ライフサイエンスコーパス: ACAID

1 ACAID is characterized by decreases in delayed-type hype

2 ACAID mitigates ocular autoimmune diseases and promotes

3 ACAID regulates harmful immune responses that can lead t

4 ACAID was induced by priming in the anterior chamber (AC

5 are necessary for the induction of ACAID; 2) ACAID B cells do not directly suppress the expression of

6 Experimental manipulations that abolished ACAID included cautery, neovascularization, and keratopl

7 al cells into normal eyes failed to abrogate ACAID, whereas LC-containing cell populations uniformly

8 o treatment with anti-CD8 antibody abrogated ACAID but had no effect on corneal allograft survival.

9 In addition, ACAID was shown to be induced in the rabbits with cornea

10 All ACAID-inducing signals created in vitro with soluble, pa

11 ti-inflammatory activities do not lead to an ACAID-inducing signal per se.

12 f ss(2)-microglobulin on both the B cell and ACAID APC, but not on the T suppressor cells.

13 unable to generate Ag-specific Tr cells and ACAID.

14 r-specific delayed hypersensitivity (DH) and ACAID, and fragment-containing eyes were tested for thei

15 ce the epithelium is lost, DH disappears and ACAID emerges.

16 fection can induce corneal endotheliitis and ACAID may play the pivotal role in this entity.

17 n active role in ocular immune privilege and ACAID by creating a local immunosuppressive microenviron

18 injected LCs preserved immune privilege and ACAID induction (P < 0.001).

19 IL-1ra preserves ocular immune privilege and ACAID through suppression of LC function.

20 treatments on corneal allograft survival and ACAID were evaluated.

21 The fact that IL-6 antagonized ACAID induction in normal eyes suggests that strategies

22 Cell-associated ACAID-inducing signals are generated in naive mice regar

23 tibility) antigens generated cell-associated ACAID-inducing signals.

24 Further discordance between ACAID and corneal allograft survival emerged in experime

25 duction of Ag-specific regulatory T cells by ACAID B cells requires histocompatibility at the TL/Qa r

26 Peripheral tolerance produced by ACAID requires the participation of ACAID B cells, which

27 as used to sort out CD4+CD25+, and CD4+CD25- ACAID T cells before they were injected into OVA-immuniz

28 at were injected with CD4+CD25+ or CD4+CD25- ACAID T cells.

29 The CD4+CD25+, but not the CD4+CD25-, ACAID T regs expressed Foxp3.

30 over, the contribution of gammadelta T cells ACAID generation could be replaced by adding exogenous r

31 d with anti-gamma delta Ab failed to develop ACAID following anterior chamber injection of either sol

32 (KO) mice retained their ability to develop ACAID post-RLB.

33 (a) CD1 knockout mice were unable to develop ACAID unless they were reconstituted with NKT cells toge

34 nal gamma delta T cells also fail to develop ACAID.

35 geneic corneal fragments in the AC developed ACAID by 8 weeks, but not at 1 week.

36 nterior chamber-associated immune deviation (ACAID) and promote corneal allograft survival.

37 nterior chamber-associated immune deviation (ACAID) induction after anterior chamber injection of bov

38 or chamber (AC)-associated immune deviation (ACAID) induction after injection of ovalbumin (OVA).

39 nterior chamber-associated immune deviation (ACAID) is a form of peripheral tolerance that is induced

40 nterior chamber-associated immune deviation (ACAID) is elicited by an antigen-specific signal that es

41 chamber (a.c.)-associated immune deviation (ACAID) model of peripheral tolerance, a.c. inoculation o

42 nterior chamber-associated immune deviation (ACAID) occurs in most mouse strains, ACAID cannot be ind

43 nterior chamber-associated immune deviation (ACAID) protocol is characterized by impairment of Th1 re

44 nterior chamber-associated immune deviation (ACAID) to demonstrate that central regulation of acquire

45 nterior chamber-associated immune deviation (ACAID) to intracamerally injected soluble antigen 1 to 2

46 nterior chamber-associated immune deviation (ACAID) Tregs were induced by injecting C57BL/6 spleen ce

47 nterior chamber-associated immune deviation (ACAID), a manifestation of ocular immune privilege, prev

48 nterior chamber-associated immune deviation (ACAID), an eye-derived tolerance evoked by injection of

49 ce, termed a.c.-associated immune deviation (ACAID), characterized by Ag-specific inhibition of delay

50 nterior chamber-associated immune deviation (ACAID), culminates in the generation of regulatory cells

51 nterior chamber-associated immune deviation (ACAID), is characterized by impairment of delayed hypers

52 nterior Chamber-Associated Immune Deviation (ACAID), the differentiation of the T regulatory (Tr) cel

53 nterior chamber-associated immune deviation (ACAID), the differentiation of the T regulatory cells de

54 nterior chamber-associated immune deviation (ACAID), this deviant response is not detected until well

55 nterior chamber-associated immune deviation (ACAID), which has been shown to participate in long-term

56 nterior chamber-associated immune deviation (ACAID).

57 nterior chamber associated immune deviation (ACAID).

58 nterior chamber-associated immune deviation (ACAID).

59 nterior chamber-associated immune deviation (ACAID).

60 nterior chamber associated immune deviation (ACAID).

61 nterior chamber associated immune deviation (ACAID).

62 rance termed AC-associated immune deviation (ACAID).

63 nterior chamber-associated immune deviation (ACAID).

64 nterior chamber-associated immune deviation (ACAID).

65 nterior chamber-associated immune deviation (ACAID).

66 nterior chamber-associated immune deviation (ACAID).

67 nterior chamber-associated immune deviation; ACAID) is associated in part with CD8+ T cells that supp

68 tention of the cauterized eyes' capacity for ACAID induction (P < 0.01) and to a profound (>80%) supp

69 ion, these eyes show a restored capacity for ACAID induction, and this appears to be unrelated to any

70 t act as ancillary APCs and are required for ACAID induction.

71 nto virgin murine corneas before testing for ACAID.

72 BCR to capture and internalize antigen from ACAID-inducing macrophages.

73 into the AC of presensitized mice generated ACAID-inducing signals that were soluble and located in

74 was highly upregulated in in vivo-generated ACAID T regs and was necessary for their suppression of

75 Hence, the present study identifies ACAID as a prototypical model of centrally induced, nond

76 The role of IL-10 in ACAID was confirmed in IL-10 knockout mice.

77 ever, the functions of gammadelta T cells in ACAID are unknown.

78 ining the functions of gammadelta T cells in ACAID.

79 e for the induction of regulatory T cells in ACAID.

80 CD8+ T regulatory cell (T reg) functions in ACAID.

81 suggest that the Th1 response is impaired in ACAID by a mechanism(s) that does not require Th2-type c

82 t CD8(+) CTL responses are also inhibited in ACAID.

83 to evaluate the role that cytokines play in ACAID.

84 Because NKT cells have a prominent role in ACAID and NKT cell-derived IL-13 is required in a tumor

85 l-derived Th2 cytokines might have a role in ACAID.

86 with which corneal tissue itself can induce ACAID, allogeneic corneal segments were inserted into an

87 inert particulate antigens could not induce ACAID, but soluble and cell-associated (minor histocompa

88 n of Ag-specific splenic B cells that induce ACAID.

89 om IL-10 knockout mice were unable to induce ACAID following in vitro treatment with TGF-beta.

90 and then evaluated for the ability to induce ACAID in naive (nonsensitized) as well as T- and B-cell-

91 AC of eyes of mice with EAU failed to induce ACAID.

92 d anti-IL-10 Ab lost their ability to induce ACAID.

93 antigen was necessary for B cells to induce ACAID; however, transporter of antigen processing (TAP)

94 iculate, or cell-associated antigens induced ACAID in vivo.

95 from which tumor has been eliminated induced ACAID.

96 Finally, OVA induced ACAID in mice depleted of CD25+ cells.

97 n of the grafted eyes' capacity for inducing ACAID to soluble antigen (OVA).

98 ACAID APC in vitro, were capable of inducing ACAID when transferred to naive mice.

99 pation of three cell populations: the ocular ACAID APC, the splenic B cell, and the splenic T cell.

100 Abolition of ACAID by splenectomy resulted in a sharp increase in the

101 ppressive microenvironment, to abrogation of ACAID.

102 In contrast, other aspects of ACAID-induced tolerance, including recruitment of iNKT c

103 function as the efferent regulatory cells of ACAID.

104 ell population prohibited the development of ACAID.

105 T cells in vivo abrogated the development of ACAID; and (c) anti-CD1 monoclonal antibody treatment of

106 gamma antibodies prevented the expression of ACAID and abolished the immune privilege of corneal allo

107 no effect on the induction or expression of ACAID.

108 t, and even necessary, for the expression of ACAID.

109 vivo during the induction and expression of ACAID.

110 ontribute to the induction and expression of ACAID.

111 ta T cells are crucial for the generation of ACAID and for corneal allograft survival.

112 crete IL-10 and facilitate the generation of ACAID Tregs.

113 (TAP) was not required for the generation of ACAID.

114 grafts by a mechanism that is independent of ACAID.

115 tor (BCR) was necessary for the induction of ACAID and conveyed antigen specificity to the suppressor

116 amero-splenic axis prevents the induction of ACAID and greatly increases the risk for corneal allogra

117 cells is not necessary for the induction of ACAID B cells.

118 Moreover, induction of ACAID before the application of TNFRII KO corneal allogr

119 e strategically located for the induction of ACAID by the sloughing of corneal cells into the AC, the

120 we wondered whether pre-emptive induction of ACAID could inhibit Th2 responses.

121 from CD25- precursors, and the induction of ACAID is not dependent on the presence of natural CD4+CD

122 Moreover, the induction of ACAID regulatory cells required histocompatibility betwe

123 The induction of ACAID required the normal expression of ss(2)-microglobu

124 The induction of ACAID requires the participation of three cell populatio

125 ) B cells are necessary for the induction of ACAID; 2) ACAID B cells do not directly suppress the exp

126 Loss of ACAID correlated variably with loss of ability of cornea

127 has a central role in the bilateral loss of ACAID.

128 B treatment, prevented the bilateral loss of ACAID.

129 oinflamatory peptide, in RLB-induced loss of ACAID.

130 Using in vitro and in vivo models of ACAID, we demonstrate that ACAID B cells must express bo

131 n, when correlated with the time of onset of ACAID, suggests that immunoregulatory T cells are formed

132 duced by ACAID requires the participation of ACAID B cells, which induce the generation of both CD4(+

133 The presence of ACAID suppressor cells in corneal allograft recipients w

134 Some of the CD4+ T regs of ACAID arise from CD25- precursors, and the induction of

135 The role of ACAID in promoting corneal allograft survival was examin

136 Two types of ACAID-inducing signals have been described: those associ

137 s for the existence of two distinct types of ACAID-inducing signals.

138 tibody treatment of wild-type mice prevented ACAID development.

139 (RLB) to one eye abrogated immune privilege (ACAID) bilaterally for an extended period of time.

140 lenic NKT cells from wild-type mice restored ACAID in Jalpha18 KO mice (iNKT cell deficient), but NKT

141 , BALB/c recipients exhibited DBA/2-specific ACAID and concomitant immunity.

142 ne their capacity to induce antigen-specific ACAID.

143 t does not alter induction of donor-specific ACAID after transplantation, suggesting that its anti-in

144 ote, or inhibit, induction of donor-specific ACAID compared with vehicle-treated controls at either t

145 Donor-specific ACAID was measured in allogeneic grafted mice at 4 and 8

146 Promotion of OVA-specific ACAID by IL-1ra suggests that suppression of IL-1-mediat

147 OVA-specific ACAID T regs were obtained from the spleens of DO11.10 m

148 iation (ACAID) occurs in most mouse strains, ACAID cannot be induced in several mutant mouse strains

149 In summary, ACAID can be induced by a class II-restricted peptide an

150 were tested as to whether they could support ACAID.

151 es were tested for their capacity to support ACAID to an irrelevant antigen.

152 Moreover, fragment-containing eyes supported ACAID induction when bovine serum albumin was injected i

153 d, these eyes remain incapable of supporting ACAID, even weeks after the initial corneal insult.

154 gment manifested as the inability to sustain ACAID.

155 ce elicited normal DTH responses rather than ACAID.

156 in vivo models of ACAID, we demonstrate that ACAID B cells must express both MHC class I and II molec

157 These results reduce the likelihood that ACAID regulates Th1 responses via a Th2-like mechanism.

158 The ACAID-inducing signal is carried by blood-borne cells fr

159 and presentation of exogenous protein in the ACAID model are discussed in light of the present data.

160 expression phases of DH are involved in the ACAID response and may mediate their effects through cyt

161 tigen is essential for the processing of the ACAID antigen before TAP-independent presentation to sup

162 An in vitro model of the ACAID spleen was used to recapitulate the events that oc

163 ut not from IL-10 KO mice, reconstituted the ACAID inducing ability in J alpha 281 KO mice.

164 adding exogenous recombinant mouse IL-10 to ACAID spleen cell cultures lacking gammadelta T cells.

165 F4/80 mAb and F4/80(-/-) APCs in an in vitro ACAID model showed that all APC cells in the culture mus

166 explore this issue further, we asked whether ACAID could be induced with a class II-restricted peptid

167 strated that splenic B cells, incubated with ACAID APC in vitro, were capable of inducing ACAID when

168 tained from the spleens of DO11.10 mice with ACAID to OVA.

169 ells are induced in the spleens of mice with ACAID, and previous studies suggest that CD8 cells are i

170 d in cultures of spleen cells from mice with ACAID.