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1 to modulate allogeneic response and control transplant rejection.
2 ples from patients experiencing acute kidney transplant rejection.
3 as a target for immunomodulatory therapy of transplant rejection.
4 sorders including autoimmunity, allergy, and transplant rejection.
5 onse prediction, cancer diagnosis, or kidney transplant rejection.
6 immunity, dermatitis, periodontitis and even transplant rejection.
7 hat is a leading reflection of chronic heart transplant rejection.
8 mph nodes and beyond and also promotes organ transplant rejection.
9 s of hIL-10-TFLs are efficient in mitigating transplant rejection.
10 toimmune and allergic responses, and prevent transplant rejection.
11 ree lymphangiogenesis in mediating high-risk transplant rejection.
12 hemical insults and is a primary mediator of transplant rejection.
13 l binding partner for PDL1 other than PD1 in transplant rejection.
14 eg-dependent suppression of autoimmunity and transplant rejection.
15 ted disorders such as autoimmune disease and transplant rejection.
16 r treatment of autoimmune diseases and organ transplant rejection.
17 nt role in characterization and treatment of transplant rejection.
18 prediction and clinical management of kidney transplant rejection.
19 dominant pathway of allorecognition in acute transplant rejection.
20 role in the development of inflammation and transplant rejection.
21 mplex class II alloantigens to suppress skin transplant rejection.
22 contrasts with their prominent role in organ transplant rejection.
23 Th17 phenotype has prompted its scrutiny in transplant rejection.
24 ccessful as cyclosporin in suppressing organ transplant rejection.
25 t role for platelets in alloantibody induced transplant rejection.
26 in the treatment of autoimmune diseases and transplant rejection.
27 hy and, in particular, alloantibody-mediated transplant rejection.
28 mune and inflammatory disorders and/or organ transplant rejection.
29 type V collagen [col(V)] contributes to lung transplant rejection.
30 une and allergic diseases, or for preventing transplant rejection.
31 activation of exocytosis may play a role in transplant rejection.
32 mage, including vascular disease and chronic transplant rejection.
33 antigens" responsible for antibody-mediated transplant rejection.
34 ll antibodies used clinically to treat acute transplant rejection.
35 immunosuppressant developed to prevent organ transplant rejection.
36 mune and inflammatory disorders and/or organ transplant rejection.
37 ying the common component C4 in mouse kidney transplant rejection.
38 allogeneic MHC complexes is a major cause of transplant rejection.
39 ole in a variety of autoimmune disorders and transplant rejection.
40 in intrarenal oxygenation occur during acute transplant rejection.
41 alignancies, autoimmune disease, and humoral transplant rejection.
42 oma components, and microbubbles for imaging transplant rejection.
43 be a novel molecular target for controlling transplant rejection.
44 r necrosis factor alpha (TNF-alpha) in liver transplant rejection.
45 ung diseases such as asthma and chronic lung transplant rejection.
46 ch as autoimmunity, anti-tumor immunity, and transplant rejection.
47 ve drug that is widely used to prevent organ transplant rejection.
48 ystem for the early detection of acute renal transplant rejection.
49 causal relationship between alloantibody and transplant rejection.
50 ost, including vascular diseases and chronic transplant rejection.
51 therapeutic potential for the prevention of transplant rejection.
52 rogenic population to treat autoimmunity and transplant rejection.
53 ng clinical trials to combat immune-mediated transplant rejection.
54 nity, it remains unstudied in the context of transplant rejection.
55 heumatoid arthritis, multiple sclerosis, and transplant rejection.
56 immunity and the amelioration of allogeneic transplant rejection.
57 human kidney and their altered expression in transplant rejection.
58 xposures to cyclosporine to prevent pancreas-transplant rejection.
59 eeks to evaluate graft opacity and determine transplant rejection.
60 me Fe-S cluster protein in acute solid organ transplant rejection.
61 er number (3 x 10(6)) was required for heart transplant rejection.
62 human conditions, including autoimmunity and transplant rejection.
63 rteries, in parallel with SODD, during acute transplant rejection.
64 A, represents an ideal strategy for reducing transplant rejection.
65 calcineurin and block T-cell activation and transplant rejection.
66 atment of autoimmune diseases and to prevent transplant rejection.
67 RA mRNA up-regulation as a marker for kidney transplant rejection.
68 ata exist to guide the treatment of pancreas transplant rejection.
69 promise in dampening allergic reactions and transplant rejection.
70 ons to treat cancer, and HIV, and to prevent transplant rejection.
71 RNA expression in blood during human corneal transplant rejection.
72 for the treatment of autoimmune disease and transplant rejection.
73 with in vitro IFNgamma production and renal transplant rejection.
74 Fas mRNA in blood may have a role in corneal transplant rejection.
75 can be targeted for noninvasive detection of transplant rejection.
76 and is a prominent feature of chronic renal-transplant rejection.
77 ction, juvenile chronic arthritis, and renal transplant rejection.
78 tivity, have implicated these eicosanoids in transplant rejection.
79 trate a role for CXCR3 in the development of transplant rejection.
80 a major aim for therapy in autoimmunity and transplant rejection.
81 for the treatment of autoimmune diseases or transplant rejection.
82 is provided has not been fully delineated in transplant rejection.
83 terns in different morphological patterns of transplant rejection.
84 the indirect pathway is involved in chronic transplant rejection.
85 pool of immunogenic antigens may drive post-transplant rejection.
86 uppression decreases the rate of acute renal transplant rejection.
87 s like RANTES appear to play a role in organ transplant rejection.
88 urine monoclonal antibodies for treatment of transplant rejection.
89 sitive for the detection of acute pancreatic transplant rejection.
90 treat T cell-mediated pathologies, including transplant rejection.
91 ene transcripts to refine diagnosis of heart transplant rejection.
92 for pathogen surveillance, autoimmunity, and transplant rejection.
93 T cells and contributes to T cell-dependent transplant rejection.
94 ventricular assist device complications and transplant rejection.
95 ecule may promote inflammatory responses and transplant rejection.
96 ction between molecules with a known role in transplant rejection.
97 fluence of host and donor microbiota on skin transplant rejection.
98 schemic reperfusion injury (IRI), and tissue transplant rejection.
99 ce of immunosuppression, to T cell-dependent transplant rejection.
100 ers such as autoimmune disease and allograft transplant rejection.
101 s in endomyocardial biopsy samples to assess transplant rejection.
102 cer, autoimmune and infectious diseases, and transplant rejection.
103 teract during allogeneic encounters and thus transplant rejection.
104 umatoid arthritis, gout, sepsis, stroke, and transplant rejection.
105 to the heart during inflammation and cardiac transplant rejection.
106 and/or ameliorating autoimmune diseases and transplant rejection.
107 ated T-cell costimulation and prevents renal transplant rejection.
108 a target for the prevention and treatment of transplant rejection.
109 nsitive and quantitative diagnostic test for transplant rejection.
110 ant model was used to study NK cell-mediated transplant rejection.
111 graft tolerance dominates over the memory of transplant rejection.
112 lex alleles, the most potent determinants of transplant rejection.
113 treatment with respect to suppressing immune transplant rejection.
114 hways may also contribute to pathogenesis of transplant rejection.
115 ls became activated, ultimately resulting in transplant rejection.
116 d autoimmune disease, cancer, infection, and transplant rejection.
117 t is particularly important in infection and transplant rejection.
118 clinical consequence of treatment to prevent transplant rejection.
119 increased memory T cells, which may promote transplant rejection.
120 ine interleukin-17, which has been linked to transplant rejection.
121 herapies of inflammatory kidney diseases and transplant rejection.
122 t include degenerative diseases, cancer, and transplant rejection.
123 erived components as immune suppressants for transplant rejection.
124 toimmunity, as well as for the prevention of transplant rejection.
125 ion secondary to infection, inflammation, or transplant rejection.
126 We showed that in models of autoimmunity and transplant rejection, adoptive transfer of antigen-speci
127 n was restricted to patients at low risk for transplant rejection; among high-risk patients, alemtuzu
128 une-mediated tissue injury following cardiac transplant rejection, an in vivo model of intense inflam
130 ells are significant mediators of hepatocyte transplant rejection and are relatively resistant to cos
132 lective immunosuppressive agents to mitigate transplant rejection and autoimmune diseases requires ef
137 fer and more convenient treatments for organ transplant rejection and autoimmune disorders such as rh
139 Th cells are the major effector cells in transplant rejection and can be divided into Th1, Th2, T
140 e latter five demonstrated at least moderate transplant rejection and caspase-3 staining, suggesting
141 AP between patients at high risk for corneal transplant rejection and control subjects (P<0.001).
142 ls for the treatment of autoimmune diseases, transplant rejection and graft-versus-host disease.
143 le of resident versus circulating T cells in transplant rejection and in providing protection to prev
145 stigated, despite the increased incidence of transplant rejection and inferior allograft outcomes in
146 ney transplant recipients who develop severe transplant rejection and malignant hypertension during t
147 pregulated in patients with kidney and heart transplant rejection and may account for perpetuation of
148 ancers, autoimmune disorders, infection, and transplant rejection and may help to design better vacci
149 ed to study the role of human macrophages in transplant rejection and other pathologies in vivo.
150 technique for the detection of acute cardiac transplant rejection and other processes characterized b
151 ping immunotherapeutic approaches to inhibit transplant rejection and potentially other immune-mediat
152 Nanoparticle macrophage PET-CT detects heart transplant rejection and predicts organ survival by repo
153 Allograft loss was associated with chronic transplant rejection and recurrence of lupus nephritis.
155 lation was also identified between high-risk transplant rejection and severe lymphatic invasion reach
156 HLA variation is a crucial determinant of transplant rejection and susceptibility to a large numbe
158 We hypothesize that prolonged T2 reflects transplant rejection and that quantitative T2 mapping wi
159 loreactive plasma cells in acute Ab-mediated transplant rejection and their autoreactive counterparts
163 for the treatment of autoimmune diseases and transplant rejection and toward modification of tumor im
165 of such diverse diseases as atherosclerosis, transplant rejection and tumor-related angiogenesis.
169 allograft survival in vivo, prevents corneal transplant rejection, and attenuates the progression and
171 nct sensitivity to growth factor blockade in transplant rejection, and CD28/CD154-independent rejecti
172 injury, end-stage renal failure, acute renal transplant rejection, and delayed allograft function.
173 ated conditions such as autoimmune diseases, transplant rejection, and graft-versus-host disease.
174 ctivity can attenuate autoimmunity and delay transplant rejection, and heat shock proteins derived fr
175 of chronic DC-triggered autoimmune diseases, transplant rejection, and hematologic malignancies with
176 expressed in a regulated manner during renal transplant rejection, and identify DR3 as a potential in
179 de novel therapies for corneal inflammation, transplant rejection, and other lymphatic-related disord
180 e forms of renal pathology, emphasizing CKD, transplant rejection, and polycystic kidney disease and
181 potent but short-lived stimulators of early transplant rejection, and recipient antigen presenting c
183 dely recognized as playing a pivotal role in transplant rejection, and several studies have shown tha
185 rodegenerative states, organ and bone marrow transplant rejection, and tumor response to chemotherapy
186 's disease, diabetes, multiple sclerosis and transplant rejection appear to be the next burgeoning ph
187 ge-based diagnosis of acute allogeneic renal transplant rejection (AR) established in a rat model.
188 progression of clinically significant heart transplant rejection are currently monitored by serial b
191 T cells resisting to CD28/CD154 blockade in transplant rejection are sensitive to OX40 blockade and
193 s, such as atherosclerosis acute and chronic transplant rejection, arthritis, influenza, and malaria
194 ons should have applications in treatment of transplant rejection as well as autoimmune diseases.
197 nt sites, as well as its known role in organ transplant rejection, autoimmune disease development and
199 d, has clinical utility for the treatment of transplant rejection based on its inhibition of IMPDH.
200 mmunity appears to extend to a lower rate of transplant rejection because patients with pretransplant
201 Bortezomib in Late Antibody-Mediated Kidney Transplant Rejection [BORTEJECT] Trial), we investigated
203 globulin (Thymoglobulin) effectively treats transplant rejection but induces anti-rabbit Ab response
204 oduces clinical immunosuppression preventing transplant rejection but is associated with transient br
205 ng effector mechanisms associated with acute transplant rejection but that it is required for initiat
206 cognized as a contributor to inflammation in transplant rejection but without detailed analysis of it
207 Platelets have been described as markers of transplant rejection, but little investigation has criti
208 elets have been long described as markers of transplant rejection, but the contribution of platelets
209 the adaptive immune system are critical for transplant rejection, but the role of the innate immune
210 the transplanted kidney are known to mediate transplant rejection, but which of the three main activa
212 may improve autoimmune diseases and prevent transplant rejection by suppressing the differentiation
213 nexin-V imaging for noninvasive detection of transplant rejection by targeting cell membrane phosphol
215 ated inhibition of alloresponses involved in transplant rejection correlates with CD86 saturation, in
217 ggest that while alloimmunity initiates lung transplant rejection, de novo autoimmunity mediated by c
218 HHV-6 reactivation has been associated with transplant rejection, delayed engraftment, encephalitis,
219 hangiogenesis mediates diseases like corneal transplant rejection, dry eye disease, and allergy.
220 plicated in costimulation blockade-resistant transplant rejection, due to their enhanced effector fun
221 causal relationship between alloantibody and transplant rejection-especially chronic rejection-has be
223 diseases, ranging from cancer metastasis to transplant rejection, for which there is little effectiv
225 ection, but the contribution of platelets to transplant rejection has not been critically examined.
228 suppressant used for the prevention of renal transplant rejection, has recently emerged as an effecti
229 tes numerous immunologic effects relevant to transplant rejection; however, its specific contribution
230 diovascular diseases including acute cardiac transplant rejection; however, the contribution of ECM-d
231 linically relevant disease states, including transplant rejection, hypertension, acute renal injury,
233 been used successfully for the treatment of transplant rejection in clinical practice, it may be a u
234 eration, abnormal growth, or immune mediated transplant rejection in either patient during the first
235 he strength, phenotype, or kinetics of heart transplant rejection in mice and (b) does not impact the
236 has now been generated and is effective for transplant rejection in nonhuman primates and other mode
238 reductions were found in risk of acute renal transplant rejection in recipients who possessed the CCR
239 ligand (aCD40L) can prevent autoimmunity and transplant rejection in several animal models and is cur
241 may actually be potent facilitators of organ transplant rejection in the absence of T-bet and RORgamm
243 es are a major factor in producing "chronic" transplant rejection, including the arteriopathy (athero
245 induce graft beds that promote high risk of transplant rejection, intrastromal corneal sutures were
246 The diagnostic gold standard for detecting transplant rejection involves a core biopsy, which is in
247 d during this study suggest that small bowel transplant rejection is associated with changes in the m
251 f their role in transplant immunobiology and transplant rejection is extremely limited and fragmentar
256 which is by itself ineffective in prolonging transplant rejection, is much more efficacious in prolon
258 nt are major determinants of the kinetics of transplant rejection, little is known about the contribu
259 on regimens that have reduced rates of acute transplant rejection, long-term allograft survival remai
260 ion injury; however, it also occurs in organ transplant rejection, major trauma, severe burns, the an
265 seases as diverse as lymphedema, filariasis, transplant rejection, obesity, and tumor metastasis.
266 ferences were sufficient to stimulate robust transplant rejection of wild-type cells in mutant mice.
267 o protect the host and chronic inflammation, transplant rejection, or other disorders may occur.
268 ional relevance of the semidirect pathway to transplant rejection, our findings provide a solution to
270 This suggests that a capacity to regulate transplant rejection pre-exists in naive mice, and may b
273 , patients with myocarditis had similar post-transplant rejection, retransplantation, and survival ra
276 they may represent the natural initiators of transplant rejection, spontaneous tumor rejection, and s
277 of CD4(+) T cells, mediate cytotoxicity and transplant rejection that is exclusively TNF-alpha/TNFR-
278 ases, including vascular disease and chronic transplant rejection, that involve vascular endothelial
279 torically, antibodies were thought to elicit transplant rejection through complement mediated damage
280 number of T cells that typically drive acute transplant rejection through their ability to directly i
281 ple of urine serine hydrolase ABPP in kidney transplant rejection to illustrate the utility and workf
282 -fits-all" immunosuppression for controlling transplant rejection to precision medicine and targeted
285 h NK cells in a model of Tcell-mediated skin transplant rejection under costimulatory blockade condit
286 development to treat autoimmune diseases and transplant rejection, underscoring the importance in und
288 hypothesize that CO may protect against lung transplant rejection via its anti-inflammatory and antia
291 vel therapeutic targets for autoimmunity and transplant rejection, we developed and performed a large
292 ys in identifying pathways involved in organ transplant rejection, we examined the gene expression pr
293 of regulatory T cells capable of preventing transplant rejection, we have developed two different st
294 haptoglobin enhanced the onset of acute skin transplant rejection, whereas haptoglobin-deficient skin
295 lant recipients and those experiencing acute transplant rejection, which revealed hundreds of differe
296 l. debunk two classical paradigms concerning transplant rejection, with important consequences for th
297 ing skin necrosis contributes to accelerated transplant rejection, with potential implications for th
299 variety of corneal abnormalities, including transplant rejection, wound healing and microbial kerati
300 for example, ischemia-reperfusion injury and transplant rejection yet is beneficial for liver tissue