ライフサイエンスコーパス: minor histocompatibility

1 The classical minor histocompatibility 3 (H3) locus was originally def

2 g tracheal grafts was examined as a model of minor histocompatibility Ag (mHAg)-induced chronic allog

3 The role of minor histocompatibility Ag (mHAg)-specific CD8+ CTLs in

4 , wherein TS1 CD4 cells specific for a model minor histocompatibility Ag (miHA) induce GVHD in miHA-p

5 The MHC-matched, minor histocompatibility Ag (miHA)-mismatched B10.BR-->C

6 naturally processed, ubiquitously expressed minor histocompatibility Ag (miHAg) with a proven role i

7 tolerance by testing whether tolerance to a minor histocompatibility Ag can be induced in newborn mi

8 mitted Ag has been previously described as a minor histocompatibility Ag composed of a mitochondriall

9 C-matched murine strains expressing multiple minor histocompatibility Ag differences.

10 H3a is a minor histocompatibility Ag gene, located within H3, tha

11 Thus, a single minor histocompatibility Ag H60 mismatch can trigger an

12 CD8 T cells specific for the immunodominant minor histocompatibility Ag H60.

13 lected from healthy mothers and analyzed for minor histocompatibility Ag HY-specific responses.

14 We show that mouse T cells responding to the minor histocompatibility Ag HYDbSmcy share an invariant

15 versity of TCRs that are specific for single minor histocompatibility Ag peptides and expressed by CT

16 + CTL clones that recognized a male-specific minor histocompatibility Ag presented by HLA-B8.

17 instrumentation to identify a male-specific minor histocompatibility Ag restricted by HLA-A*0101 (A1

18 photoxin (LT) signaling in a murine model of minor histocompatibility Ag system mismatch GVHSD by usi

19 opes, of melanoma-associated Ags, and of the minor histocompatibility Ag UTA2-1, which is currently b

20 pression of SMCY(311-319), an immunodominant minor histocompatibility Ag, as detected by cytotoxicity

21 errant allele, A*0118N, that may behave as a minor histocompatibility Ag, with implications in allore

22 uitment of T cells into MHC-matched/multiple minor histocompatibility Ag-disparate allografts during

23 chemokine expression in MHC-matched/multiple minor histocompatibility Ag-disparate allografts has not

24 grafts from transgenic animals onto MHC- and minor histocompatibility Ag-matched nontransgenic recipi

25 was also identified in BALB/b mice receiving minor histocompatibility Ag-mismatched B6 T cell-replete

26 Using a minor histocompatibility Ag-mismatched BMT (B6 --> B6 x

27 Mouse models of minor histocompatibility Ag-mismatched bone marrow trans

28 (B6)-->BALB/c and the MHC-matched, multiple minor histocompatibility Ag-mismatched C3H.SW-->B6 strai

29 s in both MHC-mismatched and MHC-matched but minor histocompatibility Ag-mismatched models driven by

30 eased graft-vs-host disease in both MHC- and minor histocompatibility Ag-mismatched murine hemopoieti

31 t B6.lpr mice as recipients in a MHC-matched minor histocompatibility Ag-mismatched murine model for

32 ly to be target tissue-related anti-multiple minor histocompatibility Ag-specific responses in each o

33 d promotes MHC class I cross-presentation of minor histocompatibility Ags (H-Ags) to CTLs in the frog

34 Minor histocompatibility Ags (HA) and their associated i

35 Minor histocompatibility Ags (HA) play prominent roles i

36 atched for MHC because of differences in the minor histocompatibility Ags (mH-Ags).

37 Human minor histocompatibility Ags (mHag) present significant

38 rly defined, partly because immunity against minor histocompatibility Ags (mHAgs) complicates the elu

39 In vitro CTL responses to multiple minor histocompatibility Ags (miHA) are governed by immu

40 T cell recognition of minor histocompatibility Ags (MiHA) plays an important r

41 inations differing in expression of multiple minor histocompatibility Ags (miHA).

42 Minor histocompatibility Ags (minor H Ags) are substanti

43 logeneic reactions are due to disparities in minor histocompatibility Ags (minor HAs).

44 es that lead to allorecognition of major and minor histocompatibility Ags and have implications on th

45 Minor histocompatibility Ags are peptides derived from p

46 Minor histocompatibility Ags elicit cell-mediated immune

47 that sex-mismatched H-Y Ags may be important minor histocompatibility Ags for GVH responses, we direc

48 dy of alloimmune responses against major and minor histocompatibility Ags has been limited by the lac

49 as they proliferate in response to major or minor histocompatibility Ags in vivo.

50 ptides corresponding to the male-specific HY minor histocompatibility Ags presented by HLA-B27 in tra

51 (GVHD) is hampered by a lack of knowledge of minor histocompatibility Ags triggering alloresponses.

52 Allorecognition of minor histocompatibility Ags was highly dependent on CD2

53 ) recipients that are mismatched at multiple minor histocompatibility Ags, including the immunodomina

54 hile responses to less abundant Ags, such as minor histocompatibility Ags, require T helper cells.

55 ) mouse model of human GVHD directed against minor histocompatibility Ags, we found that donor CD8(+)

56 ed alloantigens behave similarly in vitro to minor histocompatibility Ags, with comparable immunogeni

57 hic, suggesting that these may also serve as minor histocompatibility Ags.

58 n MHC-matched individuals is the mismatch of minor histocompatibility Ags.

59 iginate from donor mice and recognize BALB/c minor histocompatibility alloantigens and BALB/c endogen

60 or histocompatibility complex (MHC), but not minor histocompatibility, alloantigens was induced.

61 atched BALB.B spleen cells, despite multiple minor histocompatibility antigen (HA) differences.

62 In a single minor histocompatibility antigen (male to female)-depend

63 of RBC products induced BMT rejection across minor histocompatibility antigen (mHA) barriers.

64 ined the immune response to DBY, a model H-Y minor histocompatibility antigen (mHA) in a male patient

65 C with grafts supplemented with T cells in a minor histocompatibility antigen (mHA)-mismatched mouse

66 rences in susceptibility to immune pressure, minor histocompatibility antigen (mHa)-specific T-cell l

67 Minor histocompatibility antigen (mHag) discordances hav

68 astocytoma in a murine model of MHC-matched, minor histocompatibility antigen (mHAg)-mismatched bone

69 T(M) from donors vaccinated against a single minor histocompatibility antigen (miHA) expressed by leu

70 cient B6 (H-2(b)) recipients primed to donor minor histocompatibility antigen (MiHA) prior to BM tran

71 Minor histocompatibility antigen (miHA) vaccines have th

72 smatched, CD4-driven murine GVHD model and a minor histocompatibility antigen (MiHA)-mismatched, CD8-

73 The hypothesis that ICAM-1 acts as a minor histocompatibility antigen and that anti-ICAM-1 an

74 acute CD4+ T cell-mediated GVHD across this minor histocompatibility antigen barrier depends on the

75 helper-deficient CD8(+) T-cell response to a minor histocompatibility antigen by phenotypic and in vi

76 Here we describe a human minor histocompatibility antigen created by a polymorphi

77 ed this alloimmune syndrome in recipients of minor histocompatibility antigen disparate donor cells,

78 of cases across a two-haplotype class I plus minor histocompatibility antigen disparity by a 12-d cou

79 induced across a two-haplotype class I plus minor histocompatibility antigen disparity by a 12-day c

80 etinoic acid early inducible (RAE-1) and H60 minor histocompatibility antigen genes on mouse chromoso

81 totoxic T cell clones specific for the human minor histocompatibility antigen H-Y and restricted by H

82 suggested that recipient mismatching for the minor histocompatibility antigen HA-1 is associated with

83 ation produces HvG against the male specific minor histocompatibility antigen HY.

84 matched donor MHC class I and II, and of H-Y minor histocompatibility antigen was assessed by quantif

85 mice and the interaction of these cells with minor histocompatibility antigen- (miHA-) mismatched CD8

86 When transplanted into minor histocompatibility antigen-disparate allogeneic re

87 row irradiation chimeras across the multiple minor histocompatibility antigen-disparate, C57BL/6-->BA

88 test the role of donor Stat1 in MHC-matched minor histocompatibility antigen-mismatched (mHA-mismatc

89 study the mechanisms of DLI in MHC-matched, minor histocompatibility antigen-mismatched allogeneic c

90 histocompatibility complex-matched multiple minor histocompatibility antigen-mismatched alloHCT usin

91 usion may not apply to MHC-matched, multiple minor histocompatibility antigen-mismatched alloSCT, the

92 In both a minor histocompatibility antigen-mismatched as well as a

93 Recipients were H-2-matched, minor histocompatibility antigen-mismatched C57BL/6 mice

94 ed, single Y chromosome-encoded, or multiple minor histocompatibility antigen-mismatched hematopoieti

95 r Histocompatibility Antigen Complex-matched minor Histocompatibility Antigen-mismatched murine model

96 platelets, and we report that transfusion of minor histocompatibility antigen-mismatched platelets in

97 play an important role in clinical GVHD in a minor histocompatibility antigen-mismatched setting.

98 major histocompatibility complex-matched and minor histocompatibility antigen-mismatched unrelated do

99 te infusions (DLIs) were incorporated into a minor histocompatibility antigen-mismatched, T cell-depl

100 ificantly suppressed the clonal expansion of minor histocompatibility antigen-specific CD8 T cells du

101 pleen cells do not inhibit allogeneic MHC or minor histocompatibility antigen-specific CTL production

102 ted in this issue employed the redesign of a minor histocompatibility antigen.

103 , a thirteen-residue, maternally transmitted minor histocompatibility antigen.

104 tinoic acid early transcript (Rae1) and H-60 minor histocompatibility antigen.

105 cellular immune response against chaperoned minor histocompatibility antigenic peptides that effects

106 Indirect presentation of minor histocompatibility antigens (HA) as revealed by cr

107 Human minor histocompatibility antigens (mHA) and clinically r

108 Next, we immunized the donor to the minor histocompatibility antigens (mHA) of the recipient

109 Minor histocompatibility antigens (mHAg's) are peptides

110 Minor histocompatibility antigens (mHags) are immunogeni

111 le GVHD because of the presence of recipient minor histocompatibility antigens (mHAgs) in whole-cell

112 er of donor T cells that recognize recipient minor histocompatibility antigens (mHAgs) is a potential

113 he priming of donor T cells against putative minor histocompatibility antigens (mHAgs) on the tumor v

114 Minor histocompatibility antigens (mHAgs) present a sign

115 T cell recognition of minor histocompatibility antigens (mHags) underlies allo

116 herited major histocompatibility complex and minor histocompatibility antigens (mHAgs).

117 ced primarily by donor T-cell recognition of minor histocompatibility antigens (mHAgs).

118 Minor histocompatibility antigens (mHAs) are known targe

119 Alloreactive donor T cells against host minor histocompatibility antigens (mHAs) cause graft-ver

120 le for increased rejection is likely against minor histocompatibility antigens (mHAs).

121 cing alloreactive T cell responses targeting minor histocompatibility antigens (MiHA) expressed on ma

122 SCT, CD8+ stem cell memory T cells targeting minor histocompatibility antigens (MiHAs) expressed by r

123 r magnitude and diversity of CD8 T cells for minor histocompatibility antigens (MiHAs) in patients wi

124 s) initiate GVHD by directly presenting host minor histocompatibility antigens (miHAs) to donor CD8 c

125 onor and recipient were incompatible at many minor histocompatibility antigens (minor H Ags), the CD8

126 Minor histocompatibility antigens (minor H antigens) are

127 -dependent GVHD in a mouse model across only minor histocompatibility antigens (minor H antigens).

128 cells that recognize mismatched major and/or minor histocompatibility antigens and cause severe damag

129 xpansion of Tregs against major and possibly minor histocompatibility antigens and predict the feasib

130 genes and subsequent reduced presentation of minor histocompatibility antigens and reduced ligation o

131 ansplant is acquired tolerance of allogeneic minor histocompatibility antigens and that posttransplan

132 Immune responses to minor histocompatibility antigens are poorly understood

133 Minor histocompatibility antigens contribute to the cont

134 On the other hand, the importance of minor histocompatibility antigens derived from nonhemato

135 onor T cells that are specific for recipient minor histocompatibility antigens encoded by Y-chromosom

136 Allogeneic antibodies against minor histocompatibility antigens encoded on the Y chrom

137 For minor histocompatibility antigens HA-1 and HA-2, normal

138 ed the HLA-B27-restricted CTL response to HY minor histocompatibility antigens in rats and mice trans

139 In addition, a better understanding of minor histocompatibility antigens may lead to more targe

140 ansplantation, donors' T cells can recognize minor histocompatibility antigens on recipient cells and

141 eved to be mediated by T-cell recognition of minor histocompatibility antigens on recipient cells.

142 The inclusion of SNPs that encode minor histocompatibility antigens or other genetic polym

143 Minor histocompatibility antigens play a significant rol

144 The GVL effect is directed against minor histocompatibility antigens shared by normal and l

145 ying a murine model that uses differences in minor histocompatibility antigens to generate Scl GVHD.

146 grafts, skin differing from the host only by minor histocompatibility antigens undergoes slower (i.e.

147 a strong genetic disparity in both major and minor histocompatibility antigens were used for transpla

148 cognition of these hematopoietically derived minor histocompatibility antigens will induce significan

149 Minor histocompatibility antigens with expression restri

150 PK3 and the shared antigens do not represent minor histocompatibility antigens, as their sequences ar

151 to donor human leukocyte antigen molecules, minor histocompatibility antigens, endothelial cells, RB

152 ors, including recognition of sex-determined minor histocompatibility antigens, influence of sex horm

153 bone marrow is not matched in the clinic for minor histocompatibility antigens, such as those carried

154 kin and bone marrow, mismatched for multiple minor histocompatibility antigens, was induced in Fas mu

155 stent with a response to immunodominant host minor histocompatibility antigens, we detected oligoclon

156 for disparities in cytoplasmically inherited minor histocompatibility antigens, we examined one hyper

157 were oligoclonal, pointing to a response to minor histocompatibility antigens.

158 yeloid-specific differentiation antigens and minor histocompatibility antigens.

159 yngeneic antigen-presenting cells presenting minor histocompatibility antigens.

160 ing for major histocompatibility antigens or minor histocompatibility antigens.

161 ls in the development of humoral immunity to minor histocompatibility antigens.

162 ediated by donor T cells that recognize host minor histocompatibility antigens.

163 lografts that confront the host with foreign minor histocompatibility antigens.

164 duce ACAID, but soluble and cell-associated (minor histocompatibility) antigens generated cell-associ

165 01) after bone marrow transplantation across minor histocompatibility barriers (B10.BR-->CBA/J).

166 ide, graft-versus-host disease (GVHD) across minor histocompatibility barriers was induced in the B10

167 R-4 as recipients of grafts across major and minor histocompatibility barriers.

168 e B10.D2 --> BALB/c model (both H-2d) across minor histocompatibility barriers.

169 ion and induce antigen-specific tolerance in minor histocompatibility complex-mismatched recipients,

170 man mHAg and provide the first evidence that minor histocompatibility differences can result from the

171 e inhibited the MLR across several major and minor histocompatibility differences in a specific and d

172 host CD4+ T cells that recognize very subtle minor histocompatibility differences.

173 ed into BALB/c (major histocompatibility and minor histocompatibility-disparate) eyes.

174 ere rapidly rejected, even in the context of minor histocompatibility disparities, with massive graft

175 n donor-host combinations involving multiple minor histocompatibility disparity.

176 the role of cytokine-gene polymorphisms and minor histocompatibility genes in transplant outcome req

177 Minor histocompatibility (H) Ag disparities result in gr

178 The mouse H13 minor histocompatibility (H) Ag, originally detected as

179 Minor histocompatibility (H) Ags are classically describ

180 Minor histocompatibility (H) Ags elicit T cell responses

181 To model performance against minor histocompatibility (H) Ags important in allogeneic

182 Of the many minor histocompatibility (H) Ags that have been detected

183 Unexpectedly, corneas expressing minor histocompatibility (H) alloantigens are rejected a

184 matched Balb.B spleen cells despite multiple minor histocompatibility (H) antigen differences.

185 role of the hematopoietic lineage-restricted minor histocompatibility (H) antigen HA-1 in renal allog

186 The H60 minor histocompatibility (H) antigen peptide is derived

187 sues accelerates rejection of MHC identical, minor histocompatibility (H) antigen-disparate skin graf

188 hich lung injury after BMT can be induced by minor histocompatibility (H) antigenic differences betwe

189 Since minor histocompatibility (H) antigens are the main targe

190 toxic T lymphocytes (CTL) specific for human minor histocompatibility (H) antigens can be isolated fr

191 isparity at loci outside the MHC that encode minor histocompatibility (H) antigens can elicit GVHD an

192 molecular identification of these additional minor histocompatibility (H) antigens lagged behind that

193 T-cell immunotherapy that targets minor histocompatibility (H) antigens presented selectiv

194 Minor histocompatibility (H) antigens stimulate in vivo

195 present MHC class I-restricted H3aa or H3ab minor histocompatibility (H) antigens to cytotoxic T-lym

196 stem where donor and host differ by multiple minor histocompatibility (H) antigens, we investigated t

197 red by donor T cells specific for particular minor histocompatibility (H) antigens.

198 nition of tumor-specific and host-restricted minor histocompatibility (H) antigens.

199 The products of minor histocompatibility (H) loci are serious barriers t

200 ajor histocompatibility complex (MHC) and/or minor histocompatibility (H)-disparate recipient mice.

201 mammalian Y chromosome encodes male-specific minor histocompatibility (H-Y) Ags that are recognized b

202 The Y chromosome encodes male-specific minor histocompatibility (H-Y) antigens that stimulate T

203 utations in genes that produce male-specific minor histocompatibility (H-Y) antigens.

204 and CD8(+) T cell responses to male-specific minor histocompatibility (HY) Ags following injection of

205 l carcinoma (MB49) model expressing the male minor histocompatibility (HY) antigen was inoculated sub

206 jor histocompatibility complex plus multiple minor histocompatibility loci) and from NZB donors (mism

207 d from NZB donors (mismatch only at multiple minor histocompatibility loci).

208 was induced to grafts mismatched at multiple minor histocompatibility loci, Ag specificity was inferr

209 , differences between donor and recipient at minor histocompatibility loci, which encode allelic prot

210 certain strains of mice with differences in minor histocompatibility loci.

211 BA) receiving bone marrow transplants across minor histocompatibility loci.

212 des that effects an accelerated rejection of minor histocompatibility-locus disparate skin grafts in

213 mphocytes (CTL) responsive to immunodominant minor histocompatibility (minor H) Ags are thought to pl

214 arget cells bearing donor major (MHC) and/or minor histocompatibility (minor H) antigens (direct and

215 hese engrafted IK were transplanted across a minor histocompatibility mismatched barrier into pancrea

216 w that reconstitution of scid/scid mice with minor histocompatibility mismatched naive CD4+ T lymphoc

217 his phenomenon to the rejection of major and minor histocompatibility-mismatched allografts performed

218 kin disorders that is induced by transfer of minor histocompatibility-mismatched CD4(+)/CD45RB(high)

219 G-CSF mobilized allograft from MHC-matched, minor histocompatibility-mismatched donors; recipients o

220 ransplantation by transplanting MHC-matched, minor histocompatibility-mismatched grafts composed of p

221 We have developed a new minor histocompatibility-mismatched rat kidney transplan

222 By contrast, in minor histocompatibility-mismatched recipients, early bl

223 ures of an "infectious" tolerance pathway to minor histocompatibility-mismatched skin grafts, origina

224 n and suggest that strategies to account for minor histocompatibility mismatching may help to reduce

225 are more immunogenic than those derived from minor histocompatibility or other nominal Ags.

226 ivity to allogeneic MHC antigens rather than minor histocompatibility or tumor-associated antigens.