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

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

4 role in the differentiation of autoreactive pathogenic T cells.

5 where they subsequently recruit and tolerize pathogenic T cells.

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

7 tion, SMC proliferation, and infiltration 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 nto the CNS together with the first invading pathogenic T cells.

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

14 gmenting the presentation of autoantigens to pathogenic T cells.

15 the mechanisms underlying the development of pathogenic T cells.

16 ch favors differentiation of regulatory over pathogenic T cells.

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

18 lly supporting the expansion of autoreactive pathogenic T cells.

19 ates arthritis despite increasing numbers of pathogenic T cells.

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

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

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

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

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

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

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

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

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

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

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

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

32 1+ T reg depletion, with emergence of potent pathogenic T cells and severe AOD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 The pathogenic T cells driving disease in this murine model

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

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

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

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

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

68 Pathogenic T cells from donors after BM failure appeared

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

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

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

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

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

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

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

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

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

78 Pathogenic T cells in individuals with rheumatoid arthri

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

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

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

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

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

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

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

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

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

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

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

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

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

92 These pathogenic T cells initiated a cytokine storm characteri

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 Pathogenic T cells recognize two minor epitopes that are

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 Targeting pathogenic T cells using vaccines consisting of syntheti

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

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

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

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

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

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

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