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1                                The classical minor histocompatibility 3 (H3) locus was originally def
2 RC2(DC-/-) ), we show that the transplant of minor histocompatibility Ag (HY)-mismatched skin grafts
3 g tracheal grafts was examined as a model of minor histocompatibility Ag (mHAg)-induced chronic allog
4                                  The role of minor histocompatibility Ag (mHAg)-specific CD8+ CTLs in
5 , wherein TS1 CD4 cells specific for a model minor histocompatibility Ag (miHA) induce GVHD in miHA-p
6                             The MHC-matched, minor histocompatibility Ag (miHA)-mismatched B10.BR-->C
7  naturally processed, ubiquitously expressed minor histocompatibility Ag (miHAg) with a proven role i
8  tolerance by testing whether tolerance to a minor histocompatibility Ag can be induced in newborn mi
9 mitted Ag has been previously described as a minor histocompatibility Ag composed of a mitochondriall
10 C-matched murine strains expressing multiple minor histocompatibility Ag differences.
11                                     H3a is a minor histocompatibility Ag gene, located within H3, tha
12                               Thus, a single minor histocompatibility Ag H60 mismatch can trigger an
13  CD8 T cells specific for the immunodominant minor histocompatibility Ag H60.
14 lected from healthy mothers and analyzed for minor histocompatibility Ag HY-specific responses.
15 We show that mouse T cells responding to the minor histocompatibility Ag HYDbSmcy share an invariant
16 versity of TCRs that are specific for single minor histocompatibility Ag peptides and expressed by CT
17 + CTL clones that recognized a male-specific minor histocompatibility Ag presented by HLA-B8.
18  instrumentation to identify a male-specific minor histocompatibility Ag restricted by HLA-A*0101 (A1
19 photoxin (LT) signaling in a murine model of minor histocompatibility Ag system mismatch GVHSD by usi
20 opes, of melanoma-associated Ags, and of the minor histocompatibility Ag UTA2-1, which is currently b
21 pression of SMCY(311-319), an immunodominant minor histocompatibility Ag, as detected by cytotoxicity
22 errant allele, A*0118N, that may behave as a minor histocompatibility Ag, with implications in allore
23 uitment of T cells into MHC-matched/multiple minor histocompatibility Ag-disparate allografts during
24 chemokine expression in MHC-matched/multiple minor histocompatibility Ag-disparate allografts has not
25 grafts from transgenic animals onto MHC- and minor histocompatibility Ag-matched nontransgenic recipi
26 was also identified in BALB/b mice receiving minor histocompatibility Ag-mismatched B6 T cell-replete
27                                      Using a minor histocompatibility Ag-mismatched BMT (B6 --> B6 x
28                              Mouse models of minor histocompatibility Ag-mismatched bone marrow trans
29  (B6)-->BALB/c and the MHC-matched, multiple minor histocompatibility Ag-mismatched C3H.SW-->B6 strai
30 s in both MHC-mismatched and MHC-matched but minor histocompatibility Ag-mismatched models driven by
31 eased graft-vs-host disease in both MHC- and minor histocompatibility Ag-mismatched murine hemopoieti
32 t B6.lpr mice as recipients in a MHC-matched minor histocompatibility Ag-mismatched murine model for
33 ly to be target tissue-related anti-multiple minor histocompatibility Ag-specific responses in each o
34 d promotes MHC class I cross-presentation of minor histocompatibility Ags (H-Ags) to CTLs in the frog
35                                              Minor histocompatibility Ags (HA) and their associated i
36                                              Minor histocompatibility Ags (HA) play prominent roles i
37 atched for MHC because of differences in the minor histocompatibility Ags (mH-Ags).
38                                        Human minor histocompatibility Ags (mHag) present significant
39 rly defined, partly because immunity against minor histocompatibility Ags (mHAgs) complicates the elu
40           In vitro CTL responses to multiple minor histocompatibility Ags (miHA) are governed by immu
41                        T cell recognition of minor histocompatibility Ags (MiHA) plays an important r
42 inations differing in expression of multiple minor histocompatibility Ags (miHA).
43                                              Minor histocompatibility Ags (minor H Ags) are substanti
44 logeneic reactions are due to disparities in minor histocompatibility Ags (minor HAs).
45 es that lead to allorecognition of major and minor histocompatibility Ags and have implications on th
46                                              Minor histocompatibility Ags are peptides derived from p
47                                              Minor histocompatibility Ags elicit cell-mediated immune
48 that sex-mismatched H-Y Ags may be important minor histocompatibility Ags for GVH responses, we direc
49 dy of alloimmune responses against major and minor histocompatibility Ags has been limited by the lac
50  as they proliferate in response to major or minor histocompatibility Ags in vivo.
51 ptides corresponding to the male-specific HY minor histocompatibility Ags presented by HLA-B27 in tra
52 (GVHD) is hampered by a lack of knowledge of minor histocompatibility Ags triggering alloresponses.
53                           Allorecognition of minor histocompatibility Ags was highly dependent on CD2
54 ) recipients that are mismatched at multiple minor histocompatibility Ags, including the immunodomina
55 hile responses to less abundant Ags, such as minor histocompatibility Ags, require T helper cells.
56 ) mouse model of human GVHD directed against minor histocompatibility Ags, we found that donor CD8(+)
57 ed alloantigens behave similarly in vitro to minor histocompatibility Ags, with comparable immunogeni
58 hic, suggesting that these may also serve as minor histocompatibility Ags.
59 n MHC-matched individuals is the mismatch of minor histocompatibility Ags.
60 iginate from donor mice and recognize BALB/c minor histocompatibility alloantigens and BALB/c endogen
61 or histocompatibility complex (MHC), but not minor histocompatibility, alloantigens was induced.
62 atched BALB.B spleen cells, despite multiple minor histocompatibility antigen (HA) differences.
63                                  In a single minor histocompatibility antigen (male to female)-depend
64 of RBC products induced BMT rejection across minor histocompatibility antigen (mHA) barriers.
65 ined the immune response to DBY, a model H-Y minor histocompatibility antigen (mHA) in a male patient
66 C with grafts supplemented with T cells in a minor histocompatibility antigen (mHA)-mismatched mouse
67 rences in susceptibility to immune pressure, minor histocompatibility antigen (mHa)-specific T-cell l
68                                              Minor histocompatibility antigen (mHag) discordances hav
69 astocytoma in a murine model of MHC-matched, minor histocompatibility antigen (mHAg)-mismatched bone
70 -encoded major HLA disparities or expressing minor histocompatibility antigen (miHA) differences pres
71 T(M) from donors vaccinated against a single minor histocompatibility antigen (miHA) expressed by leu
72 cient B6 (H-2(b)) recipients primed to donor minor histocompatibility antigen (MiHA) prior to BM tran
73                                              Minor histocompatibility antigen (miHA) vaccines have th
74 smatched, CD4-driven murine GVHD model and a minor histocompatibility antigen (MiHA)-mismatched, CD8-
75                                              Minor histocompatibility antigen (MiHA)-specific T cells
76         The hypothesis that ICAM-1 acts as a minor histocompatibility antigen and that anti-ICAM-1 an
77  acute CD4+ T cell-mediated GVHD across this minor histocompatibility antigen barrier depends on the
78 helper-deficient CD8(+) T-cell response to a minor histocompatibility antigen by phenotypic and in vi
79                     Here we describe a human minor histocompatibility antigen created by a polymorphi
80 ed this alloimmune syndrome in recipients of minor histocompatibility antigen disparate donor cells,
81 of cases across a two-haplotype class I plus minor histocompatibility antigen disparity by a 12-d cou
82  induced across a two-haplotype class I plus minor histocompatibility antigen disparity by a 12-day c
83 etinoic acid early inducible (RAE-1) and H60 minor histocompatibility antigen genes on mouse chromoso
84 totoxic T cell clones specific for the human minor histocompatibility antigen H-Y and restricted by H
85 ignal peptide peptidase (SPP), also known as minor histocompatibility antigen H13.
86 ively mediated by T cells that recognize the minor histocompatibility antigen H60.
87 suggested that recipient mismatching for the minor histocompatibility antigen HA-1 is associated with
88 ation produces HvG against the male specific minor histocompatibility antigen HY.
89 ned when Rux-chow was fed to C.B10 mice in a minor histocompatibility antigen mismatched (B6 C.B10) A
90 matched donor MHC class I and II, and of H-Y minor histocompatibility antigen was assessed by quantif
91 an fluorescence intensity [aMFI] >= 1000), a minor histocompatibility antigen, associated with graft
92 r 2 (ARHGDIB) (adjusted MFI [aMFI]>=1000), a minor histocompatibility antigen, associated with graft
93 mice and the interaction of these cells with minor histocompatibility antigen- (miHA-) mismatched CD8
94                       When transplanted into minor histocompatibility antigen-disparate allogeneic re
95 row irradiation chimeras across the multiple minor histocompatibility antigen-disparate, C57BL/6-->BA
96  test the role of donor Stat1 in MHC-matched minor histocompatibility antigen-mismatched (mHA-mismatc
97  study the mechanisms of DLI in MHC-matched, minor histocompatibility antigen-mismatched allogeneic c
98  histocompatibility complex-matched multiple minor histocompatibility antigen-mismatched alloHCT usin
99 usion may not apply to MHC-matched, multiple minor histocompatibility antigen-mismatched alloSCT, the
100                                    In both a minor histocompatibility antigen-mismatched as well as a
101                 Recipients were H-2-matched, minor histocompatibility antigen-mismatched C57BL/6 mice
102 ed, single Y chromosome-encoded, or multiple minor histocompatibility antigen-mismatched hematopoieti
103 r Histocompatibility Antigen Complex-matched minor Histocompatibility Antigen-mismatched murine model
104 platelets, and we report that transfusion of minor histocompatibility antigen-mismatched platelets in
105 play an important role in clinical GVHD in a minor histocompatibility antigen-mismatched setting.
106 major histocompatibility complex-matched and minor histocompatibility antigen-mismatched unrelated do
107 te infusions (DLIs) were incorporated into a minor histocompatibility antigen-mismatched, T cell-depl
108 ificantly suppressed the clonal expansion of minor histocompatibility antigen-specific CD8 T cells du
109 pleen cells do not inhibit allogeneic MHC or minor histocompatibility antigen-specific CTL production
110 nd that the LIMS1 locus appeared to encode a minor histocompatibility antigen.
111 ted in this issue employed the redesign of a minor histocompatibility antigen.
112 , a thirteen-residue, maternally transmitted minor histocompatibility antigen.
113 tinoic acid early transcript (Rae1) and H-60 minor histocompatibility antigen.
114                                           In minor histocompatibility-antigen mismatched allogeneic h
115  cellular immune response against chaperoned minor histocompatibility antigenic peptides that effects
116                     Indirect presentation of minor histocompatibility antigens (HA) as revealed by cr
117                                        Human minor histocompatibility antigens (mHA) and clinically r
118          Next, we immunized the donor to the minor histocompatibility antigens (mHA) of the recipient
119                                              Minor histocompatibility antigens (mHAg's) are peptides
120                                              Minor histocompatibility antigens (mHags) are immunogeni
121 le GVHD because of the presence of recipient minor histocompatibility antigens (mHAgs) in whole-cell
122 er of donor T cells that recognize recipient minor histocompatibility antigens (mHAgs) is a potential
123 he priming of donor T cells against putative minor histocompatibility antigens (mHAgs) on the tumor v
124                                              Minor histocompatibility antigens (mHAgs) present a sign
125                        T cell recognition of minor histocompatibility antigens (mHags) underlies allo
126                T cell alloreactivity against minor histocompatibility antigens (mHAgs)-polymorphic pe
127 herited major histocompatibility complex and minor histocompatibility antigens (mHAgs).
128 ced primarily by donor T-cell recognition of minor histocompatibility antigens (mHAgs).
129                                              Minor histocompatibility antigens (mHAs) are known targe
130      Alloreactive donor T cells against host minor histocompatibility antigens (mHAs) cause graft-ver
131              In contrast, the implication of minor histocompatibility antigens (mHAs) in AMR has not
132 le for increased rejection is likely against minor histocompatibility antigens (mHAs).
133 cing alloreactive T cell responses targeting minor histocompatibility antigens (MiHA) expressed on ma
134 SCT, CD8+ stem cell memory T cells targeting minor histocompatibility antigens (MiHAs) expressed by r
135 r magnitude and diversity of CD8 T cells for minor histocompatibility antigens (MiHAs) in patients wi
136 s) initiate GVHD by directly presenting host minor histocompatibility antigens (miHAs) to donor CD8 c
137 recognizing polymorphic peptides, designated minor histocompatibility antigens (MiHAs), that are pres
138 including tumor-specific antigens (TSAs) and minor histocompatibility antigens (MiHAs).
139 onor and recipient were incompatible at many minor histocompatibility antigens (minor H Ags), the CD8
140                                              Minor histocompatibility antigens (minor H antigens) are
141 -dependent GVHD in a mouse model across only minor histocompatibility antigens (minor H antigens).
142 cells that recognize mismatched major and/or minor histocompatibility antigens and cause severe damag
143 the advances in systematic identification of minor histocompatibility antigens and neoantigens arisin
144 xpansion of Tregs against major and possibly minor histocompatibility antigens and predict the feasib
145 genes and subsequent reduced presentation of minor histocompatibility antigens and reduced ligation o
146 ansplant is acquired tolerance of allogeneic minor histocompatibility antigens and that posttransplan
147                          Immune responses to minor histocompatibility antigens are poorly understood
148                                              Minor histocompatibility antigens contribute to the cont
149         On the other hand, the importance of minor histocompatibility antigens derived from nonhemato
150 onor T cells that are specific for recipient minor histocompatibility antigens encoded by Y-chromosom
151                Allogeneic antibodies against minor histocompatibility antigens encoded on the Y chrom
152                                          For minor histocompatibility antigens HA-1 and HA-2, normal
153 ed the HLA-B27-restricted CTL response to HY minor histocompatibility antigens in rats and mice trans
154       In addition, a better understanding of minor histocompatibility antigens may lead to more targe
155 ansplantation, donors' T cells can recognize minor histocompatibility antigens on recipient cells and
156 eved to be mediated by T-cell recognition of minor histocompatibility antigens on recipient cells.
157            The inclusion of SNPs that encode minor histocompatibility antigens or other genetic polym
158                                              Minor histocompatibility antigens play a significant rol
159           The GVL effect is directed against minor histocompatibility antigens shared by normal and l
160 ying a murine model that uses differences in minor histocompatibility antigens to generate Scl GVHD.
161 grafts, skin differing from the host only by minor histocompatibility antigens undergoes slower (i.e.
162 a strong genetic disparity in both major and minor histocompatibility antigens were used for transpla
163 cognition of these hematopoietically derived minor histocompatibility antigens will induce significan
164                                              Minor histocompatibility antigens with expression restri
165 PK3 and the shared antigens do not represent minor histocompatibility antigens, as their sequences ar
166 f reproductive immunology, and how major and minor histocompatibility antigens, blood group antigens,
167  to donor human leukocyte antigen molecules, minor histocompatibility antigens, endothelial cells, RB
168 ors, including recognition of sex-determined minor histocompatibility antigens, influence of sex horm
169 bone marrow is not matched in the clinic for minor histocompatibility antigens, such as those carried
170 kin and bone marrow, mismatched for multiple minor histocompatibility antigens, was induced in Fas mu
171 stent with a response to immunodominant host minor histocompatibility antigens, we detected oligoclon
172 for disparities in cytoplasmically inherited minor histocompatibility antigens, we examined one hyper
173 lografts that confront the host with foreign minor histocompatibility antigens.
174 ing for major histocompatibility antigens or minor histocompatibility antigens.
175  were oligoclonal, pointing to a response to minor histocompatibility antigens.
176 yeloid-specific differentiation antigens and minor histocompatibility antigens.
177 yngeneic antigen-presenting cells presenting minor histocompatibility antigens.
178 ls in the development of humoral immunity to minor histocompatibility antigens.
179 ediated by donor T cells that recognize host minor histocompatibility antigens.
180 duce ACAID, but soluble and cell-associated (minor histocompatibility) antigens generated cell-associ
181 01) after bone marrow transplantation across minor histocompatibility barriers (B10.BR-->CBA/J).
182 ide, graft-versus-host disease (GVHD) across minor histocompatibility barriers was induced in the B10
183 R-4 as recipients of grafts across major and minor histocompatibility barriers.
184 e B10.D2 --> BALB/c model (both H-2d) across minor histocompatibility barriers.
185 ion and induce antigen-specific tolerance in minor histocompatibility complex-mismatched recipients,
186 man mHAg and provide the first evidence that minor histocompatibility differences can result from the
187 e inhibited the MLR across several major and minor histocompatibility differences in a specific and d
188 host CD4+ T cells that recognize very subtle minor histocompatibility differences.
189 ed into BALB/c (major histocompatibility and minor histocompatibility-disparate) eyes.
190 ere rapidly rejected, even in the context of minor histocompatibility disparities, with massive graft
191 n donor-host combinations involving multiple minor histocompatibility disparity.
192  the role of cytokine-gene polymorphisms and minor histocompatibility genes in transplant outcome req
193                                              Minor histocompatibility (H) Ag disparities result in gr
194                                The mouse H13 minor histocompatibility (H) Ag, originally detected as
195                                              Minor histocompatibility (H) Ags are classically describ
196                                              Minor histocompatibility (H) Ags elicit T cell responses
197                 To model performance against minor histocompatibility (H) Ags important in allogeneic
198                                  Of the many minor histocompatibility (H) Ags that have been detected
199             Unexpectedly, corneas expressing minor histocompatibility (H) alloantigens are rejected a
200 matched Balb.B spleen cells despite multiple minor histocompatibility (H) antigen differences.
201 role of the hematopoietic lineage-restricted minor histocompatibility (H) antigen HA-1 in renal allog
202                                      The H60 minor histocompatibility (H) antigen peptide is derived
203 sues accelerates rejection of MHC identical, minor histocompatibility (H) antigen-disparate skin graf
204 hich lung injury after BMT can be induced by minor histocompatibility (H) antigenic differences betwe
205                                        Since minor histocompatibility (H) antigens are the main targe
206 toxic T lymphocytes (CTL) specific for human minor histocompatibility (H) antigens can be isolated fr
207 isparity at loci outside the MHC that encode minor histocompatibility (H) antigens can elicit GVHD an
208 molecular identification of these additional minor histocompatibility (H) antigens lagged behind that
209 TCR-T) specific for hematopoietic-restricted minor histocompatibility (H) antigens may provide a pote
210            T-cell immunotherapy that targets minor histocompatibility (H) antigens presented selectiv
211                                              Minor histocompatibility (H) antigens stimulate in vivo
212  present MHC class I-restricted H3aa or H3ab minor histocompatibility (H) antigens to cytotoxic T-lym
213 stem where donor and host differ by multiple minor histocompatibility (H) antigens, we investigated t
214 red by donor T cells specific for particular minor histocompatibility (H) antigens.
215 nition of tumor-specific and host-restricted minor histocompatibility (H) antigens.
216                              The products of minor histocompatibility (H) loci are serious barriers t
217 ajor histocompatibility complex (MHC) and/or minor histocompatibility (H)-disparate recipient mice.
218 mammalian Y chromosome encodes male-specific minor histocompatibility (H-Y) Ags that are recognized b
219       The Y chromosome encodes male-specific minor histocompatibility (H-Y) antigens that stimulate T
220 utations in genes that produce male-specific minor histocompatibility (H-Y) antigens.
221 and CD8(+) T cell responses to male-specific minor histocompatibility (HY) Ags following injection of
222 l carcinoma (MB49) model expressing the male minor histocompatibility (HY) antigen was inoculated sub
223 jor histocompatibility complex plus multiple minor histocompatibility loci) and from NZB donors (mism
224 d from NZB donors (mismatch only at multiple minor histocompatibility loci).
225 was induced to grafts mismatched at multiple minor histocompatibility loci, Ag specificity was inferr
226 , differences between donor and recipient at minor histocompatibility loci, which encode allelic prot
227  certain strains of mice with differences in minor histocompatibility loci.
228 BA) receiving bone marrow transplants across minor histocompatibility loci.
229 des that effects an accelerated rejection of minor histocompatibility-locus disparate skin grafts in
230 mphocytes (CTL) responsive to immunodominant minor histocompatibility (minor H) Ags are thought to pl
231 arget cells bearing donor major (MHC) and/or minor histocompatibility (minor H) antigens (direct and
232 hese engrafted IK were transplanted across a minor histocompatibility mismatched barrier into pancrea
233 w that reconstitution of scid/scid mice with minor histocompatibility mismatched naive CD4+ T lymphoc
234 his phenomenon to the rejection of major and minor histocompatibility-mismatched allografts performed
235 kin disorders that is induced by transfer of minor histocompatibility-mismatched CD4(+)/CD45RB(high)
236                      We found that human and minor histocompatibility-mismatched donor mouse heart al
237  G-CSF mobilized allograft from MHC-matched, minor histocompatibility-mismatched donors; recipients o
238 ransplantation by transplanting MHC-matched, minor histocompatibility-mismatched grafts composed of p
239                      We have developed a new minor histocompatibility-mismatched rat kidney transplan
240                              By contrast, in minor histocompatibility-mismatched recipients, early bl
241 ures of an "infectious" tolerance pathway to minor histocompatibility-mismatched skin grafts, origina
242 n and suggest that strategies to account for minor histocompatibility mismatching may help to reduce
243 are more immunogenic than those derived from minor histocompatibility or other nominal Ags.
244 ivity to allogeneic MHC antigens rather than minor histocompatibility or tumor-associated antigens.

 
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