ライフサイエンスコーパス: autoimmune response

1 hat transform an alloimmune reaction into an autoimmune response.

2 nfection may culminate in an T-cell-mediated autoimmune response.

3 cleic acids as well as for prevention of the autoimmune response.

4 ansportation by MZ-P B cells to stimulate an autoimmune response.

5 n (ATG) might be effective for reducing this autoimmune response.

6 evelopment of a T cell-mediated inflammatory autoimmune response.

7 infection, followed by a bile duct-targeted autoimmune response.

8 now characterized by a more intense humoral autoimmune response.

9 roxyvitamin D(3) may not play a role in this autoimmune response.

10 and the functional roles of IFNgamma in the autoimmune response.

11 ich TREM receptors regulate inflammation and autoimmune response.

12 atin is abnormally exposed, facilitating the autoimmune response.

13 ization process and favor environment for an autoimmune response.

14 odorant binding protein 1a, targeted by the autoimmune response.

15 ial for the perpetuation of the CNS-targeted autoimmune response.

16 alpha5NC1 subunits, which in turn elicits an autoimmune response.

17 in particular, are major contributors to the autoimmune response.

18 generation of memory cells that control the autoimmune response.

19 prior to the generation of a robust adaptive autoimmune response.

20 ion involved in the development of the human autoimmune response.

21 es of HNK could be valuable for blocking the autoimmune response.

22 etermined whether this treatment altered the autoimmune response.

23 ells and their potential role in shaping the autoimmune response.

24 ces CD8(+) T cell tolerance, activation, and autoimmune response.

25 consequence of a dysregulated and persistent autoimmune response.

26 tion how a foreign Ag (gluten) can induce an autoimmune response.

27 networks consistent with an adrenal-targeted autoimmune response.

28 (OPN), a pleiotropic cytokine implicated in autoimmune responses.

29 rocess and present self-peptides to suppress autoimmune responses.

30 t for controlling excessive inflammation and autoimmune responses.

31 ed that the DC-HIL/SD-4 pathway may regulate autoimmune responses.

32 clear whether it serves a functional role in autoimmune responses.

33 from the circulation might serve to trigger autoimmune responses.

34 sion, but they often also are accompanied by autoimmune responses.

35 while also contributing to inflammatory and autoimmune responses.

36 ller cell-mediated killing modulates humoral autoimmune responses.

37 that directly contribute to a modulation of autoimmune responses.

38 otential for activation and recruitment into autoimmune responses.

39 nd might lead to the development of aberrant autoimmune responses.

40 antigenic responses and chronic inflammatory autoimmune responses.

41 B cells are important for the regulation of autoimmune responses.

42 ions in the host limit pathogenic Th1-driven autoimmune responses.

43 D exacerbated only genetically predetermined autoimmune responses.

44 gut integrity and the control of anti-islet autoimmune responses.

45 major sources of IL-17A in antimicrobial and autoimmune responses.

46 play a significant role in inflammatory and autoimmune responses.

47 intenance of immune homeostasis and blocking autoimmune responses.

48 but also to the development of IL-17-driven autoimmune responses.

49 erons (IFNs) are important for antiviral and autoimmune responses.

50 (T(H)1) and T(H)17 cells are associated with autoimmune responses.

51 tribute to viral clearance and regulation of autoimmune responses.

52 t sufficient to protect against Th1-mediated autoimmune responses.

53 here are many parallels between allergic and autoimmune responses.

54 ens, yet prevents deleterious NK cell-driven autoimmune responses.

55 s frequently associated with microbe-related autoimmune responses.

56 T cells that are crucial for the control of autoimmune responses.

57 DCs limit T cell activation and thus prevent autoimmune responses.

58 ant in CD4+ regulatory T cell suppression of autoimmune responses.

59 er protein Band 3, to the development of NZB autoimmune responses.

60 lating tissue homeostasis, inflammation, and autoimmune responses.

61 est an additional means for amplification of autoimmune responses.

62 e controls the overall outcome of immune and autoimmune responses.

63 ade of this pathway may curtail inflammatory/autoimmune responses.

64 ed suppression that leads to amelioration of autoimmune responses.

65 lian cell surface glycoconjugates triggering autoimmune responses.

66 therapeutic target to treat TH17 cell-driven autoimmune responses.

67 pients against both alloimmune and recurring autoimmune responses.

68 des, and other peptides that are relevant in autoimmune responses.

69 iator of T cell functions in both immune and autoimmune responses.

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

71 ses capable of exacerbating self-destructive autoimmune responses.

72 rt of a feedback circuit that limits further autoimmune responses.

73 ost may be crucial to limit inflammatory and autoimmune responses.

74 at microbiota are also capable of regulating autoimmune responses.

75 ce peripheral immune tolerance that prevents autoimmune responses.

76 icularly in suppressing harmful allergic and autoimmune responses.

77 ocal inflamed tissues/organs to suppress the autoimmune response after adoptive transfer, thereby avo

78 Our study indicates that the autoimmune response against aquaporin-4 in neuromyelitis

79 iety of cancer cells, but also can elicit an autoimmune response against B cells.(1).

80 ith APECED, loss of AIRE appears to cause an autoimmune response against enteric defensins and loss o

81 als that in psoriasis HLA-C*06:02 directs an autoimmune response against melanocytes through autoanti

82 e death is sufficient to trigger an adaptive autoimmune response against myelin, suggesting that a si

83 mon neurological disorder, the origin of the autoimmune response against myelin, which is the charact

84 Provocation of an autoimmune response against NaV1.5 induces conductance d

85 lmark of systemic lupus erythematosus is the autoimmune response against self nuclear Ags, including

86 hepatobiliary viral infection followed by an autoimmune response against the bile duct epithelia.

87 ught to test the hypothesis that inducing an autoimmune response against the cardiac sodium channel (

88 nd subsequent effects on the induction of an autoimmune response against the eye, we examined CD4 T c

89 ed immune cells elaborate a specific humoral autoimmune response against the von Willebrand factor A

90 lying the ability for this agent to modulate autoimmune responses against beta-cells are unclear, for

91 gh dose of DNA did not induce any detectable autoimmune responses against DNA.

92 of noxious cellular contents and to restrict autoimmune responses against self antigens.

93 disorder classic Ehlers-Danlos syndrome, and autoimmune responses against the alpha1(V) chain are lin

94 rticular pathology and enhanced T and B cell autoimmune responses against type II collagen.

95 In the absence of both a defined autoimmune response and a target autoantigen(s), the pro

96 subsequent initiation and progression of the autoimmune response and demyelinating disease.

97 OCK2 inhibitor downregulates the Th17-driven autoimmune response and improved clinical symptoms in ps

98 at underlie the continued progression of the autoimmune response and islet destruction is critical.

99 Autoimmune response and microbial translocation were not

100 lost Foxp3 expression during an inflammatory autoimmune response and might be involved in inadequate

101 Multiple sclerosis involves an aberrant autoimmune response and progressive failure of remyelina

102 ion of gut microflora, leading to an altered autoimmune response and T1D incidence in NOD mice.

103 APCs is a major regulatory mechanism curbing autoimmune responses and acts in concert with Fas-mediat

104 rate an important role of Sema7A in limiting autoimmune responses and add to growing evidence of shar

105 y Toso as a unique regulator of inflammatory autoimmune responses and an attractive target for therap

106 (MS) and for exploring the interface between autoimmune responses and CNS tissue that ultimately lead

107 led to the redevelopment of myosin-specific autoimmune responses and inflammation.

108 s plays a key role in controlling immune and autoimmune responses and is characterized by a unique tr

109 suggesting a role for DNA-PKcs in regulating autoimmune responses and maintaining AIRE-dependent tole

110 y which EBV could promote the development of autoimmune responses and might enable the identification

111 ransferred MDSCs to downregulate Ag-specific autoimmune responses and prevent diabetes onset, suggest

112 CD4(+) T cells with the hope of attenuating autoimmune responses and restoring self-tolerance.

113 ransplants revealed a complete abrogation of autoimmune responses and severe downregulation of alloim

114 toreactive T cells primed during the primary autoimmune response, and demonstrate that local antigen

115 negative selection, the ability to prime an autoimmune response, and the elimination of the relevant

116 f different cell types involved in the lupus autoimmune response, and to examine the therapeutic effe

117 itory molecule involved in immune tolerance, autoimmune responses, and antiviral immune evasion.

118 participate in the priming of the allo- and autoimmune responses, and their depletion can thus be ad

119 Propagation of autoimmune responses appears to reflect a bidirectional

120 reasons for the central role of I-Ag7 in the autoimmune response are analyzed.

121 perpetuate or even induce an organ specific autoimmune response are not yet fully understood.

122 might achieve this incorporate the idea that autoimmune responses are initially immune responses agai

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

124 these peripheral Tregs (pTregs) in averting autoimmune responses, as well as immunological mechanism

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

126 tification of Ags responsible for initiating autoimmune responses based solely on serological analysi

127 Vasectomized B6AF1 mice did not mount autoimmune response but instead developed sperm antigen-

128 a preceding infection is the trigger of the autoimmune response, but the mechanism connecting the in

129 t significantly affect anti-islet Th1 or Th2 autoimmune responses, but markedly increased inflammator

130 t commensal flora can dramatically influence autoimmune responses, but the mechanisms behind this are

131 r results suggest that IAPP triggers a broad autoimmune response by CD4 T cells in NOD mice.

132 roposed to inhibit HIV-1 replication and the autoimmune response by hydrolyzing cellular dNTPs.

133 te experimental autoimmune encephalomyelitis autoimmune response by inhibiting immune cell infiltrati

134 iNKTs suppressed the autoimmune response by reducing the germinal center (GC)

135 cells can independently support Ag-specific autoimmune responses by CD4 T cells in EAE is lacking.

136 is a pleiotropic cytokine that can regulate autoimmune responses by enhancing regulatory CD4(+)FoxP3

137 hematosus (SLE) and is postulated to enhance autoimmune responses by increasing access to intracellul

138 icate that the DC-HIL/SD-4 pathway regulates autoimmune responses by mediating the T cell suppressor

139 gs suggest a mechanism by which IL-17 drives autoimmune responses by promoting the formation of spont

140 some autoimmune diseases and participate in autoimmune responses by secreting autoantibodies.

141 ed that IDO2 expression by B cells modulates autoimmune responses by supporting the cross talk betwee

142 histocompatibility complexes (pMHC) blunted autoimmune responses by triggering the differentiation a

143 This concept implies that the autoimmune response can be theoretically stopped and per

144 These injections also lead to an anti-AChR autoimmune response characterized by a significant produ

145 This autoimmune response could be related to infection of gen

146 ticular, imaging of CD4+ T cells involved in autoimmune responses could be helpful in diagnosing myoc

147 However, the etiology and progression of autoimmune responses directed against these antigens are

148 spensible to sustain tolerance that prevents autoimmune responses directed at self-Ags during experim

149 ferentiation and a negative regulator of the autoimmune response during lupus.

150 lls, but not alpha cells, are targeted by an autoimmune response during T1D.

151 indicate that pDCs are important in quieting autoimmune responses during EAE, and that trafficking in

152 isease remain unanswered, the development of autoimmune responses during infection clearly occurs in

153 40/Ox40L pathway drives cellular and humoral autoimmune responses during lupus nephritis in NZB/W F1

154 ail, self-reactive T cells are activated and autoimmune responses ensue.

155 verting the effect of AR agonist on the Th17 autoimmune response from anti-inflammatory to proinflamm

156 olism (MYH, TRHDE, ALDH1A3), and nervous and autoimmune response (GRIA1, IL2, IL7, IL21, IL1R1) were

157 , SFB can promote IL-17-dependent immune and autoimmune responses, gut-associated as well as systemic

158 ay a critical role in the development of the autoimmune response, has not been extensively studied in

159 esides determining the target specificity of autoimmune responses, HLA molecules may influence diseas

160 tigens associated with the development of an autoimmune response in breast cancer has relevance to de

161 urpose of this study was to characterize the autoimmune response in CUS.

162 ated the statins' mechanisms that target the autoimmune response in humans, and evaluated their thera

163 This component of the autoimmune response in MG is of particular importance wh

164 However, the antigenic targets of the autoimmune response in MS have not yet been deciphered.

165 nt mechanism of selective suppression of the autoimmune response in MS.

166 olecular mechanisms of the initiation of the autoimmune response in MS.

167 m of IFN-beta1a that selectively targets the autoimmune response in multiple sclerosis.

168 insulin (Ins), which is a key target of the autoimmune response in NOD mice and patients alike.

169 to regulate alloimmunity and to abrogate the autoimmune response in NOD mice in different settings co

170 anism for generating antigens that drive the autoimmune response in RA.

171 nuclear autoantigens to sustain the specific autoimmune response in systemic lupus erythematosus.

172 ase onset may lead to the progression of the autoimmune response in T1D.

173 1 as a new cytokine that plays a role in the autoimmune response in the early phase of the disease.

174 During the initial autoimmune response in type 1 diabetes, islets are expos

175 Cs is able to modulate the development of an autoimmune response in vivo.

176 ak self-tolerance and promote a CD8-mediated autoimmune response in vivo.

177 immune responses and organize T- and B-cell autoimmune responses in advanced atherosclerosis.

178 f crosstalk between alloimmune responses and autoimmune responses in AILD is an important area that n

179 an completely suppress antigenically complex autoimmune responses in an Ag-nonspecific manner.

180 ve secondary effects on specific adaptive or autoimmune responses in AS.

181 Type I IFN can promote autoimmune responses in BXD2 mice through up-regulation

182 dy, we compared their effect on Th17 and Th1 autoimmune responses in experimental autoimmune uveitis,

183 he initial antigenic stimulants for the IgG4 autoimmune responses in FS.

184 plore biochemical alterations arising due to autoimmune responses in glioma.

185 eveals a potential mechanism for destructive autoimmune responses in humans.

186 rotect pancreatic islets from alloimmune and autoimmune responses in mice.

187 SIgA-DCs are highly potent in inhibiting autoimmune responses in mouse models of type 1 diabetes

188 rotecting these cells against alloimmune and autoimmune responses in mouse models.

189 -secreting T cells play an important role in autoimmune responses in multiple sclerosis and the model

190 d examined their activities to stimulate the autoimmune responses in NOD mice, a model for human type

191 t insulinoma-released EXOs can stimulate the autoimmune responses in nonobese diabetic (NOD) mice, a

192 standing of the role of leptin in modulating autoimmune responses in SLE can open possibilities of le

193 ht the critical role of Stat4 Th1 signals in autoimmune responses in suppressing Foxp3(+) Treg respon

194 perones may play a role in the initiation of autoimmune responses in T1D.

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

196 tem also has a key involvement in regulating autoimmune responses in the central nervous system.

197 effects of such a blockade on development of autoimmune responses in the CNS should be considered.

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

199 e to blunt polyclonal, multiantigen-specific autoimmune responses in vivo without impairing systemic

200 onses can still be decoupled from pathologic autoimmune responses in vivo, which may provide novel in

201 T helper type 17 (T(H)17) and T(H)1-mediated autoimmune responses in vivo.

202 ines and augmented T(H)17 and T(H)1-mediated autoimmune responses in vivo.

203 expansion and function during anti-viral and autoimmune responses in vivo.

204 Such autoimmune responses include direct damage on tissue-con

205 isease focus mainly on downstream targets of autoimmune responses, including effector cells and cytok

206 -17-producing helper T (T(H)17) cells during autoimmune responses, including experimental autoimmune

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

208 These results are direct evidence for an autoimmune response initiated by CS exposure.

209 hey may be useful for assessment of cellular autoimmune responses involved in type 1 diabetes.

210 Development of an immune or autoimmune response involves T-cell activation in lympho

211 The genesis of the ANCA autoimmune response is a multifactorial process that inc

212 n 2 unrelated TTP patients suggests that the autoimmune response is antigen driven, because the proba

213 How the autoimmune response is initiated, identity of provoking

214 Autoimmune response is polyspecific and can be controlle

215 The progression of autoimmune responses is associated with an avidity matur

216 y demonstrated that TSHR, the target of this autoimmune response, is also a key susceptibility gene f

217 Given the proinflammatory nature of autoimmune responses, it is not surprising that studies

218 er, is subverted during infection, injury or autoimmune response leading to increased population of M

219 hat absence of pDCs during the priming of an autoimmune response leads to increased mobilization of M

220 Initiation of autoimmune responses likely reflects the presentation of

221 A localized autoimmune response may, however, be involved in the pat

222 anisms that trigger vitiligo remain elusive, autoimmune responses mediate its progression.

223 tions of the major players in the pathogenic autoimmune response, namely, T cells, B cells, dendritic

224 C3aR on APC and T cells, a heightened local autoimmune response occurs in which myelin destruction i

225 Importantly, the pattern of organ-specific autoimmune response of Sf.Il2-/-mice resembled IL-2 knoc

226 or oxidative/nitrosative stress to elicit an autoimmune response or to contribute to disease pathogen

227 human protein, which may also contribute to autoimmune responses or enhanced pathology in some scrub

228 First, we defined blood autoimmune response phenotypes by combinatorial, multipa

229 indicate potentially related islet and blood autoimmune response phenotypes that coincide with and pr

230 sues leads to an attenuation of pathological autoimmune responses, possibly as a means to mitigate in

231 e model of SLE-like serology, that during an autoimmune response, RAG was reinduced in antigen-activa

232 stratification, together with enrichment of autoimmune response-related (nucleotide binding site-leu

233 ll populations responsible for dysfunctional autoimmune responses remained unclear.

234 Whether HDL affects the development of an autoimmune response remains elusive.

235 uring the priming phase of an organ-specific autoimmune response remains unclear.

236 C9orf72 regulates immune homeostasis and an autoimmune response reminiscent of systemic lupus erythe

237 d the induction of T-helper 17 cell-mediated autoimmune responses resembling those observed in patien

238 apies that enhance or diminish antitumor and autoimmune responses, respectively.

239 Thus, Treg cells act to restrain autoimmune responses, resulting in an organized and cont

240 in order to identify target antigens of the autoimmune response (see the related article beginning o

241 The induction of undesired autoimmune responses should be considered when using cyt

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

243 itiated by a virus infection, followed by an autoimmune response targeting bile ducts.

244 mportant role for complement in the adaptive autoimmune response than previously recognized, possibly

245 y to microbes and xenobiotics, and regulates autoimmune responses that can affect the central nervous

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

247 changes occurred in the absence of adaptive autoimmune responses, the findings show that brain infec

248 cumulation of NLRs can result in unwarranted autoimmune responses, their cellular concentrations must

249 to HIV-1 restriction and suppression of the autoimmune response through direct cleavage of viral and

250 une privileges by suppressing alloimmune and autoimmune responses through its receptor, CD200R, expre

251 he gut commensal flora in sustaining ongoing autoimmune responses through the local fine tuning of T-

252 istent with the idea that hypertension is an autoimmune response to altered self.

253 The question considered is, "What causes the autoimmune response to begin and what causes it to worse

254 Autoimmune response to cardiac troponin I (TnI) induces

255 , and CD6(-/-) mice presented an exacerbated autoimmune response to collagen.

256 ce of this strategy is the development of an autoimmune response to HLA-presented epitopes encoded do

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

258 mmune system by restraining inflammation and autoimmune response to intracellular Ags released from d

259 n environment or lifestyle alter the humoral autoimmune response to islet antigens should help explai

260 termine the specificity and magnitude of the autoimmune response to islet antigens.

261 provide the first tangible evidence that an autoimmune response to retina is causally involved in pa

262 This intriguing connection between an autoimmune response to self-antigen and an immune respon

263 h progressive neurodegeneration caused by an autoimmune response to self-antigens in a genetically su

264 ort a mechanism by which host cells avert an autoimmune response to self-nucleic acids.

265 a critical role for HLA-DR3 in generating an autoimmune response to SmD and lupus nephritis in the NZ

266 vation in thyroiditis needed to maintain the autoimmune response to the thyroid.

267 n influence the divergent tolerogenic versus autoimmune response to vasectomy.

268 fectious and noninfectious causes, including autoimmune responses to cardiac antigens.

269 Here we examined sex-specific autoimmune responses to cardiac self and their impact on

270 n made in clarifying mechanisms of allo- and autoimmune responses to FVIII and in suppression of thes

271 Autoimmune responses to meiotic germ cell antigens (MGCA

272 enia gravis (EAMG) are caused by Ab-mediated autoimmune responses to muscle nicotinic acetylcholine r

273 antly delays and attenuates inflammatory and autoimmune responses to myelin Ags in the mouse experime

274 noma paradigm, little is known about whether autoimmune responses to normal tissue can induce rejecti

275 Regulatory T cells suppress autoimmune responses to self-antigens.

276 Ag transfer may perpetuate chronic autoimmune responses to specific self-proteins and help

277 ivo lymphotoxin blockade link these systemic autoimmune responses to the formation of gut-associated

278 uggest that posttransplantation induction of autoimmune responses to tissue-specific antigens contrib

279 Autoimmune responses to vimentin occur after solid organ

280 ivity to nT reg cells in controlling ongoing autoimmune responses under homeostatic conditions.

281 condary necrosis of beta-cells can prime the autoimmune response via uptake by and activation of anti

282 ell lineage is important in inflammatory and autoimmune responses, via its ability to produce interle

283 This autoimmune response was also able to induce the rejectio

284 To gain more insight into this autoimmune response we have characterized the binding of

285 ether oligodendrocyte death could cause this autoimmune response, we examined the oligodendrocyte abl

286 Because Treg suppress autoimmune responses, we asked whether B cells control a

287 B cells play a crucial role in induction of autoimmune responses, we defined the role of B cells and

288 underlying mechanisms of HMGB1 regulation of autoimmune response were further explored.

289 The targets of the adaptive autoimmune response were polyspecific and not focussed o

290 These autoimmune responses were independent of the location of

291 in T1D patients may account for the chronic autoimmune response when damage-associated molecular pat

292 mast cells has no discernible effect on the autoimmune response, which involves both innate and adap

293 How to diminish the autoimmune response while not augmenting infectious risk

294 patibility protein (pMHC) interactions limit autoimmune responses while enhancing T cell response to

295 lace to prevent such potentially deleterious autoimmune responses while preserving immunity integral

296 ular metabolism and detection, triggering an autoimmune response with an increase in cerebral IFN-alp

297 matosus (SLE) is characterized by a systemic autoimmune response with profound and diverse T cell cha

298 that preferentially target disease-relevant autoimmune responses within the CD8(+) T-cell compartmen

299 to wild-type mice induce a transient primary autoimmune response without apparent anti-nuclear Ab rea

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