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1 irteen-residue, maternally transmitted minor histocompatibility antigen.
2 acid early transcript (Rae1) and H-60 minor histocompatibility antigen.
3 this issue employed the redesign of a minor histocompatibility antigen.
4 t the LIMS1 locus appeared to encode a minor histocompatibility antigen.
5 oligoclonal, pointing to a response to minor histocompatibility antigens.
6 ens, although they remained tolerant to host histocompatibility antigens.
7 -specific differentiation antigens and minor histocompatibility antigens.
8 r major histocompatibility antigens or minor histocompatibility antigens.
9 ic antigen-presenting cells presenting minor histocompatibility antigens.
10 the development of humoral immunity to minor histocompatibility antigens.
11 d by donor T cells that recognize host minor histocompatibility antigens.
12 n mismatching for cellular peptides known as histocompatibility antigens.
13 affected tissues and giving rise to multiple histocompatibility antigens.
14 ammation and up-regulation of class I and II histocompatibility antigens.
15 iated with sensitization to mismatched donor histocompatibility antigens.
16 ts that confront the host with foreign minor histocompatibility antigens.
17 is controlled by genetic factors, especially histocompatibility antigens.
18 in receptor protein 1 (TFRC) and HLA class I histocompatibility antigen A, B and C (HLA-ABC) enabled
19 The hypothesis that ICAM-1 acts as a minor histocompatibility antigen and that anti-ICAM-1 antibodi
20 ells in the glands; 4) upregulation of major histocompatibility antigens and adhesive molecules by ep
21 regulate surface expression of class I major histocompatibility antigens and also inhibit tumor necro
22 that recognize mismatched major and/or minor histocompatibility antigens and cause severe damage to h
23 o operational tolerance to the donor's major histocompatibility antigens and long-term acceptance to
24 vances in systematic identification of minor histocompatibility antigens and neoantigens arising from
25 on of Tregs against major and possibly minor histocompatibility antigens and predict the feasibility
26 and subsequent reduced presentation of minor histocompatibility antigens and reduced ligation of acti
27 nt is acquired tolerance of allogeneic minor histocompatibility antigens and that posttransplant immu
28 rolling the production of antibodies against histocompatibility antigens are of prime importance in o
30 ong MHC matched mouse strains, a few unknown histocompatibility antigens are targeted by the cytotoxi
31 the ubiquitous light chain of class I major histocompatibility antigens, as the amyloid fibril prote
32 d the shared antigens do not represent minor histocompatibility antigens, as their sequences are iden
33 orescence intensity [aMFI] >= 1000), a minor histocompatibility antigen, associated with graft failur
34 RHGDIB) (adjusted MFI [aMFI]>=1000), a minor histocompatibility antigen, associated with graft failur
35 ry pathway which reduces expression of major histocompatibility antigens at the plasma membrane and s
36 CD4+ T cell-mediated GVHD across this minor histocompatibility antigen barrier depends on the expres
37 ls (HSCs) when transplanted across the major histocompatibility antigen barriers if transplanted alon
38 ize bone marrow grafts bearing hematopoietic histocompatibility antigens bear surface markers of natu
40 ssion and near to complete mismatch of major histocompatibility antigens between the diabetic cynomol
41 oductive immunology, and how major and minor histocompatibility antigens, blood group antigens, and t
42 ed specific tolerance to both host and donor histocompatibility antigens, but normal anti-third party
43 -deficient CD8(+) T-cell response to a minor histocompatibility antigen by phenotypic and in vivo ima
48 ficient B6.gld mice as recipients in a Major Histocompatibility Antigen Complex-matched minor Histoco
51 On the other hand, the importance of minor histocompatibility antigens derived from nonhematopoieti
52 s alloimmune syndrome in recipients of minor histocompatibility antigen disparate donor cells, showin
54 radiation chimeras across the multiple minor histocompatibility antigen-disparate, C57BL/6-->BALB.B c
55 urrent dogma dictates that this is driven by histocompatibility antigen disparities between donor and
56 es across a two-haplotype class I plus minor histocompatibility antigen disparity by a 12-d course of
57 ed across a two-haplotype class I plus minor histocompatibility antigen disparity by a 12-day course
59 cells that are specific for recipient minor histocompatibility antigens encoded by Y-chromosome gene
61 nor human leukocyte antigen molecules, minor histocompatibility antigens, endothelial cells, RBCs, or
62 epends on an orchestrated immune response to histocompatibility antigens expressed by the grafted tis
63 CAID, but soluble and cell-associated (minor histocompatibility) antigens generated cell-associated A
64 c acid early inducible (RAE-1) and H60 minor histocompatibility antigen genes on mouse chromosome 10
65 c T cell clones specific for the human minor histocompatibility antigen H-Y and restricted by HLA-A*0
66 Antibody response to Y-chromosome encoded histocompatibility antigens (H-Y antigens) was also asso
69 ted that recipient mismatching for the minor histocompatibility antigen HA-1 is associated with acute
73 f alloantibody responses against foreign HLA histocompatibility antigens has never been delineated.
74 rkers (intercellular adhesion molecule-1 and histocompatibility antigen HLA-DR) in arteries and arter
75 ition mediated by Ly-49A in the mouse, human histocompatibility antigen (HLA)-B*2705-specific NK clon
76 to late phase trials and to evaluate closely histocompatibility antigen (HLA)-matched banked antigen-
80 morphic genes are known to encode functional histocompatibility antigens in mismatched individuals, b
81 HLA-B27-restricted CTL response to HY minor histocompatibility antigens in rats and mice transgenic
83 ncluding recognition of sex-determined minor histocompatibility antigens, influence of sex hormones o
84 ed by the indirect recognition of allogeneic histocompatibility antigens late in transplantation may
85 CD1 family of evolutionarily conserved major histocompatibility antigen-like molecules, controls the
87 In addition, a better understanding of minor histocompatibility antigens may lead to more targeted im
89 he immune response to DBY, a model H-Y minor histocompatibility antigen (mHA) in a male patient with
90 grafts supplemented with T cells in a minor histocompatibility antigen (mHA)-mismatched mouse model.
91 in susceptibility to immune pressure, minor histocompatibility antigen (mHa)-specific T-cell lines o
93 Next, we immunized the donor to the minor histocompatibility antigens (mHA) of the recipient by me
95 toma in a murine model of MHC-matched, minor histocompatibility antigen (mHAg)-mismatched bone marrow
98 D because of the presence of recipient minor histocompatibility antigens (mHAgs) in whole-cell tumor
99 donor T cells that recognize recipient minor histocompatibility antigens (mHAgs) is a potential strat
100 ming of donor T cells against putative minor histocompatibility antigens (mHAgs) on the tumor vaccine
107 lloreactive donor T cells against host minor histocompatibility antigens (mHAs) cause graft-versus-ho
110 ed major HLA disparities or expressing minor histocompatibility antigen (miHA) differences presented
111 rom donors vaccinated against a single minor histocompatibility antigen (miHA) expressed by leukemia
112 B6 (H-2(b)) recipients primed to donor minor histocompatibility antigen (MiHA) prior to BM transplant
114 ed, CD4-driven murine GVHD model and a minor histocompatibility antigen (MiHA)-mismatched, CD8-driven
116 lloreactive T cell responses targeting minor histocompatibility antigens (MiHA) expressed on malignan
117 nd the interaction of these cells with minor histocompatibility antigen- (miHA-) mismatched CD8+ T ce
118 D8+ stem cell memory T cells targeting minor histocompatibility antigens (MiHAs) expressed by recipie
119 itude and diversity of CD8 T cells for minor histocompatibility antigens (MiHAs) in patients with sel
120 tiate GVHD by directly presenting host minor histocompatibility antigens (miHAs) to donor CD8 cells.
121 izing polymorphic peptides, designated minor histocompatibility antigens (MiHAs), that are presented
123 nd recipient were incompatible at many minor histocompatibility antigens (minor H Ags), the CD8 T-cel
126 en Rux-chow was fed to C.B10 mice in a minor histocompatibility antigen mismatched (B6 C.B10) AA mode
129 the role of donor Stat1 in MHC-matched minor histocompatibility antigen-mismatched (mHA-mismatched) a
130 the mechanisms of DLI in MHC-matched, minor histocompatibility antigen-mismatched allogeneic chimera
131 compatibility complex-matched multiple minor histocompatibility antigen-mismatched alloHCT using bone
132 may not apply to MHC-matched, multiple minor histocompatibility antigen-mismatched alloSCT, the most
135 ngle Y chromosome-encoded, or multiple minor histocompatibility antigen-mismatched hematopoietic cell
136 ocompatibility Antigen Complex-matched minor Histocompatibility Antigen-mismatched murine model for G
137 ets, and we report that transfusion of minor histocompatibility antigen-mismatched platelets induced
139 histocompatibility complex-matched and minor histocompatibility antigen-mismatched unrelated donors a
140 usions (DLIs) were incorporated into a minor histocompatibility antigen-mismatched, T cell-depleted,
143 ntation, donors' T cells can recognize minor histocompatibility antigens on recipient cells and gener
146 by increased recipient mismatching for major histocompatibility antigens or minor histocompatibility
147 The inclusion of SNPs that encode minor histocompatibility antigens or other genetic polymorphis
148 cagon receptor, a ras-related protein (Rad), histocompatibility antigens, PC-1, and fatty acid bindin
150 (TCR) to peptide antigen presented by major histocompatibility antigens (pMHC) on antigen-presenting
151 when recipient lymphocytes encounter foreign histocompatibility antigens presented by the graft's end
152 ymes to cleavage sites and of class II major histocompatibility antigen-presenting proteins to helper
153 s that humoral and cellular sensitization to histocompatibility antigens prior to and after islet tra
155 poorly defined minor (i.e., other than HLA) histocompatibility antigens remains a serious problem in
156 The GVL effect is directed against minor histocompatibility antigens shared by normal and leukemi
157 tly suppressed the clonal expansion of minor histocompatibility antigen-specific CD8 T cells during t
158 cells do not inhibit allogeneic MHC or minor histocompatibility antigen-specific CTL production), dep
159 arrow is not matched in the clinic for minor histocompatibility antigens, such as those carried by pl
161 , skin differing from the host only by minor histocompatibility antigens undergoes slower (i.e., chro
162 d donor MHC class I and II, and of H-Y minor histocompatibility antigen was assessed by quantifying p
163 d bone marrow, mismatched for multiple minor histocompatibility antigens, was induced in Fas mutant a
164 with a response to immunodominant host minor histocompatibility antigens, we detected oligoclonal liv
165 sparities in cytoplasmically inherited minor histocompatibility antigens, we examined one hypervariab
166 ng genetic disparity in both major and minor histocompatibility antigens were used for transplantatio
168 ion of these hematopoietically derived minor histocompatibility antigens will induce significant graf