanding autoimmune diseases.

152 fective in patients with antibody-associated autoimmune diseases.

153 uishing normal from tumor tissue and trigger autoimmune diseases.

154 channel is observed at the onset of several autoimmune diseases.

155 ls may be a potential target for therapy for autoimmune diseases.

156 the same direction of effect for allergy and autoimmune diseases.

157 not be sufficient to prevent tissue-specific autoimmune diseases.

158 an constant eQTLs in GWAS signals of several autoimmune diseases.

159 ing therapeutic agents against TH17-mediated autoimmune diseases.

160 une response, and is also the main driver of autoimmune diseases.

161 dates for the prevention and amelioration of autoimmune diseases.

162 tential as a therapeutic target for treating autoimmune diseases.

163 ome a focus of research in the area of human autoimmune diseases.

164 ole of these cells in human inflammatory and autoimmune diseases.

165 nt seemed to be a general characteristic for autoimmune diseases.

166 t self, and thus to avoid the development of autoimmune diseases.

167 immune response, as shown for infectious and autoimmune diseases.

168 s play an important role in the pathology of autoimmune diseases.

169 to cure human chronic infections, cancer, or autoimmune diseases.

170 ions of this selectivity filter give rise to autoimmune diseases.

171 romising target for treatment of a number of autoimmune diseases.

172 insight for understanding the regulation of autoimmune diseases.

173 l loci and their pathways involved in PD and autoimmune diseases.

174 patients treated at 10 mg/kg dose level, and autoimmune disorder (one [5%]), increased amylase (one [

175 d a serious treatment-related adverse event: autoimmune disorder (two [13%]), lower abdominal pain (o

176 ently published study suggests that NS is an autoimmune disorder based on findings of cross-reacting

177 ng a previously reported type 1 diabetes and autoimmune disorder locus.

178 pathogenesis of multiple sclerosis (MS), an autoimmune disorder of the CNS and thus analyzed the mic

179 Rheumatoid arthritis is a chronic autoimmune disorder resulting in synovial inflammation.

180 nd function, leading to a fatal, early-onset autoimmune disorder.

181 B cells contribute to multiple aspects of autoimmune disorders and may play a role in triggering d

182 The initial trigger for both systemic autoimmune disorders and organ-specific autoimmune disor

183 cognized, role for AS in the pathogenesis of autoimmune disorders and particularly for T1D.

184 Infections and autoimmune disorders are more frequent in Down syndrome,

185 s with multiple myeloma and B cell-dependent autoimmune disorders but exert toxicity from inhibition

186 ly unclear if T reg cell deficiency-mediated autoimmune disorders can be treated by targeting the ent

187 The relationship between allergy and autoimmune disorders is complex and poorly understood.

188 ential therapeutic intervention for managing autoimmune disorders of the CNS.

189 emic autoimmune disorders and organ-specific autoimmune disorders probably involves the recognition o

190 ement functions occur in many infectious and autoimmune disorders that have been linked to schizophre

191 alarial drugs (AMDs) on clinical features of autoimmune disorders were discovered by chance during Wo

192 , FcRn can contribute to the pathogenesis of autoimmune disorders when an abnormal immune response ta

193 ples from patients with varied infectious or autoimmune disorders, and in the case of Sjogren's syndr

194 as a potential treatment for alloimmune and autoimmune disorders, but it is unknown whether disturba

195 s pathogens contribute to the development of autoimmune disorders, but the mechanisms connecting thes

196 d in many pathological conditions, including autoimmune disorders, cancer, and cardiovascular and all

197 ia (CSU) are widely held to often have other autoimmune disorders, including autoimmune thyroid disea

198 rgeted for the treatment of Th17 cell-driven autoimmune disorders.

199 However, overproduction is associated with autoimmune disorders.

200 he treatment of multiple sclerosis and other autoimmune disorders.

201 cture in major infectious, inflammatory, and autoimmune disorders.

202 nisms present in several diseases, including autoimmune disorders.

203 necroptosis may underlie human fibrotic and autoimmune disorders.

204 d the role of neuroimaging in the setting of autoimmune encephalitides, comparing the utility of (18)

205 cytokine in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) and, ostensibly, in m

206 resistant to the development of experimental autoimmune encephalomyelitis (EAE) as a result of an inc

207 the development of spontaneous experimental autoimmune encephalomyelitis (EAE) during adolescence an

208 ursor cells (NPCs) in mice with experimental autoimmune encephalomyelitis (EAE) impairs the accumulat

209 151-induced relapsing-remitting experimental autoimmune encephalomyelitis (EAE) mice.

210 el CNS infiltration by B cells, experimental autoimmune encephalomyelitis (EAE) was induced in transg

211 D supplementation protects from experimental autoimmune encephalomyelitis (EAE), a model of MS.

212 UV light suppresses experimental autoimmune encephalomyelitis (EAE), a widely used animal

213 ient mice developed more severe experimental autoimmune encephalomyelitis (EAE), an animal model of h

214 sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), expansion of pathoge

215 mat prevents TH17 cell-mediated experimental autoimmune encephalomyelitis (EAE), it also disrupts thy

216 in pregnant animals undergoing experimental autoimmune encephalomyelitis (EAE), the animal model of

217 We used a murine model of MS, experimental autoimmune encephalomyelitis (EAE), to evaluate the hypo

218 glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis (EAE).

219 ease-modulating activity on the Experimental Autoimmune Encephalomyelitis (EAE).

220 erve neurologic function in the experimental autoimmune encephalomyelitis animal model of multiple sc

221 ing disease severity in a mouse experimental autoimmune encephalomyelitis model, demonstrating the vi

222 -/-) mice display an attenuated experimental autoimmune encephalomyelitis phenotype accompanied by de

223 ven prevent signs of disease in experimental autoimmune encephalomyelitis, as well as maintain normog

224 rhesus monkey brain induced by experimental autoimmune encephalomyelitis, which is the most-studied

225 17 immune responses are seen in experimental autoimmune encephalomyelitis.

226 e exhibited reduced severity of experimental autoimmune encephalomyelitis.

227 sclerosis and its animal model, experimental autoimmune encephalomyelitis.

228 immunotherapeutic reduction in, experimental autoimmune encephalomyelitis.

229 cts in autoimmune diseases like experimental autoimmune encephalomyelitis; however, its role in the p

230 An autoimmune etiology is suspected but not yet proven.

231 least half of patients with CSU may have an autoimmune etiology that can be determined in vitro usin

232 Serum Abs suggesting a potential autoimmune etiology were detected in 39 (34.8%) cases.

233 ority had detectable serum Abs suggesting an autoimmune etiology.

234 adulthood, with a predominant anti-ADAMTS13 autoimmune etiology.

235 We report a "polyclonal" autoimmune event occurring in the airways of prednisone-

236 common with uncharacteristic laboratory and autoimmune findings that often slow or mask the diagnosi

237 tially narrowed, yet the recipients remained autoimmune-free.

238 In 2 patients early transient autoimmune hemolysis settled after treatment and did not

239 Autoimmune hemolytic anemia (AIHA) is an uncommon entity

240 oms of certain autoimmune diseases including autoimmune hepatitis (AIH).

241 ction is highly associated with ESCCs in non-autoimmune human patients.

242 Autoimmune hypophysitis (AH) is a chronic inflammatory d

243 uitary was confirmed in patients affected by autoimmune hypophysitis.

244 These findings support the autoimmune hypothesis.

245 3(+) Tregs is essential for Tregs to control autoimmune inflammation in the central nervous system (C

246 ffective at reversing disease by suppressing autoimmune inflammation in the skin and promoting melano

247 Giant cell arteritis (GCA) causes autoimmune inflammation of the aorta and its large branc

248 ed in a prophylactic or therapeutic fashion, autoimmune inflammation was markedly attenuated in vivo.

249 e CNS during multiple infections, as well as autoimmune inflammation, but the behavior of this cell t

250 erved in patients with new-onset and chronic autoimmune inflammatory arthritis.

251 Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease of the CNS

252 wide range of human diseases, which include autoimmune, inflammatory, and degenerative conditions.

253 1-IFN potentiates diabetogenicity within the autoimmune islet.

254 n ulcer has been considered as an idiopathic autoimmune keratitis.

255 mors and the other associated with prostatic autoimmune lesions, recognized distinct non-overlapping

256 Primary biliary cholangitis (PBC) is an autoimmune liver disease with a strong hereditary compon

257 ed-coil domain of STAT5B that presented with autoimmune lymphoproliferative syndrome-like features.

258 Autoimmune manifestations, such as skin infiltration and

259 ons in normal numbers and exhibited no overt autoimmune manifestations.

260 In this study, we used the experimental autoimmune myocarditis (EAM) model to determine the role

261 ted in P0106-125-induced murine experimental autoimmune neuritis.

262 ht how HuR contributes to Th17 cell-mediated autoimmune neuroinflammation and support the notion that

263 nd tic disorders, a concept termed pediatric autoimmune neuropsychiatric disorders associated with st

264 apeutic strategy to attenuate the underlying autoimmune pathogenesis of ophthalmopathy.

265 this polymorphism on both viral sensing and autoimmune pathogenesis remains poorly understood.

266 arbor dysregulated Th1 responses and develop autoimmune pathology, these disease phenotypes are not d

267 CD4(+) T cells are central mediators of autoimmune pathology; however, defining their key effect

268 Here we summarize the most prominent autoimmune pathways and identify key issues that require

269 actors that promote LIP as a tool to predict autoimmune potential and to inform tumor immunotherapy a

270 The other 5 experienced ongoing autoimmune problems, including thyroiditis (3), hemolysi

271 hat therapies specifically directed at these autoimmune processes could have therapeutic efficacy.

272 ed inflammatory signature indicates that the autoimmune program was active at the time of weaning.

273 The autoimmune regulator (AIRE) protein is the key factor in

274 Autoimmune regulator expression was also demonstrated.

275 flammation occurs in the basal ganglia as an autoimmune response to infections.

276 generally thought to be driven by a systemic autoimmune response, increasing evidence suggests that i

277 disease and the clinical relevance of these autoimmune responses are still being explored.

278 es may be disadvantageous by contributing to autoimmune responses associated with antibiotic-refracto

279 Evidence indicates that maladaptive autoimmune responses in the arterial wall play critical

280 nstrated that Foxp3+ Tregs potently suppress autoimmune responses in vivo through inhibition of the a

281 The immune and autoimmune responses that characterize IgAN indicate a p

282 Autoimmune responses to meiotic germ cell antigens (MGCA

283 ic human gut bacteria that regulate adaptive autoimmune responses, suggesting therapeutic targeting o

284 Skin microbiota can impact allergic and autoimmune responses, wound healing, and anti-microbial

285 relationship in MHC-II-dependent normal and autoimmune responses.

286 ed suppression that leads to amelioration of autoimmune responses.

287 ting, including adaptive optics, outcomes in autoimmune retinopathy (AIR) patients treated with ritux

288 roduction of type I interferons driven by an autoimmune risk variant and triggered by ligand function

289 m by which CCL1 produced by Treg cells at an autoimmune site up-regulates the expression of its own r

290 f bullous pemphigoid (BP), the most frequent autoimmune skin-blistering disease, involves matrix meta

291 (resulting from a malignant, infectious, or autoimmune stimulus without an identifiable underlying g

292 d by regulatory T cells contributed to their autoimmune-suppressive function in this model.

293 regs via a Cre-inducible transgene causes an autoimmune syndrome.

294 mited mechanistic insight into self-reactive autoimmune T cell development and their escape from nega

295 lity of autoimmune tissues and the rarity of autoimmune T cells in the blood hinder their study.

296 We describe a method to enrich and harvest autoimmune T cells in vivo by using a biomaterial scaffo

297 n have other autoimmune disorders, including autoimmune thyroid disease.

298 ate autoimmunity, but the inaccessibility of autoimmune tissues and the rarity of autoimmune T cells

299 Using animal models for autoimmune type 1 diabetes (T1D), we found that CRIg(+)

300 lls and can be used therapeutically to limit autoimmune uveitis in mice.