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1 a treatment option in sepsis associated with immunosuppression.
2 ncreas tissue and (b) the need for life-long immunosuppression.
3 acept-based, compared with tacrolimus-based, immunosuppression.
4 ge and limits extrinsic myeloid and lymphoid immunosuppression.
5 orted by RANK-expressing tumor cells, induce immunosuppression.
6 omplicated infection (eg, abscess) or severe immunosuppression.
7 buting to both immune homeostasis and cancer immunosuppression.
8 nomodulator were frail in the 2 years before immunosuppression.
9 , on tumor-infiltrating leukocytes eliciting immunosuppression.
10 umorigenicity and lung metastasis is through immunosuppression.
11 tumor effects and to inhibit surgery-induced immunosuppression.
12 higher risk for long-term complications from immunosuppression.
13 ted in cancers to inhibit T cells and elicit immunosuppression.
14 medical advice, the patient discontinued all immunosuppression.
15 not receive a transplant (11.6%) are without immunosuppression.
16 immunosuppression.
17 ical technique, type of donor, and induction immunosuppression.
18 in 28.5% of the cases after minimization of immunosuppression.
19 cancer, independently from age, gender, and immunosuppression.
20 antation in addition to post-transplantation immunosuppression.
21 d tacrolimus for partial lymphocyte-directed immunosuppression.
22 prolong graft function and elicit localized immunosuppression.
23 B1 and is important for T(reg) cell-mediated immunosuppression.
24 ystem, early surgery, indwelling devices, or immunosuppression.
25 rrhosis had excessive alcohol consumption or immunosuppression.
26 900 days, with rejection only after reducing immunosuppression.
27 into consideration the potential effects of immunosuppression.
28 transplant to minimise the burden of general immunosuppression.
29 acellular matrix remodelling, metastasis and immunosuppression.
30 rejection and the requirement for long-term immunosuppression.
31 They are linked by the net state of immunosuppression.
32 impair nanomedicine delivery can also cause immunosuppression.
33 ature with upregulation of genes involved in immunosuppression.
34 hesized that IL17 triggers and sustains PDAC immunosuppression.
35 ic infections attributable to induced global immunosuppression.
36 0 copies/ml that resolved after reduction of immunosuppression.
37 transplant model in the absence of exogenous immunosuppression.
38 demonstrated a dramatic clinical response to immunosuppression.
39 from latency beyond their general effects on immunosuppression.
40 epatocytes were rejected but engrafted after immunosuppression.
41 odies, but they are unresponsive to standard immunosuppression.
42 mal tumor microenvironment (TME)-that causes immunosuppression.
43 monitored closely in the setting of lowered immunosuppression.
44 key diabetes-related genes in the context of immunosuppression.
45 imilar risks across strata of viral load and immunosuppression.
46 T (iNKT) cells with glycolipid antigen drove immunosuppression.
47 -host disease (GVHD) results from inadequate immunosuppression.
48 e used to guide personalized post-transplant immunosuppression.
49 thus, contribute to tumor proliferation and immunosuppression.
50 ft thickness in a murine model of transplant immunosuppression.
51 tation of engineered cells in the absence of immunosuppression.
52 robial constituents promote inflammation and immunosuppression.
53 ontrols islet autoimmunity without long-term immunosuppression.
54 male Mecp2 mutant mice that was overcome by immunosuppression.
55 for treatment thereby removing the need for immunosuppression.
56 nfection, cancer, and other complications of immunosuppression.
57 ons in markers and cytokines associated with immunosuppression.
58 he Cxcl8 pathway exhibited dominance despite immunosuppression.
59 life-threatening infections due to lifelong immunosuppression.
60 ent-dependent cytotoxicity through relief of immunosuppression.
61 he potential to obviate the need for chronic immunosuppression.
62 ed therapeutic interventions such as reduced immunosuppression.
63 nucleosis that showed a dramatic response to immunosuppression.
64 months following a standardized reduction in immunosuppression.
65 ion corresponded with indicators of systemic immunosuppression.
66 compare outcomes of SLKT, based on induction immunosuppression.
67 by activating cellular pathways that lead to immunosuppression.
68 sistant bacteria-induced sepsis in mice with immunosuppression.
69 tional tolerance after complete cessation of immunosuppression.
70 togenic genes dysregulated in the context of immunosuppression.
71 ted with increased mortality and features of immunosuppression.
72 r promotion by severe, prolonged HIV-induced immunosuppression.
73 on of Treg in AA, which predicts response to immunosuppression.
74 tore self-tolerance without inducing chronic immunosuppression.
75 rvival depends on reversal of the underlying immunosuppression.
76 ieving transplantation without the requisite immunosuppression.
80 ologic response rates even in the setting of immunosuppression after transplantation, these HCV-virem
82 ne cells [MICs]), induced long-term specific immunosuppression against the allogeneic donor.METHODSIn
84 9 due the high prevalence of co-morbidities, immunosuppression and ageing, a detailed analysis of the
85 es are being studied(7), which often involve immunosuppression and are not efficient in removing pre-
88 most significantly upregulated genes in both immunosuppression and diabetes subsets and were appropri
89 transplantation (HT), where the advances in immunosuppression and donor selection strategies have le
90 d STING agonists could help to reduce tumour immunosuppression and enhance the efficacy of a wide ran
91 TANCE Chronic viral infections may result in immunosuppression and enhanced susceptibility to infecti
94 in vivo mechanisms underlying sepsis-induced immunosuppression and identify TNFR2pos Treg as targets
95 In addition to established risk factors (immunosuppression and infectious mononucleosis), allergi
96 Kgamma constitutes an opportunity to mediate immunosuppression and inflammation within the tumor micr
97 Rubcn(-/-) mice are resistant to UV-induced immunosuppression and instead display exaggerated inflam
101 strate that brain cancers cause multifaceted immunosuppression and pinpoint circulating factors as a
102 /TA-encapsulated islets can elicit localized immunosuppression and potentially delay graft destructio
103 is the most important agent for maintenance immunosuppression and prevention of immunologic injury t
104 lant and patient outcomes due to advances in immunosuppression and prevention of posttransplantation
105 observed, most likely due to advancements in immunosuppression and preventive strategies, including p
108 -cleaving Cas nucleases, which cause limited immunosuppression and require multiple infections to byp
109 felong disease activity, implying a need for immunosuppression and risk of malignancy, must be weighe
110 matory phase of sepsis improves, post-sepsis immunosuppression and secondary infection have increased
111 d acute rejection correlates with troughs in immunosuppression and subsides when immunosuppressive ta
112 e or inhibition of mTOR by rapamycin reduced immunosuppression and susceptibility to secondary Candid
113 onstrate that LAP is required for UV-induced immunosuppression and that UV exposure induces a broadly
116 t can lead to minimization or elimination of immunosuppression and, it is hoped, help revitalize the
117 of tacrolimus/mammalian target of rapamycin immunosuppression, and an acute rejection event were ind
118 regulatory T (Treg)-cells, where it mediates immunosuppression, and by a subset of T-helper (Th) 17-c
119 y recapitulates the persistent inflammation, immunosuppression, and catabolism syndrome observed in a
121 ion, but the procedure is invasive, requires immunosuppression, and could cause other complications s
122 ase, lung disease, kidney disease, diabetes, immunosuppression, and liver disease were associated wit
124 lection, donor and HTx recipient management, immunosuppression, and pretransplant mechanical circulat
125 stic response that promotes hypovascularity, immunosuppression, and resistance to chemo- and immunoth
126 er the expansion of those cells that survive immunosuppression, and this expansion could be associate
127 Clinical presentation, laboratory values, immunosuppression, and treatment strategies were reviewe
128 nse, tests for quantifying the "net state of immunosuppression," and genetic polymorphisms associated
130 icantly dysregulated genes in the context of immunosuppression are implicated in insulin signaling an
131 rent paramyxoviruses, like neurotoxicity and immunosuppression, are now understood in the light of re
134 lects meticulous attention to the details of immunosuppression, balancing risks for graft rejection a
135 to Tac withdrawal or maintenance of standard immunosuppression beginning 6 months after transplant.
136 Ms promote tumor-associated angiogenesis and immunosuppression by altering metabolism in breast cance
137 ese findings characterize a new mechanism of immunosuppression by hypoxia via downregulation of the t
138 reduced due to immunological immaturity and immunosuppression by RSV-specific maternal antibodies.
140 ts have been made to circumvent the need for immunosuppression by using various techniques to achieve
141 ting the expression of genes associated with immunosuppression, chemotaxis, and tumor matrix remodeli
142 ults provide a possible mechanism behind the immunosuppression commonly seen in breast cancer patient
146 We hypothesized that patients with advanced immunosuppression could be stratified into inflammatory
147 In a threshold analysis, the extension of immunosuppression coverage was cost-effective at a willi
148 graft survival in the absence of continuing immunosuppression, defined as operational tolerance, has
149 We demonstrate that IDO-Kyn-AHR-mediated immunosuppression depends on an interplay between Tregs
152 Metastasis is a molecularly late event, and immunosuppression driven by different molecular events,
153 tment with corticosteroids and a second-line immunosuppression drug and treated with biologic agents
154 tment with corticosteroids and a second-line immunosuppression drug experienced satisfactory disease
156 the oncolytic virus overcomes PD-L1-mediated immunosuppression during both the priming and effector p
159 a conceptual framework for the management of immunosuppression during infection in organ recipients.
160 warranted to assess the optimal maintenance immunosuppression during the use of checkpoint inhibitor
162 cribed the use of sirolimus (SRL) as primary immunosuppression following heart transplantation (HT).
165 as World Health Organization advanced/severe immunosuppression for age) at 1 year of VS was described
166 P prophylaxis in those receiving intensified immunosuppression for graft rejection, CMV infection, hi
167 engraftment, and to those receiving systemic immunosuppression for graft-versus-host disease treatmen
169 There is scant data on the use of induction immunosuppression for simultaneous liver/kidney transpla
172 nfections are an important adverse effect of immunosuppression for treatment of inflammatory bowel di
174 CNI-based mammalian target of rapamycin-free immunosuppression (group A, n = 264) was compared with a
175 ith the following criteria: tacrolimus-based immunosuppression, >1-year graft survival, no initial us
176 1.08, 1.7]; P < 0.05) CONCLUSION.: Induction immunosuppression had no impact on patient and allograft
177 New surgical techniques and conventional immunosuppression have enabled some success, but outcome
178 splantation (1.7-4.6-fold) in the absence of immunosuppression, homed to allografts, and suppressed p
181 ant or systemic therapy (corticosteroid plus immunosuppression in >90%) were followed prospectively f
182 dom from rejection following withdrawal from immunosuppression in a clinical trial of kidney transpla
183 ejection because of unnecessary reduction of immunosuppression in case of self-limiting BKPyV-DNAemia
187 ratio of ADO/AMP significantly and reversed immunosuppression in mouse models, indicating its potent
188 made in understanding immune dysfunction and immunosuppression in multiple myeloma (MM), and various
192 Frailty was associated with infections after immunosuppression in patients with IBD after we adjust f
193 (MLVI), a surrogate measure of adherence to immunosuppression in pediatric liver transplant recipien
194 Interestingly, the factor responsible for immunosuppression in serum is non-steroidal and of high
195 ate for the first time that CDDO-Me relieves immunosuppression in the breast TME and unleashes host a
196 ove to have unique clinical consequences for immunosuppression in the growing population of elderly t
201 thymic involution was a hallmark feature of immunosuppression in three distinct models of brain canc
202 d effect of repeated GEM treatment promoting immunosuppression in TME via upregulation of GM-CSF and
205 ponses, balancing inflammatory processes and immunosuppression; indeed, alterations in extracellular
208 Age and underlying comorbidities rather than immunosuppression intensity-related measures were major
210 utopsy cases and animal models confirms that immunosuppression is also present in extracranial metast
212 in solid organ recipients, the management of immunosuppression is based largely on clinical experienc
215 A consequence of the need for this permanent immunosuppression is the high risk of opportunistic, com
216 -2) adaptive immune response despite chronic immunosuppression is unknown and has important implicati
224 een mostly focused in countering MDSC-driven immunosuppression, little is known about the mechanisms
225 e risk of alloimmune injury that would guide immunosuppression management in renal transplant patient
226 about the presentation, clinical course, and immunosuppression management of this novel infection amo
228 transplant recipients treated by belatacept immunosuppression may be at increased risk for Cytomegal
230 s, infliximab dosage information, additional immunosuppression medications, and numbers of and times
231 o cancer therapy, tumor relapse, malignancy, immunosuppression, metastasis, cancer stem cell producti
232 vide an update on the progress of studies of immunosuppression minimization or withdrawal in solid or
233 cells, or macrophages; patient selection and immunosuppression mirrored the RGT, except basiliximab i
235 rofile at the DTH biopsy site corresponds to immunosuppression of an Ag-induced T cell response.
236 hy seen at our center in three patients with immunosuppression of different origins: one with stage I
237 or knockdown of GM-CSF can partially reduce immunosuppression of Ly6C(high) cells induced by GEM-con
242 [1.04-1.46]; P = 0.01), and minimization of immunosuppression (OR, 26.2 [5.48-166.6]; P < 0.001).
243 hibitor therapy is effective for maintenance immunosuppression, our preliminary data suggest that eve
245 t clinical consequences, including prolonged immunosuppression, poor vaccine responses and increased
246 mplex patients given their high net state of immunosuppression prior to CAR-T-cell infusion coupled w
247 lar adenosine/A2 adenosine receptor-mediated immunosuppression protects tissues from collateral damag
252 mbining low-dose EVL and CNIs in maintenance immunosuppression regimen (quadritherapy) and compare it
253 er a delayed (ie, 28 +/- 4 d posttransplant) immunosuppression regimen based on everolimus (EVR) redu
254 s regarding recurrence prevention, including immunosuppression regimen or secondary prevention with a
255 ng-term deleterious effects of combinatorial immunosuppression regimens and allograft failure cause s
258 ave a high percentage of failure and lead to immunosuppression, repair GPCRs have promising therapeut
260 Treatment protocol consisted of reduction of immunosuppression (RIS), rituximab (from 2000), cytotoxi
263 ukoencephalopathy, regardless of the type of immunosuppression, so this finding should routinely asse
264 ase control (87.2%), reduced use of systemic immunosuppression, stable visual acuity, and a 23.7% ris
265 observed in those patients having underlying immunosuppression such as, diabetes, organ transplantati
266 could be responsible for mediating systemic immunosuppression that antagonizes anti-PD-1 checkpoint
267 ation and chronic inflammatory disease cause immunosuppression that can be difficult to reverse.
268 w-up visits 2 and 3 years after cessation of immunosuppression, the patient exhibited normal graft fu
269 in the kidneys of healthy people, but during immunosuppression, the virus can reactivate and cause pr
270 ansplant patients have been able to decrease immunosuppression, this is the first instance of true op
271 hese data demonstrate a mechanism of TGFbeta immunosuppression through inhibition of CXCR3 in CD8(+)
273 esponse sensor, PERK, enhances MDSC-mediated immunosuppression through the NRF2 transcription factor,
274 g regimens, in parallel with more aggressive immunosuppression to better control graft-versus-host di
276 e with belatacept did not provide sufficient immunosuppression to reliably prevent pancreas rejection
277 ery of a nationalized database for VCA type, immunosuppression treatment, and clinical outcomes for V
283 may be more widely performed if maintenance immunosuppression was not essential for graft acceptance
284 gical disease models, we determined that the immunosuppression was not unique to cancer itself, but r
285 ld be increased in patients in whom relative immunosuppression was the major feature of their sepsis
289 Both thymic involution and serum-derived immunosuppression were reversible upon clearance of brai
291 esults suggest that hypoxic exposure induces immunosuppression which could increase vulnerability to
292 reveal a powerful mechanism of HPV-mediated immunosuppression, which can be exploited to improve res
293 (TAMs) mediate angiogenesis, metastasis, and immunosuppression, which inhibits infiltration of tumor-
295 ar disease (HR, 2.19; 95% CI, 1.2-3.98), and immunosuppression with cyclosporine A (HR, 1.93; 95% CI,
297 ned graft survival in the absence of chronic immunosuppression with potential clinical implications.
300 or cells (MDSCs) are immune cells that exert immunosuppression within the tumor, protecting cancer ce