ライフサイエンスコーパス: pathogenic T cell

1 AIL ligand (capable of inhibiting activated, pathogenic T cells).

2 most immune system cells including APCs and pathogenic T cells.

3 juvant (CFA) or passively by the transfer of pathogenic T cells.

4 cell activity, suggesting direct effects on pathogenic T cells.

5 role in the differentiation of autoreactive pathogenic T cells.

6 where they subsequently recruit and tolerize pathogenic T cells.

7 but not that induced by adoptive transfer of pathogenic T cells.

8 his repertoire encompasses the precursors of pathogenic T cells.

9 ng studies alone, could activate such highly pathogenic T cells.

10 -CD40L blocked disease expression induced by pathogenic T cells.

11 stion of tissue specificity determination by pathogenic T cells.

12 lation necessary for the activation of these pathogenic T cells.

13 gmenting the presentation of autoantigens to pathogenic T cells.

14 lly supporting the expansion of autoreactive pathogenic T cells.

15 tion, SMC proliferation, and infiltration of pathogenic T cells.

16 nto the CNS together with the first invading pathogenic T cells.

17 insulin epitope results in escape of highly pathogenic T cells.

18 ential for ameliorating diseases mediated by pathogenic T cells.

19 he gut with both colitogenic pathobionts and pathogenic T cells.

20 the mechanisms underlying the development of pathogenic T cells.

21 ch favors differentiation of regulatory over pathogenic T cells.

22 rograms and effector functions of these rare pathogenic T cells.

23 the development of IFN-gamma(+) and IL-17(+) pathogenic T cells.

24 ability and restrained iTreg conversion into pathogenic T cells.

25 ates arthritis despite increasing numbers of pathogenic T cells.

26 development and activation of self-reactive pathogenic T cells(1,2).

27 The origin, phenotype, and function of pathogenic T cells across the spectrum of severity requi

28 nctional in RA and that favor continuous and pathogenic T-cell activation.

29 in LECs could lead to lymphatic disease and pathogenic T-cell activation.

30 e initiation of the intestinal damage by the pathogenic T cells altered ambient oxygen levels in the

31 In an attempt to identify the pathogenic T cells among the many expanded T cell clones

32 altered peptide ligand selectively silences pathogenic T cells and actively signals for the efflux o

33 d arthritis by eliminating or downregulating pathogenic T cells and consequently blocking the develop

34 ytic disease and reduced the accumulation of pathogenic T cells and expression of IL-6 in the CNS.

35 l apoptotic clearance pathways to inactivate pathogenic T cells and halt the disease process in autoi

36 A link between IL-23-driven pathogenic T cells and IL-7/IL-7R signaling has previous

37 which IL-1 is involved in the generation of pathogenic T cells and in disease development remains la

38 ows that inhibiting calcineurin can generate pathogenic T cells and indicates that T cell-mediated vi

39 nsferase G9A was required for development of pathogenic T cells and intestinal inflammation.

40 diverse antigen receptor repertoire suppress pathogenic T cells and maintain immune homeostasis durin

41 unopathology by prohibiting the expansion of pathogenic T cells and other pro-inflammatory lymphocyte

42 1+ T reg depletion, with emergence of potent pathogenic T cells and severe AOD.

43 sB(9-23) by both limiting the development of pathogenic T cells and supporting the selection of Tregs

44 g in a failure to suppress the generation of pathogenic T cells and the development of colitis.

45 the Tr cells to inhibit the proliferation of pathogenic T cells and the development of diabetes.

46 ion in IL-23R-deficient mice could not drive pathogenic T cells and the development of EAE.

47 munoglobulin mucin-3 (Tim-3) is expressed on pathogenic T cells, and its ligand galectin-9 (gal-9) is

48 To understand how these pathogenic T cells are generated and the role of dendrit

49 Previous work has indicated that pathogenic T cells arise from deleterious interactions b

50 ot protected from insulitis and still harbor pathogenic T-cells, as demonstrated by transfer studies.

51 DO controls the accumulation of Th1 and Th17 pathogenic T cells at the site of inflammation during co

52 The ability to target a consistent set of pathogenic T cells between individuals and across class

53 ated by a role of both motifs for priming of pathogenic T cells by DCs.

54 rapy that inhibits and reduces the number of pathogenic T cells by targeting the OX40 receptor expres

55 ells were titrated in the presence of CD4(+) pathogenic T cells (CD4(+Path) T cells) in reconstitutio

56 ic mice expressing a receptor derived from a pathogenic T cell clone do develop spontaneous disease.

57 function contributed to the activation of a pathogenic T-cell clone, BDC2.5.

58 TNF-alpha produced in the pancreas by pathogenic T cell clones and recruited macrophages was n

59 ective set of immunodominant Treg as well as pathogenic T cell clones can be targeted for potential i

60 We examined the frequency of the candidate pathogenic T cell clones in the peripheral blood and CSF

61 Sequence analysis of the pathogenic T cell clones reveals a marked heterogeneity

62 All of the 70 most frequent putative pathogenic T cell clones were alphabeta T cells.

63 Our goal was to track individual candidate pathogenic T cell clones, selected on the basis of previ

64 Here we determined whether pathogenic T-cell clones could be derived by serial adop

65 may allow a pathway to selective ablation of pathogenic T-cell clones ex vivo or in vivo without dist

66 -23))-induced proliferative responses of NOD pathogenic T-cell clones.

67 inflamed atheroma and in arteritic lesions, pathogenic T cells coordinate multiple injury pathways.

68 To discover if pathogenic T cells could be selectively deleted, we inve

69 ent Tregs failed to control the expansion of pathogenic T cells derived from scurfy mice, failed to m

70 Given the importance of CD40 for pathogenic T cell development, BDC2.5.CD40(-/-) mice wer

71 independently of Foxp3(+) Tregs to suppress pathogenic T cell development.

72 regulators of gene expression, contribute to pathogenic T-cell differentiation in multiple sclerosis.

73 settings that include expansion of activated pathogenic T cells, differentiation of Th1/Th2 cells, an

74 upus erythematosus: 1) Antigen-specific and "pathogenic" T cells display a limited T cell receptor re

75 An advantage of this model is that the pathogenic T cells driving disease (donor strain) can be

76 The pathogenic T cells driving disease in this murine model

77 es and are considered the main population of pathogenic T cells driving experimental autoimmune encep

78 Definitive identification of pathogenic T cell epitopes as is now known in celiac dis

79 Our data suggest that cardiac myosin and its pathogenic T cell epitopes may link innate and adaptive

80 , experimental autoimmune encephalomyelitis, pathogenic T cells exhibit a Th1-like phenotype characte

81 reduction in inflammation due to blockade of pathogenic T cell expansion.

82 in islets and expand cognitively interactive pathogenic T cells from a pool of naive precursors.

83 Pathogenic T cells from donors after BM failure appeared

84 roteomics with mechanistic studies to assess pathogenic T cell functions and inducing signals.

85 responses, the precise Ags recognized by the pathogenic T cells have often been difficult to identify

86 licular helper (Tfh), regulatory (Treg), and pathogenic T cells (IL17A+ and IFNG+), alongside extensi

87 we examined the role of TRAIL expression on pathogenic T cells in an induced model of murine lupus,

88 CD8(+) T cells act specifically to suppress pathogenic T cells in autoimmune and infectious diseases

89 Therapeutically targeting pathogenic T cells in autoimmune diseases has been chall

90 can potentially be used as tools to suppress pathogenic T cells in autoimmune diseases such as type 1

91 To elucidate the role of pathogenic T cells in autoimmunity further, we have dire

92 can shift the balance between Treg cells and pathogenic T cells in chronic GVHD recipients and amelio

93 t decrease in tumour growth without inducing pathogenic T cells in colonic tissue, indicating that al

94 omeostasis in the steady-state but activates pathogenic T cells in conditions of inflammation.

95 TCR transgenic (tg) models, the emergence of pathogenic T cells in diabetes-prone NOD mice has been a

96 gesting that IGRP also may be an antigen for pathogenic T cells in human type 1 diabetes and, thus, a

97 odeficient mice demonstrated the presence of pathogenic T cells in I-E+ donors, and that continuous e

98 Pathogenic T cells in individuals with rheumatoid arthri

99 produced by malignant T cells in CTCL and by pathogenic T cells in ISD, respectively, are likely both

100 ing function that has also been proposed for pathogenic T cells in ISD.

101 eans of developing therapies that target the pathogenic T cells in multiple sclerosis (MS) without co

102 However, the phenotype of pathogenic T cells in peripheral blood remains to be def

103 ells likely represent the disease-initiating pathogenic T cells in psoriasis, suggesting that lasting

104 The epitopes recognized by pathogenic T cells in systemic autoimmune disease remain

105 ovide a systemic, antigen-specific signal to pathogenic T cells in the absence of costimulation and,

106 The entry and survival of pathogenic T cells in the CNS are crucial for the initia

107 prone mice contribute to the reactivation of pathogenic T cells in the eye, leading to intraocular in

108 and Blimp-1, allowing active suppression of pathogenic T cells in the inflamed central nervous syste

109 en-presenting cells (APCs) for activation of pathogenic T cells in the multiple sclerosis model exper

110 ndent differences in the effects of Tregs on pathogenic T cells in the pancreas.

111 To test whether the development of pathogenic T cells in the two colitis models was directl

112 ts the harmful accumulation of self-reactive pathogenic T cells in vital organs.

113 d consequent hyperproliferation of psoriatic pathogenic T cells in vivo.

114 The presence of pathogenic T-cells in the absence of disease indicates p

115 el modalities in suppressing the activity of pathogenic T cells including cardiac myosin-specific T c

116 bility of myeloid cells to directly react to pathogenic T cell infiltration by engulfing living T cel

117 o reduce rosacea inflammation by restricting pathogenic T-cell infiltration.

118 These pathogenic T cells initiated a cytokine storm characteri

119 e of CNS CD11c(+) cells in the attraction of pathogenic T cells into and their survival within the CN

120 Infiltration of these pathogenic T cells into the CNS has been correlated with

121 P-10 was not required for the trafficking of pathogenic T cells into the CNS in EAE but played an une

122 n resistance is associated with an influx of pathogenic T cells into visceral adipose tissue (VAT), b

123 Moreover, the repertoire of the pathogenic T cells is highly conserved with respect to V

124 onic experimental colitis the development of pathogenic T cells is influenced predominantly, though n

125 in patients with established disease harbors pathogenic T cells is less investigated.

126 ession were studied in cultured splenocytes, pathogenic T cells isolated from C3H/HeJBir mice, and HT

127 to sites of inflammation and target diverse pathogenic T cells, likely without prior conditioning by

128 Surprisingly, young Tregs that modulated pathogenic T cells maintained stable frequency over time

129 To contain autoimmunity, pathogenic T cells must be eliminated or diverted from r

130 itic cell transfer, we show that neither the pathogenic T cells nor CNS-resident cells are required t

131 in resolved psoriatic lesions represent the pathogenic T cells of origin in this disease.

132 hat IFN-gamma is not required for priming of pathogenic T cells or for effecting the retinal damage a

133 e diseases is a link between osteopontin and pathogenic T cells, particularly T helper 17 cells, wher

134 of dysfunctional Tregs and the resistance of pathogenic T cells, particularly Th17 cells, to Treg sup

135 nd the corresponding microorganism-specific, pathogenic T cell phenotypes remain largely unknown.

136 tes regulatory APC properties and suppresses pathogenic T cell polarization, thereby reducing the cli

137 e IL-12 cytokine family that drives a highly pathogenic T cell population involved in the initiation

138 cell responses; however, the identity of the pathogenic T cell populations responsible for dysfunctio

139 tial for the generation and proliferation of pathogenic T cell populations upon immunization with mye

140 The present studies show that pathogenic T cells produce type 1 cytokines (IL-2; IFN-g

141 We have shown that IL-23-dependent, pathogenic T cells produced IL-17 A, IL-17 F, IL-6, and

142 of the central nervous system (CNS) to sense pathogenic T cell-produced IFN-gamma during EAE initiati

143 demonstrate disease remission, inhibition of pathogenic T cell proliferation, decreased cytokine prod

144 This was related to the inhibition of pathogenic T-cell proliferation and to reduced pro-infla

145 Pathogenic T cells recognize two minor epitopes that are

146 the breakdown of self tolerance, potentially pathogenic T cells recognizing dominant myosin epitopes

147 diabetes effectively in young NOD mice whose pathogenic T cells remain peripheral to the islets.

148 ecognition of beta-cell-specific epitopes by pathogenic T-cells remains ill defined; we seek to furth

149 Moreover, pathogenic T cells require the continuous presence of co

150 system, however, the optimal protective, non-pathogenic T cell response against Mtb is still elusive.

151 eripheral immune organs and their control of pathogenic T cell response and CNS pathology.

152 We conclude that neonatal NK cells promote pathogenic T cell response at multiple stages during neo

153 the precise molecular mechanisms driving the pathogenic T cell response in ARLA remain unclear.

154 igens and foreign antigens recognized by the pathogenic T cell response in NT1 is ongoing.

155 HLA-DQ8-associated celiac disease (CD), the pathogenic T cell response is directed toward an immunod

156 ve of an Ag-specific response and triggers a pathogenic T cell response sufficient to cause alveolar

157 accompanied by almost complete inhibition of pathogenic T cell response to critical peptide autoepito

158 ic T regs accumulate and continuously negate pathogenic T cell response.

159 rovides a strategy to selectively target the pathogenic T cell response.

160 functions during RSV infection, suppressing pathogenic T cell responses and inhibiting lung eosinoph

161 Thus, IL-27 signaling in DCs limited pathogenic T cell responses and the development of autoi

162 used as novel therapeutic agents to abrogate pathogenic T cell responses by selective depletion of ac

163 integrin alphavbeta8 were unable to suppress pathogenic T cell responses during active inflammation.

164 ave implications for the immunomodulation of pathogenic T cell responses during transplantation.

165 mmunotherapeutic tool for the attenuation of pathogenic T cell responses in autoimmune arthritis.

166 f therapies for multiple sclerosis targeting pathogenic T cell responses remains imperative.

167 goal of immunotherapy remains the control of pathogenic T cell responses that drive autoimmunity and

168 idence of gammac cytokines as key drivers of pathogenic T cell responses, offering a potential strate

169 cific T cells before they differentiate into pathogenic T cell responses.

170 role in diabetes pathogenesis by regulating pathogenic T cell responses.

171 d T cell activation and, thus, suppress Th17 pathogenic T cell responses.

172 rohibited EAU development by inhibiting Th17 pathogenic T cell responses.

173 ial role for NLRP12 in negatively regulating pathogenic T cell responses.

174 autoimmune diseases mediated by Th17 or Th1 pathogenic T cell responses.

175 achieved through a delicate balance between pathogenic T-cell responses directed at tissue-specific

176 er, the mechanisms by which B cells suppress pathogenic T-cell responses likely vary across disease s

177 Thus, combining ABT with GABA can inhibit pathogenic T-cell responses, induce Treg responses, prom

178 l models indicate that dendritic cells drive pathogenic T-cell responses, partly through the producti

179 + T cells plays a central role in regulating pathogenic T-cell responses.

180 es, which may contribute to the induction of pathogenic T-cell responses.

181 In rheumatoid arthritis (RA), pathogenic T cells shift glucose away from adenosine tri

182 essed the same target TCR BV8S2 chain as the pathogenic T cells specific for myelin basic protein (MB

183 ed endogenous CD8 T cell responses using the pathogenic T cell stimulant Staphylococcus aureus entero

184 lucidate involvement of a previously unknown pathogenic T cell subset (Th17) in DED that is associate

185 stead, it facilitated generation of a highly pathogenic T cell subset exhibiting multiple hallmarks o

186 icate that CD8(+)CD28(-) T cells represent a pathogenic T-cell subset in SSc and likely play a critic

187 udies provide strong evidence that the major pathogenic T cell subsets in EAE are Th17 cells.

188 ma-expressing Th1 cells, represent two major pathogenic T cell subsets in experimental autoimmune enc

189 dings demonstrate that AEA suppresses highly pathogenic T cell subsets through CB1-mediated mammalian

190 Pathogenic T-cell subsets, their clonality, and downstre

191 how that STAT3 is a master regulator of this pathogenic T cell subtype, acting at multiple levels in

192 Pathogenic T cells that adhered to cholangiocytes up-reg

193 T cell-mediated disease primarily driven by pathogenic T cells that produce high levels of IL-17 in

194 lonal antibody may involve direct effects on pathogenic T cells, the induction of populations of regu

195 alter the activation and differentiation of pathogenic T cells through an effect on antigen presenti

196 the recipient can influence the expansion of pathogenic T cells, thus increasing long-term the burden

197 r by the ability of B cells to interact with pathogenic T cells to dampen harmful immune responses.

198 on-T cells must express HSA in order for the pathogenic T cells to execute their effector function.

199 d by the ability of B cells to interact with pathogenic T cells to inhibit harmful immune responses.

200 demonstrate that CXCR4 mediates migration of pathogenic T cells to the BM in AA mice, and inhibiting

201 impaired the homing of neuroantigen-reactive pathogenic T cells to the CNS in a VCAM-1-dependent fash

202 ier and thereby facilitates the migration of pathogenic T cells to the CNS.

203 cid/scid mice, which allows easy tracking of pathogenic T cells, to show that when anti-IL-12 mAb is

204 Autoreactive pathogenic T cells (Tpaths) and regulatory T cells (Treg

205 This gene is not expressed in T1D pathogenic T cells (Tpaths) or non-Tpath T cells.

206 Thus, contrary to pathogenic T cells, Tregs require avid TCR-ligand intera

207 decreased in depigmented hair follicles, and pathogenic T cells upregulated activation markers when e

208 Targeting pathogenic T cells using vaccines consisting of syntheti

209 To test whether the development of pathogenic T cells was dependent on their production of

210 quences have previously been unavailable for pathogenic T cells which react with a defined autoantige

211 resentation of an autoantigen, as the weakly pathogenic T cells, which remained silent in the untreat

212 bition as a therapeutic strategy to suppress pathogenic T cells while not interfering with myeloid ce

213 ertoire by increasing levels of autoreactive pathogenic T cells while suppressing development and/or

214 Targeting pathogenic T cells with Ag-specific tolerizing DNA vacci

215 sease severity due to impaired enrichment of pathogenic T cells within the CNS.

216 which induced proinflammatory cytokines and pathogenic T cells, zymosan induced a mixture of pro- an