ライフサイエンスコーパス: autoimmunity

1 hether beneficial or harmful (in the case of autoimmunity).

2 expression and alternative splicing (AS) in autoimmunity.

3 ll function in models of viral infection and autoimmunity.

4 OXP3(+) T cells results in lethal multiorgan autoimmunity.

5 of immune dysregulation, such as early-onset autoimmunity.

6 ng TLRs, blocking these pathways rescues the autoimmunity.

7 e-dependent type I IFN response and systemic autoimmunity.

8 diseases, including infections, cancer, and autoimmunity.

9 ogens and tumors, allergic inflammation, and autoimmunity.

10 ynapses and in resulting T cell functions in autoimmunity.

11 ew model for how these proteins can initiate autoimmunity.

12 diated gut-lung crosstalk and dual TCR-based autoimmunity.

13 the carrier state itself is associated with autoimmunity.

14 autoantigen-specific CD4+ T cells to mediate autoimmunity.

15 ression in Treg cells-resulted in severe TH1 autoimmunity.

16 but has also been implicated as a pathway to autoimmunity.

17 ial targets for therapies of T cell-mediated autoimmunity.

18 echanism offers a link between infection and autoimmunity.

19 egatively regulates TFH cell development and autoimmunity.

20 se to self-antigens, subsequently leading to autoimmunity.

21 role of TCR affinity in Treg function during autoimmunity.

22 ith mutations identified as risk factors for autoimmunity.

23 ors on microbiota composition and pancreatic autoimmunity.

24 with expanded CD21(low) B cells and humoral autoimmunity.

25 are key tools in the treatment of cancer and autoimmunity.

26 before seroconversion and the development of autoimmunity.

27 orted to lead to increased susceptibility to autoimmunity.

28 ein ABIN1 as risk factors for GN in systemic autoimmunity.

29 tion, such as infectious disease, cancer, or autoimmunity.

30 y of self-reactive T cells and resistance to autoimmunity.

31 cine design and to develop new therapies for autoimmunity.

32 ammatory pathway that promotes female-biased autoimmunity.

33 -antigens has been suggested to initiate CNS autoimmunity.

34 osed to increased risk of lymphomagenesis or autoimmunity.

35 high- and low-affinity Tregs in controlling autoimmunity.

36 ng drugs initially developed in oncology and autoimmunity.

37 cy, infection susceptibility, and multiorgan autoimmunity.

38 lation or with only targeted protection from autoimmunity.

39 preclinical models of acute inflammation and autoimmunity.

40 t the cost of modestly promoting the risk of autoimmunity.

41 tem (CNS) tissue and protected the mice from autoimmunity.

42 pathogenic conditions such as infection and autoimmunity.

43 ariety of antigenic stimuli while preventing autoimmunity.

44 sition, but rare cases result from monogenic autoimmunity.

45 infections, as well as multiorgan atopy and autoimmunity.

46 thma, eczema, and food allergies, as well as autoimmunity.

47 TLA-4 that was associated with resistance to autoimmunity.

48 involved in host defence, inflammation, and autoimmunity.

49 ially representing an early marker of T-cell autoimmunity.

50 ontributes to antibody-mediated immunity and autoimmunity.

51 sult in immune activation, inflammation, and autoimmunity.

52 nd subsequent occurrence of secondary B-cell autoimmunity.

53 but have not been previously associated with autoimmunity.

54 ribute to the patients' immunodeficiency and autoimmunity.

55 g how to optimize vaccine responses or limit autoimmunity.

56 immune dysregulation that often presents as autoimmunity.

57 risk of developing islet autoimmunity or CD autoimmunity.

58 olution for full understanding of pathogenic autoimmunity.

59 ms that might be related to the induction of autoimmunity.

60 ol overt activation and prevent the onset of autoimmunity.

61 aling in APCs regulates B cell selection and autoimmunity.

62 t plays crucial roles in the pathogenesis of autoimmunity.

63 FB epitope and self-antigen, thus augmenting autoimmunity.

64 tibodies in experimental models of prostatic autoimmunity.

65 fection or cancer, at the cost of heightened autoimmunity.

66 rbations of the gut microbiome to pancreatic autoimmunity.

67 systemic inflammation, tissue fibrosis, and autoimmunity.

68 votal balance between antiviral defences and autoimmunity.

69 ing the Treg cell antigens relevant to human autoimmunity.

70 new applications in infectious diseases and autoimmunity.

71 sis affects the onset and progression of CNS autoimmunity.

72 CR) repertoire are proposed to predispose to autoimmunity.

73 /-) mice, the secondary recipients developed autoimmunity.

74 TLRs in the development of GC responses and autoimmunity.

75 results in pathological conditions, such as autoimmunity.

76 cells are an important therapeutic target in autoimmunity.

77 g pregnancy or in individuals predisposed to autoimmunity.

78 gical T-cell responses in transplantation or autoimmunity.

79 important for cells and damaged DNA triggers autoimmunity.

80 result in uncontrolled immune activation and autoimmunity.

81 interventions of diseases such as cancer and autoimmunity.

82 lls that leads to protection or causation of autoimmunity.

83 uently detected but were not associated with autoimmunity.

84 , and whether they have a pathogenic role in autoimmunity.

85 a focus on their contribution to LIP-driven autoimmunity.

86 kines to peripheral tolerance and control of autoimmunity.

87 e GC responses to prevent the development of autoimmunity.

88 ant role that these cells play in preventing autoimmunity.

89 cell driven and sustained diseases, such as autoimmunity, adult T cell leukemia and HIV-1.

90 Thus, protection from autoimmunity afforded by particular MHC/HLA alleles can

91 and the development of alloimmunity-induced autoimmunity after allogeneic hematopoietic transplantat

92 f many non-infectious human diseases such as autoimmunity, allergy and cancer.

93 l for protection against infectious disease, autoimmunity, allergy, cancer, and atherosclerosis.

94 t deletion of S1P1 in Treg cells resulted in autoimmunity and acute deletion rendered mice more susce

95 ise in "immune-mediated" diseases, including autoimmunity and allergy.

96 nses, and are protected from T cell-mediated autoimmunity and alloimmunity in models of colitis and g

97 thogenesis, discusses the connection between autoimmunity and ALS/FTD, and explores the possibility t

98 lls (PCs) play central roles in immunity and autoimmunity and are enriched among the subpopulation of

99 ew summarizes the investigations implicating autoimmunity and autoantibodies in ASD.

100 agnostic, and predictive signatures in human autoimmunity and autoinflammation.

101 y associated with self-specificities such as autoimmunity and cancer, were linked to network clusters

102 an activity with widespread implications for autoimmunity and cancer.

103 ty, including vaccine responses, infections, autoimmunity and cancer.

104 oint system that is essential for preventing autoimmunity and cancer.

105 re combined immunodeficiency associated with autoimmunity and caused by defects in lymphoid-specific

106 Islet autoimmunity and CD autoimmunity were defined as being p

107 iew explores the association between thyroid autoimmunity and complications during and after pregnanc

108 checkpoint blockade, and conversely to treat autoimmunity and CTLA-4 deficiency.

109 st is probably due to the adverse effects of autoimmunity and curtailment of horizontal gene transfer

110 including the treatment of antibody-mediated autoimmunity and diagnostic imaging.

111 e the best currently available biomarker for autoimmunity and disease risk.

112 co-inhibitory pathway for both prevention of autoimmunity and failure of tumor rejection.

113 heir dysfunction and multiple diseases where autoimmunity and immunodeficiency are major components.

114 vel type I IFN-independent model of systemic autoimmunity and implicate TLR-mediated NF-kappaB proinf

115 Autoimmunity and infection caused by STAT1 GOF mutations

116 Th17-mediated pathology in murine models of autoimmunity and infection.

117 We aimed at determining the incidence of autoimmunity and inflammation in patients with PIDs.

118 sis for a detailed prospective evaluation of autoimmunity and inflammation in the context of PIDs, wi

119 for approaching therapeutic intervention in autoimmunity and inflammatory disease.

120 poptotic cells (AC) is pivotal in preventing autoimmunity and is a potent immunosuppressive stimulus.

121 ven after disease onset ameliorated systemic autoimmunity and kidney histopathology.

122 l for adaptive immunity, but also a risk for autoimmunity and lymphoid malignancies.

123 ave implications in human diseases involving autoimmunity and malignancy.

124 ial to promote protective immunity and limit autoimmunity and neoplasia.

125 esponses to neuroinflammation, brain injury, autoimmunity and neurogenesis.

126 ciency (CID) syndrome that is accompanied by autoimmunity and nonimmunologic symptoms.

127 model that recapitulates several aspects of autoimmunity and organ fibrosis observed in patients wit

128 Autoimmunity and peripheral lymphoid hyperplasia were fo

129 ssect the role of IL-23 in the expression of autoimmunity and related pathology, we generated IL-23 r

130 7) and have critical roles in the control of autoimmunity and resolution of inflammation.

131 as determine susceptibility to infection and autoimmunity and responsiveness to antibody-based therap

132 of the immune response in animals models of autoimmunity and Th17-skewing human cell culture in vitr

133 at initiate and sustain autoinflammation and autoimmunity and that are caused by disturbances in the

134 target antigen selection in testis and sperm autoimmunity and the immune responses to CTA in male can

135 tor Foxp3 are critical for the prevention of autoimmunity and the suppression of anti-tumor immunity.

136 ate cell death to limit T-cell survival (eg, autoimmunity and transplantation) or enhance T-cell surv

137 mployed to regulate immune responses in both autoimmunity and transplantation.

138 Such mechanisms likely impact autoimmunity and tumor formation, respectively.

139 FN-alpha/beta-mediated conditions, including autoimmunity and viral infections, may have an increased

140 cofactors have equal ability to precipitate autoimmunity and we have recently shown that in some cir

141 provide insight into the etiology of anti-PE autoimmunity and, because endosomes are of central impor

142 ular helper cells impact immunodeficiencies, autoimmunity, and cancer.

143 ogens and are also implicated in thrombosis, autoimmunity, and cancer.

144 R4 in a range of diseases, including cancer, autoimmunity, and HIV.

145 erogeneous disorders like chronic infection, autoimmunity, and immunodeficiency.

146 munotherapeutic targets for treating cancer, autoimmunity, and infectious diseases.

147 ncer and immune diseases, including allergy, autoimmunity, and inflammation.

148 tasis, wound healing, inflammation, allergy, autoimmunity, and oncogenesis.

149 in response to sepsis, transplantation, and autoimmunity, and preventing oxidative damage associated

150 s, plasma samples from patients with anti-PE autoimmunity, and purified anti-PE antibodies.

151 cations for tumor immunity, transplantation, autoimmunity, and reproductive success.

152 tant implications for pathogen surveillance, autoimmunity, and transplant rejection.

153 ious disease and immunotherapies for cancer, autoimmunity, and transplantation.

154 nt-induced arthritis but not antigen-induced autoimmunity, and with unique effects on priming of auto

155 d second-line treatments, immunotoxicity and autoimmunity are emerging as the Achilles' heel of immun

156 We show that inflammation and autoimmunity are prevented upon expression of kinase ina

157 This has led to the view of LIP-driven autoimmunity as a two hit model; however, not all cofact

158 Rather than viewing LIP-associated autoimmunity as an n-hit model, we suggest a more quanti

159 cols that exploit Tregs for the treatment of autoimmunity as well as diseases in which disturbed tole

160 HA in patients who did not have a history of autoimmunity; asplenic patients appeared to be particula

161 ucing both immunity and tolerance, increased autoimmunity associated with decreased DCs suggests thei

162 sion in all T cells causes fatal multi-organ autoimmunity associated with hyperactive conventional T

163 s of rotavirus-infected mice, similar to the autoimmunity associated with T1D.

164 y relevant with respect to human allergy and autoimmunity because a possible modulation of B cell dif

165 ndrome of BACH2-related immunodeficiency and autoimmunity (BRIDA) that results from BACH2 haploinsuff

166 s that selectively target TH17 cell-mediated autoimmunity but do not affect thymocyte development or

167 ide complexes are known triggers of systemic autoimmunity, but a role in organ-specific autoimmune di

168 Dysfunctional T cells can mediate autoimmunity, but the inaccessibility of autoimmune tiss

169 usceptibility to systemic and organ-specific autoimmunity, but the mechanism by which T-bet expressio

170 at C1 could help protect against antinuclear autoimmunity by broadly degrading nucleolar proteins or

171 However, infections may play a role in autoimmunity by changing the homeostatic balance of proi

172 High salt may additionally drive autoimmunity by inducing T helper 17 (TH17) cells, which

173 sis by which dual TCR expression can promote autoimmunity by limiting agonist selection of self-react

174 ceptor (A2aR) signaling acts as a barrier to autoimmunity by promoting anergy, inducing regulatory T

175 se results suggest that TRAILPEG ameliorates autoimmunity by targeting the Th 17-Tregs axis, making i

176 comes were the development of celiac disease autoimmunity (CDA) or celiac disease.

177 Post-HSCT hematological autoimmunity (cytopenias) was reported in 4 patients, ac

178 he victim of destructive inflammation during autoimmunity, degeneration, or injury has been rapidly c

179 ance of T-B cellular cross-talk in mediating autoimmunity, demonstrating that its interruption impact

180 II mice did not display signs of spontaneous autoimmunity despite the fact that their OVA-specific CD

181 partmentalized within the nucleus to prevent autoimmunity; despite this, cyclic GMP-AMP synthase (cGA

182 We observed accelerated autoimmunity development even under conditions where Sle

183 sion of Treg signature genes, causing severe autoimmunity due to Treg cell deficiency.

184 ly defined mechanism confers protection from autoimmunity during pregnancy and represents a potential

185 ons in ORAI1 in unrelated kindreds with CID, autoimmunity, ectodermal dysplasia with anhidrosis, and

186 Is) were proposed as a therapeutic option in autoimmunity ensuing from defects of TREX1.

187 tment, double-deficient mice did not develop autoimmunity even when aged to more than 1 y, suggesting

188 , was not associated with the development of autoimmunity for T1D or CD.

189 n or activity, manifest in immunodeficiency, autoimmunity, genomic instability, and lymphoid and othe

190 Those with both infections and autoimmunity had low %DHR(+) values (n = 6; range, 3% to

191 eous parents and with additional early-onset autoimmunity had recessive LRBA mutations.

192 nity than they do in progression to T1D once autoimmunity has appeared.

193 Autoimmunity has been implicated in the pathogenesis of

194 Such autoimmunity has been shown to be highly toxic in severa

195 (causal relationship suggested), and type II autoimmunity has level 2 causality (causal relationship

196 ugh numerous genetic factors contributing to autoimmunity have been identified in recent years, our k

197 Efforts to understand autoimmunity have been pursued relentlessly for several

198 ences in immune responses, especially during autoimmunity, have been studied predominantly within the

199 aling in xenobiotic systemic mercury-induced autoimmunity (HgIA).

200 (IL)-10 production by IL-10(+ve) B cells to autoimmunity, highlighting the importance of improving t

201 plasticity contributes to both immunity and autoimmunity; however, the factors that control lineage

202 yvitamin D [25(OH)D] concentration and islet autoimmunity (IA) and whether vitamin D gene polymorphis

203 Type I and II autoimmunity (ie, IgE to autoallergens and IgG autoantib

204 However, this involves the risk of autoimmunity if immune memory against host DNA is mistak

205 Autoimmunity in cfs1 is dependent on ENHANCED DISEASE SU

206 inal virome from birth to the development of autoimmunity in children at risk for type 1 diabetes (T1

207 the literature on the prevalence of thyroid autoimmunity in CSU and vice versa.

208 dence in support of a role for type I and II autoimmunity in CSU with the help of Hill's criteria of

209 tical effectors mediating the ocular surface autoimmunity in dry eye disease (DED).

210 ibiotic use and islet or celiac disease (CD) autoimmunity in genetically at-risk children prospective

211 and gut dysbiosis on the development of CNS autoimmunity in humanized transgenic mice expressing the

212 -beta) is essential for GN, but not systemic autoimmunity in LysM(Cre)Bim(fl/fl) mice.

213 that loss of CD28 signaling in Tregs caused autoimmunity in mice (termed CD28-DeltaTreg mice), chara

214 contexts of both acute infection and chronic autoimmunity in mice.

215 rate that Prdm1 functions in TECs to prevent autoimmunity in mice.

216 ous presentation of PLP178-191 attenuate CNS autoimmunity in models of EAE, implicating the potential

217 e mechanisms by which this cytokine promotes autoimmunity in murine lupus.

218 A hallmark of autoimmunity in murine models of lupus is the formation

219 signed levels of causality for type I and II autoimmunity in patients with CSU from level 1 (causal r

220 idence in support of Hill's criteria, type I autoimmunity in patients with CSU has level 3 causality

221 omain-containing 7A (THSD7A) is a target for autoimmunity in patients with membranous nephropathy (MN

222 gulatory T cells and probably contributes to autoimmunity in patients with this disease.

223 leads to devastating lymphoproliferation and autoimmunity in scurfy mutant mice and immunodysregulati

224 ition that the alarming surge in allergy and autoimmunity in the industrialised and developing worlds

225 s, changes in the intestinal virome preceded autoimmunity in this cohort.

226 e a critical source of the IFN-alpha driving autoimmunity in this lupus model.

227 ia Foxp3-independent mechanisms and prevents autoimmunity in this model by repressing the cross talk

228 ent-derived cDNA as key triggers of systemic autoimmunity in Trex1-deficient humans and mice and moti

229 t and distinct cellular contributions during autoimmunity in vitiligo, and we found that the epidermi

230 e and experimentally induced mouse models of autoimmunity, increased serum levels of IgM anti-histone

231 issue inflammation, and an ultimately severe autoimmunity, indicating the importance of diversity and

232 immunologic signaling networks; and impacts autoimmunity, infection, and inflammation.

233 Diagnosing monogenic autoimmunity is crucial for patients' prognosis and clin

234 Autoimmunity is largely prevented by medullary thymic ep

235 etback in improving current therapeutics for autoimmunity is the lack of antigen specificity.

236 Autoimmunity is thought to be one of the most frequent c

237 role in the pathogenesis of inflammation and autoimmunity is unclear.

238 The ability of LAP to attenuate autoimmunity likely occurs through the dampening of pro-

239 perience immune dysregulation manifesting as autoimmunity, lymphoproliferation, and organ inflammatio

240 enic mechanisms in CSU patients with thyroid autoimmunity may include IgE against autoantigens, immun

241 hat early factors contributing to peripheral autoimmunity may promote CNS lupus symptoms.

242 in various neurological pathologies, such as autoimmunity, mechanical injury, neurodegeneration, and

243 have been implicated in the pathogenesis of autoimmunity, most notably systemic lupus erythematosus

244 t a risk of islet or tissue transglutaminase autoimmunity need not influence the recommendations for

245 sociated immune dysregulation manifesting as autoimmunity or allergic inflammation.

246 months, particularly if they have additional autoimmunity or are born to consanguineous parents.

247 d not influence the risk of developing islet autoimmunity or CD autoimmunity.

248 d formula reduced the risk of celiac disease autoimmunity or celiac disease.

249 /injectable disease, and without symptomatic autoimmunity or clinically significant immunosuppression

250 intaining immune memory, they also can cause autoimmunity or neoplasia if misdirected or dysregulated

251 c and nonlymphocytic cells during infection, autoimmunity or neoplasms.

252 ial strain typing, immunization of cultures, autoimmunity or self-targeted cell killing, and the engi

253 es typically manifest with immunodeficiency, autoimmunity, or autoinflammation.

254 tential immune-modifying effects of obesity, autoimmunity, or diabetogenic agents like streptozotocin

255 iency results in gut microbial dysbiosis and autoimmunity over the lifespan of scurfy (SF) mouse.

256 e sought to identify novel genetic causes of autoimmunity presenting with neonatal diabetes (NDM) (di

257 t least 182 days, blocked the development of autoimmunity, prevented lymphocyte infiltration into reg

258 Thyroid autoimmunity refers to the presence of antibodies to thy

259 ough TCR avidity enhancement, it produced no autoimmunity, reflecting sequestration of GUCY2C to inte

260 immunoregulation but their effect on mucosal autoimmunity remains largely unknown.

261 g autoreactive Th17 cells and organ-specific autoimmunity remains largely unknown.

262 etabolic determinant leading to an increased autoimmunity risk in GSD-1b patients.

263 more than 100 kilobases) surrounding two key autoimmunity risk loci, CD69 and IL2RA.

264 eeks to determine whether factors related to autoimmunity risk remain significant after the initiatio

265 including an IL2RA enhancer that harbours an autoimmunity risk variant.

266 apeutic potential of ruxolitinib in treating autoimmunity secondary to STAT1 GOF mutations.

267 modulators and effectors during allergy and autoimmunity should be considered when designing new the

268 B cells and DCs, in a TLR7-mediated model of autoimmunity, similar to systemic lupus erythematosus, w

269 seph's Hospital in Denver, from the Diabetes Autoimmunity Study in the Young.

270 the molecular phenotypes of CA-MPK3 and mpk4 autoimmunity suggested convergence between the MPK3- and

271 U is more prevalent in patients with thyroid autoimmunity than in controls (weak evidence).

272 y play a different role in the initiation of autoimmunity than they do in progression to T1D once aut

273 ed with a high incidence of secondary B-cell autoimmunities that limit use.

274 tes, such as the gut microbiota, may promote autoimmunity that affects joints.

275 true for B cells using a mouse model of CNS autoimmunity that incorporates both T and B cell recogni

276 adenopathy and CD4(+) T cell activation, and autoimmunity that mainly targeted skin and lung tissues.

277 humans, which range from immunodeficiency to autoimmunity, that are caused by mutations in ZAP-70.

278 east 2 distinct pathways, type I and type II autoimmunity, that contribute to the pathogenesis of thi

279 In its presence, ACQOS causes detrimental autoimmunity, thereby reducing osmotolerance.

280 If associated with infections or autoimmunity, they represent profound combined immunodef

281 trate that Th17 cells mediate ocular surface autoimmunity through both IL-17A and IFN-gamma.

282 regions suggests they contribute to risk of autoimmunity through effects on gene expression in the i

283 nding of the origin of diseases ranging from autoimmunity to cancer.

284 with a coexisting disease or trigger such as autoimmunity, transplantation, cancer, infection, certai

285 Autoimmunity triggered by interaction of this NLR pair t

286 toimmune diabetes associated with additional autoimmunity usually reflects a polygenic predisposition

287 ation genetic signatures indicated that this autoimmunity variant has been evolutionarily advantageou

288 connective tissue disorder characterized by autoimmunity, vasculopathy, and extensive cutaneous and

289 Autoimmunity was not associated with %DHR(+) values.

290 mechanism could be an endogenous trigger for autoimmunity, we examined the impact of granzyme A defic

291 pact of Mer deficiency on the development of autoimmunity, we generated autoimmune-prone B6.Sle1b mic

292 transcripts associated with inflammation and autoimmunity were analyzed.

293 Islet autoimmunity and CD autoimmunity were defined as being positive for islet or

294 L-2Rbeta recipients showed fewer symptoms of autoimmunity when they received donor Tregs that were pr

295 estinal microbiota; moreover, they developed autoimmunity when treated with certain antibiotics or ra

296 cell regulation recovers may limit secondary autoimmunity, which does not occur with other B-cell-dep

297 that are responsible for the development of autoimmunity will be critical for developing efficient t

298 n 1 (STAT1) manifest in immunodeficiency and autoimmunity with impaired TH17 cell differentiation and

299 plaining efficacy and the risk for secondary autoimmunity with treatment of MS.

300 pping phenotypes of immune dysregulation and autoimmunity, with dramatically increased frequencies of