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1 lator (Aire), a critical mediator of central immune tolerance.
2 cids, and particularly butyrate, can promote immune tolerance.
3 urenine pathway which augments tumor-induced immune tolerance.
4  in HM is able to modulate the mechanisms of immune tolerance.
5 3, and can suppress inflammation and promote immune tolerance.
6 f the present understanding of fetus-induced immune tolerance.
7 direct targeting of immune cells to generate immune tolerance.
8 ion phase and their ability to persist under immune tolerance.
9 ed on activated T cells for the induction of immune tolerance.
10 mediated gene induction to establish central immune tolerance.
11 le to regulate adaptive immunity and promote immune tolerance.
12  for mature Treg identity and maintenance of immune tolerance.
13 fibrotic liver was tightly related to innate immune tolerance.
14 d function but is dispensable for peripheral immune tolerance.
15 s that regulate mucosal barrier function and immune tolerance.
16 n in vivo role for granzyme A in maintaining immune tolerance.
17 f T cell function contributing to peripheral immune tolerance.
18 cal modulators of both thymic and peripheral immune tolerance.
19 l population capable of facilitating durable immune tolerance.
20 n of DC maturation is a central mechanism of immune tolerance.
21 ating DCs as key mediators of organ-specific immune tolerance.
22 vity of this enzyme has been associated with immune tolerance.
23 -10(+) regulatory T cells, which may promote immune tolerance.
24 atory T (Treg) cells, a lineage critical for immune tolerance.
25 been recognized as an important mechanism in immune tolerance.
26 an attractive way to induce antigen-specific immune tolerance.
27 NS) resulting from a breakdown in peripheral immune tolerance.
28 Tregs) are critical regulators of peripheral immune tolerance.
29  a process critical for establishing central immune tolerance.
30  regulated to balance immune activation with immune tolerance.
31 ectly to T cells, resulting in a bias toward immune tolerance.
32 ll immunity, whereas immature DCs can induce immune tolerance.
33 reducing osteoclast precursors and promoting immune tolerance.
34 ng miR-155 have an impaired ability to break immune tolerance.
35 which drives regulatory T-cell responses and immune tolerance.
36 ells via the receptor MerTK is important for immune tolerance.
37  of this regulatory DNA element in promoting immune tolerance.
38 esolution of organ damage and maintenance of immune tolerance.
39 e T-regulatory cells in tumor tissue promote immune tolerance.
40 ve processes to promote Treg homeostasis and immune tolerance.
41 age mouse blastocysts, which induces central immune tolerance.
42 is immune-mediated and adaptation represents immune tolerance.
43 umans, and it was accomplished by inhibiting immune tolerance.
44 diated DNA demethylation of Foxp3 to promote immune tolerance.
45 ing the oral mucosa to antigen may stimulate immune tolerance.
46 commensal microbiota and its contribution to immune tolerance.
47 nt a suitable approach to induce Ag-specific immune tolerance.
48 tolerance and ultimately in the breakdown of immune tolerance.
49 s being developed with the goal of restoring immune tolerance.
50  have potential as powerful tools to mediate immune tolerance.
51 through the PD-1/PD-L1 pathway is central to immune tolerance.
52 s through which ATRA may contribute to liver immune tolerance.
53 tion of environmental factors that influence immune tolerance.
54  are each independently required to maintain immune tolerance.
55 f which may promote the development of fetal immune tolerance.
56 at it may be a therapeutic target to promote immune tolerance.
57 ed neoantigen expression, and tumor-specific immune tolerance.
58 se activities may be titrated to break tumor immune tolerance.
59 ddition, at steady-state, cDCs help maintain immune tolerance.
60 prevents excessive inflammation and supports immune tolerance.
61 t plays a recognized role in promoting tumor immune tolerance.
62 ation of immune responses and maintenance of immune tolerance.
63 e essential for establishing and maintaining immune tolerance.
64 tion in recipient lymphoid organs to acquire immune tolerance.
65  (Tregs) contribute to maintaining mammalian immune tolerance.
66 lecules of attention as targets for inducing immune tolerance.
67 mmation and contribute to the maintenance of immune tolerance.
68 liver regulates innate immunity and adaptive immune tolerance.
69 rgan graft survival and that they can induce immune tolerance, accelerate recovery from AKI, and prom
70           The development and maintenance of immune tolerance after allogeneic hematopoietic stem cel
71 of antithymocyte globulin [ATG]) facilitates immune tolerance after bone marrow transplantation (BMT)
72 sible pathogenic TCRs that can cause loss of immune tolerance against elastin.
73    The mechanistic insights into UVR-induced immune tolerance against skin cancers, particularly cuta
74 a maternal T1D environment improves neonatal immune tolerance against the autoantigen (pro)insulin.
75 godendrocyte glycoprotein-loaded DCs carried immune tolerance against the subsequent development of M
76                                              Immune tolerance and active immune suppression results i
77 rrant tryptophan catabolism reduces maternal immune tolerance and adversely impacts pregnancy outcome
78 ential of 1,25D3-mDCs to restore Ag-specific immune tolerance and arrest autoimmune disease progressi
79  the general principles, such as breaches in immune tolerance and barriers, leading to the promotion
80 eplication but is implicated in establishing immune tolerance and chronic infection.
81 ullination have been linked to the breach of immune tolerance and clinical autoimmunity.
82 r, which has a critical role in establishing immune tolerance and determining the fate of tumors.
83 ls (MDSCs) play a critical role in promoting immune tolerance and disease growth.
84           Prostaglandin E2 promotes not only immune tolerance and epithelial homeostasis but also the
85  is continuously required for maintenance of immune tolerance and for a major part of their character
86 onal fitness of Treg cells in the control of immune tolerance and homeostasis.
87 h17) and regulatory T (Treg) cells maintains immune tolerance and host defense.
88 tes asthma by modulating the balance between immune tolerance and inflammation.
89 observed for higher FOXP3(+) T-cell-mediated immune tolerance and lower CD8(+) T-cell-mediated cytoto
90  elevated 12,13-diHOME concentrations impede immune tolerance and may be produced by bacterial EHs in
91 Foxp3(+) regulatory T cells (Tregs) maintain immune tolerance and play an important role in immunolog
92    Epitope-optimization is required to break immune tolerance and potently activate AFP-specific CD8
93 es as a homeostatic rheostat that safeguards immune tolerance and prevents age-dependent development
94 pTregs, but not tTregs, mediates the loss of immune tolerance and promotes allograft rejection.
95 hronic inactivation of pickle causes loss of immune tolerance and shortened lifespan.
96 mmune reconstitution and re-establishment of immune tolerance and their therapeutic potential followi
97                With our growing knowledge of immune tolerance and ways to overcome it, combination tr
98 ked in human PDA where it is associated with immune-tolerance and diminished patient survival.
99  pharmacologically reduce serum HBsAg, break immune tolerance, and increase functional cure rates.
100 phages (MZMs) are important for establishing immune tolerance, and loss of their number or function c
101 f the immune system but also for maintaining immune tolerance, and more recent work has begun to iden
102  cell function and maintenance of peripheral immune tolerance, and mutations in its coding gene cause
103 ease in these cells implies the induction of immune tolerance, and the alanine aminotransferase (ALT)
104 role in the establishment and maintenance of immune tolerance, and this role is disrupted in diabetes
105      To protect mucosal tissues and maintain immune tolerance, animal hosts actively sequester bacter
106 stion will provide fundamental insights into immune tolerance, antiviral signaling, and complex autoi
107 olecular mechanisms underlying tumor-induced immune tolerance are largely unknown.
108         However, the drivers of intratumoral immune tolerance are uncertain.
109 ory T cells (Treg) are essential to maintain immune tolerance, as their loss leads to a fatal autoimm
110 naturally formed nanoparticles expressed the immune tolerance-associated molecule 'programmed death-l
111 ce instead of having the normal TH1 bias and immune tolerance because of repeated exposure to pathoge
112 nism, which can contribute to maintenance of immune tolerance, becomes insufficient in allergic disea
113                                              Immune tolerance between the fetus and mother represents
114 esents a new type of immune cell involved in immune tolerance, but it also is a potential candidate f
115           LSECs are involved in induction of immune tolerance, but little is known about their functi
116              Dietary proteins usually induce immune tolerance, but may trigger life-threatening immun
117  bypasses many of the mechanisms involved in immune tolerance by allowing for expansion of tumor-spec
118                                 Induction of immune tolerance by an increase in regulatory T (Treg) c
119 er tyrosine kinase (Mer) signaling maintains immune tolerance by clearing apoptotic cells (ACs) and i
120 hat GARP exerts oncogenic effects, promoting immune tolerance by enriching and activating latent TGFb
121                          Thus, Aire enforces immune tolerance by ensuring that distinct autoreactive
122 ells (mTECs) play a critical role in central immune tolerance by mediating negative selection of auto
123                       Thus, PPARgamma favors immune tolerance by promoting regulatory T cell generati
124 ays a key role in the development of central immune tolerance by promoting thymic presentation of tis
125 l repressor Capicua/CIC maintains peripheral immune tolerance by suppressing aberrant activation of a
126                     We provide evidence that immune tolerance can be overcome in a murine model of ha
127 at cancer immunotherapy designed to overcome immune tolerance can be useful for a growing number of p
128 tumor inflammatory response, which increases immune tolerance, cell survival, and proliferation.
129                                              Immune tolerance checkpoint inhibition has been transfor
130  we supply a comprehensive overview of human immune tolerance checkpoints with associated mechanisms
131  has opposing effects on pre-immune and post-immune tolerance checkpoints, and suggest that B cell to
132                                    Moreover, immune tolerance could be induced that precluded inducti
133 ent mechanisms involved in the regulation of immune tolerance could lead to new strategies to enhance
134  questions with regard to the role of DCs in immune tolerance could lead to the development of novel
135 es, these three Ags exert major functions in immune tolerance, defense against infections, and antica
136 n this position paper, we review insights on immune tolerance derived from allergy and from cancer in
137 th food allergy who were not able to acquire immune tolerance during childhood.
138                                              Immune tolerance during human pregnancy is maintained by
139 of a state of operationally defined clinical immune tolerance during peanut OIT.
140 nta, is a central component of fetus-induced immune tolerance during pregnancy.
141 ycin, to induce durable and antigen-specific immune tolerance, even in the presence of potent Toll-li
142 ing stem cell-derived islets while fostering immune tolerance, exemplified in Yoshihara et al., holds
143 (Treg) are critical elements for maintaining immune tolerance, for instance to exogenous antigens tha
144 ious mechanisms that have been described for immune tolerance govern our ability to control self-reac
145                   A growing understanding of immune tolerance has been the foundation for new approac
146 ivo at the start or stop of therapy impaired immune tolerance, highlighting the dependence of the the
147  wild-type (WT) mice, which induced dominant immune tolerance, identical treatment of DAF(-/-) mice o
148 lar type-II (AT-II) cells is associated with immune tolerance in an inflammatory microenvironment.
149  laboratory changes associated with clinical immune tolerance in antigen-induced T cells, basophils,
150 tion while concurrently restoring peripheral immune tolerance in autoimmune disease.
151 boost regulatory T cells (Tregs) and promote immune tolerance in autoimmune patients.
152 s were required for long-term maintenance of immune tolerance in both the CD4+ and CD8+ T cell compar
153              This suggests that the presumed immune tolerance in chronic HBV infections needs to be r
154 mplete characterization of the mechanisms of immune tolerance in hematological malignancies is critic
155 deficient emphysema implicates regulation of immune tolerance in lung macrophages through Nr4a1.
156 d function in inhibiting aTreg-cell-mediated immune tolerance in mice.
157 mmune surveillance in MGUS and to break down immune tolerance in MM.
158 provide critical insight into how to achieve immune tolerance in organ transplantation.
159 antigen-presenting cells was shown to induce immune tolerance in other animal models of autoimmune di
160 are a subset of CD4(+) T cells that maintain immune tolerance in part by their ability to inhibit the
161 ch to regulate immune homeostasis to promote immune tolerance in patients with autoimmune diseases, i
162 ng cells might enable therapies that promote immune tolerance in patients with autoimmune diseases.
163 uman cartilage proteoglycan (PG) can promote immune tolerance in PG-induced arthritis (PGIA).
164 lar aspects of immune dynamics: breakdown of immune tolerance in response to an infection with a path
165 r low-dose IL-2 therapy to enhance Tregs for immune tolerance in T1D.
166 ism to allergic sensitization and disrupting immune tolerance in the airways of patients with asthma
167 inoid receptor 2 (CB2), in the regulation of immune tolerance in the gut and the pancreas.
168 ne diseases but may come at risk for reduced immune tolerance in the intestinal tract.
169 the regulatory T cells (Tregs) and maintains immune tolerance in the pancreas.
170 al period is a critical time for shaping the immune tolerance in the progeny, influencing development
171 ne-two punch injury that profoundly disrupts immune tolerance in this devastating disease.
172 ing the immune response to establish durable immune tolerance in type 1 diabetes remains a substantia
173 nt of iNKT-based therapies aiming to restore immune tolerance in type 1 diabetes.
174 ammatory potential and the ability to induce immune tolerance in vitro.
175 icity of RLN2 and highlight the weak central immune tolerance induced against this self-hormone.
176              These observations suggest that immune tolerance induced by peptide immunotherapy can be
177 f tolerogenic therapies, other than standard immune tolerance induction (ITI), is an unmet goal.
178 ggest that the approach can also be used for immune tolerance induction to prevent or eliminate inhib
179 herapy; thus, developing strategies to break immune tolerance is a high priority.
180 e an active autoimmune reaction, wherein the immune tolerance is already broken.
181                           DC-mediated T cell immune tolerance is an active process that is influenced
182 ciphering cellular and molecular pathways of immune tolerance is an important goal, with the expectat
183 utologous cells as antigen carriers inducing immune tolerance is appreciated.
184 ls targeting hybrid peptides may explain how immune tolerance is broken in T1D.
185 more efficient methods to induce Ag-specific immune tolerance is critical to advancing allergy treatm
186                                              Immune tolerance is critical to the avoidance of unwarra
187 n this study, we demonstrate that peripheral immune tolerance is critically dependent on posttranscri
188                                              Immune tolerance is executed partly by Foxp3(+)regulator
189        These data may explain how peripheral immune tolerance is impaired in tissues under autoimmune
190 ource of antigenic peptides to which central immune tolerance is lacking.
191  for tissue-restricted self antigens, or how immune tolerance is maintained for self-antigen-specific
192                                          How immune tolerance is maintained in the skin remains uncle
193 ffective immune responses to pathogens while immune tolerance is maintained to protect the host.
194                                              Immune tolerance is necessary to prevent the immune syst
195  contribution to either immune activation or immune tolerance is still not entirely understood.
196                       A major contributor to immune tolerance is the tumor physiologic microenvironme
197 reactive cells are silenced by mechanisms of immune tolerance, islet antigen-reactive B lymphocytes a
198 e a mechanism by which loss of AIRE-mediated immune tolerance leads to intestinal disorders in patien
199 sts an interplay of macrophages with IgG4 in immune tolerance, likely relevant in allergen immunother
200 osition as a key determinant of immunity and immune tolerance, linked to the risk for the development
201         This study is the first to show that immune tolerance may be impaired in spaceflight, leading
202 rus (AAV) gene therapy, exploiting a natural immune tolerance mechanism induced by human leukocyte an
203 erapy approach was used to exploit a natural immune tolerance mechanism induced by the human leukocyt
204 e findings implicate the PSGs in a potential immune tolerance mechanism of cancers.
205 asion is achieved through multiple layers of immune tolerance mechanisms including immune editing, re
206                    This approach has allowed immune tolerance mechanisms limiting bnAb production to
207 iduals with autoimmune disease and defective immune tolerance mechanisms may produce BnAbs more readi
208 nization initiates CD4bs-bnAb responses, but immune tolerance mechanisms restrict their development,
209                                 Discovery of immune tolerance mechanisms, which inhibit pre-existing
210  cell receptor axis that can be targeted for immune tolerance modulation.
211  response, the National Institutes of Health Immune Tolerance Network and JDRF established a multicen
212  liver transplant recipients enrolled in the Immune Tolerance Network immunosuppression withdrawal (I
213              MIC-treated patients showed the Immune Tolerance Network operational tolerance signature
214              Longitudinal specimens from the Immune Tolerance Network's A Cooperative Clinical Study
215 tion approach with the potential to overcome immune tolerance observed in pregnancy, and lower vaccin
216 esponsible IgG receptors for the breaking of immune tolerance of microglia.
217 ngeneic bile duct antigens efficiently break immune tolerance of recipient mice, capturing several ke
218                                     Specific immune tolerance of transplanted organs in association w
219 taneous, or intramuscular), and induction of immune tolerance or encapsulation of islets.
220 s B virus exploits these naturally occurring immune tolerance pathways to establish persistent postna
221 ensal Staphylococcus epidermidis facilitates immune tolerance preferentially in neonates via inductio
222 n Treg cells can be titrated to break tumour immune tolerance preferentially.
223 m implies the concept of naturally occurring immune tolerance, presumably activated by overloading of
224 an and mouse, results in compromised central immune tolerance processes that may significantly impact
225 re), a transcription coordinator involved in immune tolerance processes, is a critical spindle-associ
226 presence of tumor cells in the ALN causes an immune tolerance profile that contrasts with that of the
227 ce, and may inform the development of future immune tolerance protocols.
228 nts respond to microorganisms through biased immune tolerance rather than resistance strategies.
229 tion-induced cell death (AICD) essential for immune tolerance regulation.
230 opment of therapeutic interventions in other immune tolerance-related diseases.
231  Therapeutic approaches for the induction of immune tolerance remain an unmet clinical need for the t
232                                  Maintaining immune tolerance requires the production of Foxp3-expres
233 r, characterized by impaired, or exaggerated immune tolerance, respectively.
234 -/-) and PD-1(-/-) mice, which have impaired immune tolerance, resulted in a slightly greater injury.
235 gulatory cells, consistent with induction of immune tolerance, resulting in decreased inflammatory re
236 nduce transplantation tolerance in neonates, immune tolerance strategies have been actively pursued.
237 n the context of the clinical translation of immune tolerance strategies, we discuss the significant
238    Our studies thus identify Notch4-mediated immune tolerance subversion as a fundamental mechanism t
239  higher concentrations of markers related to immune tolerance than luminal A.
240 cells (Tregs) are non-redundant mediators of immune tolerance that are critical to prevent autoimmune
241 rt-term costimulation blockade led to robust immune tolerance that could be transferred independently
242 une system immaturity by inducing a state of immune tolerance that facilitates HBV persistence.
243  Dendritic cells (DCs) can induce peripheral immune tolerance that prevents autoimmune responses.
244  autoimmune regulator (AIRE, which regulates immune tolerance) that allow self-reactive T cells to en
245 that APCs have a crucial role in maintaining immune tolerance, the underlying mechanisms are poorly u
246 esponse to inflammatory stimuli and promotes immune tolerance through effector T-cell anergy and enha
247 oenvironment of established tumours promotes immune tolerance through poorly understood mechanisms.
248           Regulatory T (Treg) cells maintain immune tolerance through the master transcription factor
249 ignificant impact on subsequent immunity and immune tolerance, thus placing them in a unique position
250 disease, as well as the processes that drive immune tolerance to allergens, will be instrumental in d
251 T (Treg) cells play a key role in sustaining immune tolerance to allergens, yet mechanisms by which T
252                                              Immune tolerance to allografts has been pursued for deca
253                                              Immune tolerance to alpha-Gal in blood type B individual
254                                              Immune tolerance to avoid chronic immunosuppression is a
255 Finally, we suggest a unified model in which immune tolerance to beta cells can be broken by several
256 underlying immune dysregulation that impairs immune tolerance to both food allergens and autoantigens
257                                              Immune tolerance to both self-antigens and innocuous non
258 pecific T cell response because of a lack of immune tolerance to C-terminal epitopes as a consequence
259 S) mainly in young adults, and a breakage of immune tolerance to CNS self-antigens has been suggested
260  we sought to determine whether induction of immune tolerance to col(V) might ameliorate atherosclero
261     Mucosal inoculation successfully induced immune tolerance to col(V) with an accompanying reductio
262 on and anti-T-cell antibodies safely induces immune tolerance to combined hematopoietic cell and orga
263 ry T cells (Tregs) are required to establish immune tolerance to commensal microbes.
264  neonatal life was required for establishing immune tolerance to commensal microbes.
265 V) vector-mediated gene therapy that induced immune tolerance to factor IX (FIX) in a hemophilia B (H
266                                      Loss of immune tolerance to gut microflora is inextricably linke
267  will guide future studies into induction of immune tolerance to intervene in the initiation and prog
268      It is assumed that newborns may develop immune tolerance to milk-transmitted pathogens similarly
269  that maternal microchimerism induces stable immune tolerance to non-inherited maternal antigens in o
270  autoimmune disease characterized by loss of immune tolerance to nuclear and cell surface antigens.
271 ing pathways would make blocking of neonatal immune tolerance to retroviruses an achievable goal.IMPO
272 controller 2 (vic2), that abrogates neonatal immune tolerance to retroviruses.
273           Regulatory T cells (Tregs) mediate immune tolerance to self and depend on IL-2 for homeosta
274                                      Loss of immune tolerance to self-antigens can promote chronic in
275 oimmune disease that results from a break in immune tolerance to self-antigens, leading to multi-orga
276  overcoming multiple mechanisms that mediate immune tolerance to self-antigens.
277 Cs) is recognized as a critical mechanism of immune tolerance to self-antigens.
278 n has been associated with a break in innate immune tolerance to self-DNA.
279 P3 play a pivotal role in the maintenance of immune tolerance to self.
280 e immunological factors that promote loss of immune tolerance to self.
281 y known therapy that provides long-term host immune tolerance to the allergen, but is time-consuming
282                At this age, neonates acquire immune tolerance to the conditionally responsive lucifer
283 cating the importance of LRP5/6 in mediating immune tolerance to the gut flora.
284  In contrast, END showed strong evidence for immune tolerance to the parasite, with high levels of ci
285    Therapeutic vaccines might be used to end immune tolerance to the virus in patients with chronic i
286 al epitopes in humans results in the loss of immune tolerance to this epitope and production of abund
287 erapy and the vital protagonists that shape 'immune tolerance' to allergens.
288             Tregs play a fundamental role in immune tolerance via control of self-reactive effector T
289                                          The immune tolerance was confirmed by marked reduction in ai
290                                              Immune tolerance was confirmed in all dogs after challen
291 (+) T regulatory cells (Treg), essential for immune tolerance, was significantly reduced.
292     A majority of tumors exist in a state of immune tolerance where the patient's immune system has b
293                 Pregnancy induces a state of immune tolerance, which can result in spontaneous improv
294 tal adenocarcinoma (PDA) is characterized by immune tolerance, which enables disease to progress unab
295 ory T (Treg) cells are critical mediators of immune tolerance whose activity depends upon T cell rece
296    In this review, we describe principles of immune tolerance with a focus on its breakdown during pa
297                             The induction of immune tolerance with HSCs has led to isolation of other
298 e liver appears to be privileged in terms of immune tolerance, with a low incidence of antibody-media
299 insights on the failure of the mechanisms of immune tolerance, with potential implications in designi
300 ry T (T reg) cells are pivotal regulators of immune tolerance, with T cell receptor (TCR)-driven acti

 
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