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1 eases such as cancer, lymphedema, and tissue allograft rejection.
2 eyes developed typical clinical signs of an allograft rejection.
3 al in directing host immune reactions toward allograft rejection.
4 ications, bleedings, anastomotic leakage, or allograft rejection.
5 y have a protective role and attenuate overt allograft rejection.
6 phology were found to "announce" an upcoming allograft rejection.
7 reactivity including autoimmune diseases and allograft rejection.
8 Little data exist on these markers during allograft rejection.
9 pendently predicts a decreased risk of acute allograft rejection.
10 tute promising approaches for the control of allograft rejection.
11 ell numbers in naive mice and hastened islet allograft rejection.
12 ffector T cells in situ, and correlated with allograft rejection.
13 latation and permeability is observed during allograft rejection.
14 play an important role in acute and chronic allograft rejection.
15 unopathology in human autoimmune disease and allograft rejection.
16 dy-producing plasma cells to reverse humoral allograft rejection.
17 T cell responses that drive autoimmunity and allograft rejection.
18 that underlies IL-4 neutralization-resistant allograft rejection.
19 rate with other effector mechanisms to cause allograft rejection.
20 mation, and that NK-cell deficiency enhanced allograft rejection.
21 hat extent NK cells can influence mouse lung allograft rejection.
22 o the response to steroid treatment of acute allograft rejection.
23 yte globulin (ATG) have been shown to reduce allograft rejection.
24 is reported to promote KS regression without allograft rejection.
25 llular and humoral mechanisms of acute renal allograft rejection.
26 fic activated (Bonzo) T cells during corneal allograft rejection.
27 nt activation leading to accelerated cardiac allograft rejection.
28 plantation model was used for studying acute allograft rejection.
29 -fms kinase inhibitor (fms-I) in acute renal allograft rejection.
30 r the amelioration of human autoimmunity and allograft rejection.
31 gets in some liver diseases, including acute allograft rejection.
32 wly generated host Tregs can prevent chronic allograft rejection.
33 nologic mechanism underlying smoking-related allograft rejection.
34 ssion of Bcl-xL in Drak2-/- T cells restored allograft rejection.
35 h revokes immune privilege, prevents corneal allograft rejection.
36 terize the metabolomic profile of intestinal allograft rejection.
37 red to reflect the evolution of chronic lung allograft rejection.
38 he predominant manifestation of chronic lung allograft rejection.
39 but its clinical applicability is limited by allograft rejection.
40 eficiency prevented T-cell priming and islet allograft rejection.
41 SF25 agonists expand Tregs in vivo and delay allograft rejection.
42 ective cure of HCV infection without risk of allograft rejection.
43 ST), although it failed to alter acute islet allograft rejection.
44 ched, life-sustaining murine model of kidney allograft rejection.
45 s also play a role in bone marrow cell (BMC) allograft rejection.
46 city and endothelial vasculopathy in chronic allograft rejection.
47 efined roles in the pathophysiology of renal allograft rejection.
48 enal ischemia reperfusion injury and cardiac allograft rejection.
49 -6 production affects Th1/Th2 balance during allograft rejection.
50 ferentiation of the immune cells involved in allograft rejection.
51 bitors R507 and R545 for prevention of acute allograft rejection.
52 hallmark of antibody-mediated chronic renal allograft rejection.
53 moking is one of major risk factors for late allograft rejection.
54 h AKI and 9 (4.9%) were diagnosed with acute allograft rejection.
55 entify plasma proteins associated with renal allograft rejection.
56 ng that B cells can also negatively regulate allograft rejection.
57 o detect medication nonadherence and prevent allograft rejection.
58 as also been implicated in cardiac and renal allograft rejection.
59 as early serum markers for monitoring acute allograft rejection.
60 e impact of DSA in the setting of intestinal allograft rejection.
61 mbers or function can cause autoimmunity and allograft rejection.
62 atibility complex (MHC)-incompatible cardiac allograft rejection.
63 for novel therapeutic treatment for cardiac allograft rejection.
64 this is associated with acute cellular renal allograft rejection.
65 should be considered for preventing cardiac allograft rejection.
66 s during an infection, malignancy, and acute allograft rejection.
67 anti-endothelial cell antibodies (AECAs) in allograft rejection.
68 , allergic keratoconjunctivitis, and corneal allograft rejection.
69 post-transplant and demonstrated a delay in allograft rejection.
70 nd airway hyperreactivity exacerbate corneal allograft rejection.
71 cient (gld) CD4 T cells demonstrated delayed allograft rejection.
72 antagonist-mediated HSC release and restored allograft rejection.
73 zation increases the risk of T cell-mediated allograft rejection.
74 as a potential prognosis marker for chronic allograft rejection.
75 e for an important role of IL-6 in mediating allograft rejection.
76 es the loss of immune tolerance and promotes allograft rejection.
77 novo after lung transplantation and mediate allograft rejection.
78 Treg were insufficient to prevent acute lung allograft rejection.
79 osuppressants which are essential to prevent allograft rejection.
80 e T lymphocytes are the primary mediators of allograft rejection.
81 stablish the role of RIP3 in chronic cardiac allograft rejection.
82 olid organ transplants, primarily because of allograft rejection.
83 ly, our study demonstrated that aging delays allograft rejection.
84 on and T cell priming, ultimately leading to allograft rejection.
85 ched, life-sustaining, murine model of renal allograft rejection.
86 microRNAs (miRNAs), leading to chronic lung allograft rejection.
87 s of kidney dysfunction and acute or chronic allograft rejection.
88 sM(C)(re) Mtor(fl/fl) ) did not affect acute allograft rejection.
89 22 SNPs on the susceptibility to acute liver allograft rejection.
90 une responses that drive atherosclerosis and allograft rejection.
91 raft model, resulting in rapid acute cardiac allograft rejection.
92 and have been implicated in the mediation of allograft rejection.
93 mphoma, graft-versus-host disease, and organ allograft rejection.
94 tion of the alloantibody response, and rapid allograft rejection.
95 otoxic CD8 T-cell responses that cause rapid allograft rejection.
96 cells (ECs) damaged during transplant drives allograft rejection.
97 peutic target to reduce this form of corneal allograft rejection.
98 c kidney disease and a history of hyperacute allograft rejections.
99 After 6 months, the main complications were allograft rejection (2.4%) and secondary graft failure (
100 hways involved in immune responses including allograft rejection (6.69) and graft-versus-host disease
101 repress recipient DC activation and suppress allograft rejection after DST, and suggest CD47 as a pot
102 lograft function and diagnosing chronic lung allograft rejection after lung transplantation (LTx).
104 as multiple sclerosis, rheumatoid arthritis, allograft rejection after transplantation, and also in c
105 cell depletion did not affect acute cardiac allograft rejection, although CD19 mAb treatment prevent
106 tively deplete monocyte/macrophages in acute allograft rejection, although this did not result in sig
107 development of future strategies to prevent allograft rejection.Although both direct and indirect pa
109 19 mAb treatment significantly reduced renal allograft rejection and abrogated allograft-specific IgG
110 e of CSE with propargylglycine delayed heart allograft rejection and abrogated type IV hypersensitivi
111 contrast, B cell depletion exacerbated skin allograft rejection and augmented the proliferation of a
112 inting efficacy in the prevention of chronic allograft rejection and carry unacceptable risks includi
113 risks associated with incidences of chronic allograft rejection and decreased survival in transplant
117 currently being tested in trials to control allograft rejection and graft versus host disease.Thymic
118 ate goal of utilising Tregs as treatment for allograft rejection and graft-versus-host disease (GvHD)
119 T cells (Tregs) is a promising treatment for allograft rejection and graft-versus-host disease (GVHD)
120 ntitative technique for serial monitoring of allograft rejection and has potential application in hum
121 h protected them from both acute and chronic allograft rejection and increased their survival after t
124 quences would provide essential insight into allograft rejection and lead to better therapies for tra
125 , where infections have been associated with allograft rejection and may be a causal event precipitat
129 hysiologic mechanisms involved in intestinal allograft rejection and potentially to identify noninvas
130 more, exogenous endostatin treatment delayed allograft rejection and promoted survival secondary to a
131 s in the phenotype of BEC during acute liver allograft rejection and the mechanism driving these chan
132 aim to define the role of P2XRs during islet allograft rejection and to establish a novel anti-P2XRs
133 determine the function of IL-6 in regulating allograft rejection and tolerance, BALB/c cardiac grafts
134 of a nonmucosal tissue would affect corneal allograft rejection and whether Th2 cells alone accounte
135 emonstrate signatures of 'PD-1 signalling', 'allograft rejection' and 'T-cell receptor signalling', a
136 HHV-6 on the occurrence of other infections, allograft rejection, and outcomes after liver transplant
137 t macrophages are essential in acute cardiac allograft rejection, and selective depletion of macropha
138 cal role in the development of autoimmunity, allograft rejection, and spontaneous as well as therapy-
139 M2 cells is critical for preventing chronic allograft rejection, and that graft survival under such
140 ed a role for the purinergic system in islet allograft rejection, and the targeting of P2X7R is a nov
142 ximab for the treatment of CD20+ acute renal allograft rejection (AR) demonstrated transient depletio
144 l of understanding how immune adaptation and allograft rejection are linked, and conversely how a sys
146 required for in vivo-mismatched bone marrow allograft rejection as well as for NK memory responses t
147 eutralized IL-6 in settings of acute cardiac allograft rejection associated with either CD8(+) or CD4
148 e evidence regarding antibody-mediated liver allograft rejection at the 11th, 12th, and 13th meetings
149 e have been implicated as effectors in acute allograft rejection based on short-term depletion studie
150 on and adaptive immunity under conditions of allograft rejection, but little is known regarding their
151 phages are recognized as a hallmark of acute allograft rejection, but the roles that they play are no
152 igate the role of macrophages in acute heart allograft rejection by cellular and functional MRI with
153 ecific mechanisms involved in suppression of allograft rejection by helminth parasites could lead tow
155 on and intimal expansion in a model of human allograft rejection by inhibiting an increase in CD161(+
156 in murine models of acute or chronic cardiac allograft rejection by transplanting recipients that eit
160 (CsA), an immunosuppressant used to prevent allograft rejection, can also increase the risk of RCC i
161 expressing Th2 cells, which promptly induced allograft rejection characterized by a Th2-type intragra
163 T cell-deficient mice resulted in decreased allograft rejection compared with wild-type controls.
164 flammatory cell infiltration and accelerated allograft rejection compared with WT DCs from transferre
166 can either positively or negatively regulate allograft rejection depending on the nature of the allog
167 f bm12 allografts led to accelerated cardiac allograft rejection, despite similar mean BP and serum s
169 The primary endpoint of the study was acute allograft rejection during a 1-year follow-up period.
170 t functions in cancer immunosurveillance, BM allograft rejection, fighting infections, tissue homeost
171 ally by us and others as a means of reducing allograft rejection following organ transplantation.
173 ate a rejection episode and/or to prevent an allograft rejection from clinically manifesting itself.
174 tive cut-off, accurately discriminates acute allograft rejection from other causes of AKI in follow-u
175 osis of AKI, accurately discriminating acute allograft rejection from other causes of AKI in renal al
177 to estimate the time-related probability of allograft rejection, graft failure, and KC recurrence.
178 ations were performed to study acute cardiac allograft rejection, graft survival, suppression of cell
179 sed to prevent or treat organ or bone-marrow allograft rejection, graft versus host disease, and auto
180 ly confirmed and clinically relevant chronic allograft rejection (group 2); 16 of these have already
184 A antiendothelial cell antibodies (AECAs) in allograft rejection; however, evidence linking AECAs of
185 ory populations have the capacity to inhibit allograft rejection; however, their compensatory capacit
186 that, whereas Th17 cells predictably promote allograft rejection, IL-4-producing GATA-3(+) Th2 cells,
189 vo expanded human T(reg) to inhibit vascular allograft rejection in a humanized mouse model of arteri
191 e examine the participation of TLR4 in acute allograft rejection in an orthotopic mouse model of SIT.
199 in type A receptor (ETAR) is associated with allograft rejection in kidney and heart transplantation.
200 ntibodies and autoantibodies are involved in allograft rejection in kidney and heart transplantation.
203 CD4 TFH/GC B cell numbers and hastened islet allograft rejection in naive 12-week old Qa-1 deficient
204 154 pathway has been effective at preventing allograft rejection in numerous transplantation models.
205 dication nonadherence and the possibility of allograft rejection in pediatric renal transplantation.
206 e to CD154 has been successful at preventing allograft rejection in preclinical models, there have be
207 tute for Th1 cells and produced 100% corneal allograft rejection in recipients of Th2 cells alone.
210 Moreover, Eomes may rescue Th1-mediated allograft rejection in the absence of IL-4, T-bet, and R
211 therapy that provides protection from early allograft rejection in the absence of systemic immunosup
217 increased T-cell activation and exacerbated allograft rejection, indicating a previously unrecognize
219 d CD8 T cells also did not prevent the renal allograft rejection induced by memory helper T cells sta
220 mma neutralization did not prevent the renal allograft rejection induced by memory helper T cells, an
221 ked, and conversely how a system works where allograft rejection is a desired outcome rather than an
223 nsplant models, the authors demonstrate that allograft rejection is accelerated in mice with a normal
227 unosuppressive reagents for preventing islet allograft rejection is associated with severe complicati
234 The profound involvement of cytokines in allograft rejection makes the molecules that control the
237 ade of OX40-OX40L interactions prevents skin allograft rejection mediated by either subset of T cells
239 ations after transplantation include chronic allograft rejection, nephrotoxicity from calcineurin inh
240 statistical data that associate smoking with allograft rejection, no any study has been conducted to
241 sly described in vivo effects on bone marrow allograft rejection observed with anti-Ly49A treatment i
243 transplantation, we demonstrated that acute allograft rejection occurred equally in MyD88-sufficient
245 their immunoglobulin products participate in allograft rejection of transplanted human kidneys in whi
249 m rs1050501 affected susceptibility to renal allograft rejection or loss and transplant recipient sur
250 dministration in rats, and prevented corneal allograft rejection over the entire 9-week study when ad
251 ert different effects on mechanisms of renal allograft rejection, particularly at the level of Tfh ce
252 he effect of complement inhibition on kidney allograft rejection phenotype and the clinical response
253 ciated with a specific histomolecular kidney allograft rejection phenotype that can be abrogated by c
254 is study that following T cell initiation of allograft rejection, platelets contribute to T cell recr
255 approach, however, is severely curtailed by allograft rejection primarily initiated by pathogenic ef
258 ntation (SIT) have improved in recent years, allograft rejection rates remain among the highest of so
259 periodate-oxidized ATP [oATP]) delays islet allograft rejection, reduces the frequency of Th1/Th17 c
262 the use of immunosuppressive drugs, chronic allograft rejection remains a major hurdle in transplant
267 whether the development of acute and chronic allograft rejection requires TLR signaling is unknown.
269 s of dd-cfDNA and correlated the levels with allograft rejection status ascertained by histology in 1
270 easured in urinary cells and correlated with allograft-rejection status with the use of logistic regr
272 clodronate-liposomes protects hearts against allograft rejection, suggesting a potential therapeutic
273 like PDL1 blockade failed to accelerate bm12 allograft rejection, suggesting a role for an additional
274 The non-HLAabs group had a higher rate of allograft rejection than controls (80% vs 55%), especial
275 l avenues for the treatment or prevention of allograft rejection that complement contemporary immunos
276 ed interplay between specific mRNA/miRNAs in allograft rejection that drive both immune-mediated inju
277 gs describe a distinct late phase of corneal allograft rejection that is likely mediated by Th17 cell
278 f antidonor class I MHC antibody can mediate allograft rejection, that donor-reactive CD8 T cells syn
279 ncreasingly recognized to contribute to lung allograft rejection, the significance of endogenous inna
280 tion (OHT) and correlated it with pathologic allograft rejection, tissue iNOS levels, and calculated
281 myocardium, cardiac fibrosis due to chronic allograft rejection up to 15 years after transplantation
283 10 displayed no significant features of skin allograft rejection upon histological analysis at 70 day
285 , we investigated the role of TLR4 in kidney allograft rejection using a fully major histocompatibili
286 of BLyS-directed immunotherapy in preventing allograft rejection using a murine islet transplantation
288 investigated the role of MRP-8/14 in cardiac allograft rejection using MRP-14(-/-) mice that lack MRP
294 use these immune cells are involved in islet allograft rejection, we hypothesized that transplantatio
295 transplantation; A/H antigen expression and allograft rejection were assessed in graft biopsies.
296 = 0.0014), as well as the diagnosis of acute allograft rejection, which is preceded by increased immu
299 vant biologic target for controlling GVHD or allograft rejection without broader immune impairment.
300 r protein is an important mediator of kidney allograft rejection, yet the precise role of MyD88 signa
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