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1  inducing regulatory T and B lymphocytes and immune deviation.
2  of animals with anterior chamber-associated immune deviation.
3 iform tolerance but did not prevent Th2-type immune deviation.
4 fective in mediating tumor regression, i.e., immune deviation.
5 C of these eyes still promoted AC-associated immune deviation.
6 monocytes facilitated graft prolongation via immune deviation.
7  subretinal space or the VC of eyes elicited immune deviation.
8 ion of antigen-specific T cells and not with immune deviation.
9 and CD40, molecules associated with Th1-type immune deviation.
10 fas ligand-mediated apoptosis and Th1 to Th2 immune deviation.
11 e induction of high-dose T cell tolerance or immune deviation.
12 e of effector response-a phenomenon known as immune deviation.
13 perimental autoimmune encephalomyelitis, via immune deviation.
14 tropenia and immature dendritic cells to the immune deviation.
15 suppressed, but rather displayed evidence of immune deviation.
16 model of tolerance is called a.c.-associated immune deviation.
17 to normal recipients to test for transfer of immune deviation.
18  anaphylactic shock, and thus does not cause immune deviation.
19 ogeneic-specific anterior chamber-associated immune deviation.
20 ation similar to anterior chamber-associated immune deviation.
21 failed to induce anterior chamber-associated immune deviation.
22 bility to induce anterior chamber-associated immune deviation.
23 be-defined immunologic background leading to immune deviations.
24 the induction of anterior chamber-associated immune deviation; 3) Tregs require IL-17A to mediate a c
25 f DBA/2J mice fail to induce antigen induced immune deviation (a form of tolerance) when treated with
26 c mice to induce anterior chamber-associated immune deviation (ACAID) and promote corneal allograft s
27  eyes to support anterior chamber-associated immune deviation (ACAID) induction after anterior chambe
28  to support anterior chamber (AC)-associated immune deviation (ACAID) induction after injection of ov
29                  Anterior chamber-associated immune deviation (ACAID) is a form of peripheral toleran
30                  Anterior chamber-associated immune deviation (ACAID) is elicited by an antigen-speci
31 e in vivo anterior chamber (a.c.)-associated immune deviation (ACAID) model of peripheral tolerance,
32  animal model of anterior chamber-associated immune deviation (ACAID) occurs in most mouse strains, A
33  elicited by the anterior chamber-associated immune deviation (ACAID) protocol is characterized by im
34 tudy, we use the anterior chamber-associated immune deviation (ACAID) to demonstrate that central reg
35 bility to induce anterior chamber-associated immune deviation (ACAID) to intracamerally injected solu
36                  Anterior chamber-associated immune deviation (ACAID) Tregs were induced by injecting
37                  Anterior chamber-associated immune deviation (ACAID), a manifestation of ocular immu
38 ens of mice with anterior chamber-associated immune deviation (ACAID), an eye-derived tolerance evoke
39 s systemic tolerance, termed a.c.-associated immune deviation (ACAID), characterized by Ag-specific i
40 enomenon, termed anterior chamber-associated immune deviation (ACAID), culminates in the generation o
41 , referred to as anterior chamber-associated immune deviation (ACAID), is characterized by impairment
42 tolerance called anterior chamber-associated immune deviation (ACAID), the differentiation of the T r
43 tolerance called Anterior Chamber-Associated Immune Deviation (ACAID), the differentiation of the T r
44 y donor-specific anterior chamber-associated immune deviation (ACAID), this deviant response is not d
45 hways, including anterior chamber-associated immune deviation (ACAID), which has been shown to partic
46 antigen-specific anterior chamber-associated immune deviation (ACAID).
47 n (OVA)-specific anterior chamber associated immune deviation (ACAID).
48 henomenon termed anterior chamber-associated immune deviation (ACAID).
49 mechanism called anterior chamber-associated immune deviation (ACAID).
50 ity (DH), termed anterior chamber associated immune deviation (ACAID).
51 nomenon known as anterior chamber-associated immune deviation (ACAID).
52 tory phenomenon, anterior chamber associated immune deviation (ACAID).
53 pheral immune tolerance termed AC-associated immune deviation (ACAID).
54 , referred to as anterior chamber-associated immune deviation (ACAID).
55 henomenon termed anterior chamber-associated immune deviation (ACAID).
56  made of induced anterior chamber-associated immune deviation (ACAID).
57 nterior chamber (anterior chamber-associated immune deviation; ACAID) is associated in part with CD8+
58 ells was a prerequisite for the induction of immune deviation after antigen presentation in the eye.
59 r of purified DC2 may be exploited to induce immune deviation after transplantation of hematopoietic
60 e immune system in a fashion that results in immune deviation, allowing tumor progression and establi
61                                    Thus, Th2 immune deviation alone does not account for the exacerba
62 e is increasing evidence that the process of immune deviation already begins in utero, but the underl
63 he subretinal space or the VC did not induce immune deviation, although the AC of these eyes still pr
64 fic regulation of T cells that involves both immune deviation and a new form of cytokine- dependent T
65              Tolerization to dnaJP1 leads to immune deviation and a trend toward clinical efficacy.
66 munization and treated with CT, counteracted immune deviation and abrogated protection.
67 tion mechanism that differs from eye-derived immune deviation and arises even when the BBB is comprom
68 cells are likely expanded in response to Th2 immune deviation and may contribute to tumor progression
69 adhesin 1 (BAD1) exploits host receptors for immune deviation and pathogen survival.
70 ch the PPARalpha agonist gemfibrozil induces immune deviation and protects mice from EAE.
71  the mechanisms of chronic fungal infection, immune deviation, and fungi as disease cofactors.
72  to support anterior chamber (AC)-associated immune deviation, and loss of ocular immune privilege.
73 he eye to support induction of AC-associated immune deviation, and the integrity of the blood/ocular
74 identified novel susceptibility genes, early immune deviations, and metabolomic alterations associate
75  and reduces priming, but does not result in immune deviation; and 3) protection is dependent on pers
76 rafts (>100-day survival) showed evidence of immune deviation, because the MLR to ACI stimulator cell
77  a deviant immune response (brain-associated immune deviation (BRAID)) that was deficient in OVA-spec
78 re B7.2, a molecule associated with Th2-type immune deviation, but not by those expressing more B7.1
79 nyl-coupled T cells into normal mice induced immune deviation, but TNFR2(-/-) 2,4,6-trinitrophenyl-co
80 act not only in the lung to prevent systemic immune deviations, but also within the progenitor compar
81   Our study thus reveals a type of bacterial immune deviation by increasing nutrient supply.
82     The objective of this work was to induce immune deviation by mucosal peptide-specific immunothera
83 nt of these T(reg) cells in conjunction with immune deviation by Th2 cells optimally induced protecti
84                  Anterior chamber-associated immune deviation can be induced by allogeneic corneal ti
85                                 A Th1 to Th2 immune deviation can explain the discordant biological r
86                                        Thus, immune deviation can increase concentrations of pathogen
87 ecessary for tolerance induction, Th1 to Th2 immune deviation cannot be sufficient for tolerance indu
88 e unresponsive state was not associated with immune deviation due to selective secretion of Th1- or T
89                               In contrast to immune deviation elicited via the eye, an intact spleen
90 ells is particularly relevant in view of the immune deviation existing in immune-privileged sites suc
91 and p35 peptides were not associated with an immune deviation, expressing levels of IFN-gamma charact
92        These findings demonstrate pronounced immune deviation favoring Th2-type responses after pulse
93                       Despite the lack of Th immune deviation, Flt3L ligand-pretreated lymph nodes ex
94 le for promoting anterior chamber-associated immune deviation following injection of Ag into the eye.
95 have considered contributing roles of innate immune deviations following otherwise innocuous infectio
96 BM cells into conditioned recipients induced immune deviation for adaptive B-cell immunity, preventin
97                The subretinal space supports immune deviation for histoincompatible tumor cells and s
98 KL as an adjuvant for immunotherapy mediates immune deviation from a pathological Th2-dominated respo
99 antation and has recently been thought to be immune deviation from the inflammatory Th1 response to a
100                      We conclude that type 2 immune deviation has differential effects on CD4+ and CD
101 the severity of allograft rejection, as such immune deviation has proven highly effective in the trea
102                                   Typically, immune deviation helps pathogens to avoid destructive im
103 votal early events in other systems, such as immune deviation in childhood to a helper T cell type 2
104 e studied the therapeutic benefit vs risk of immune deviation in experimental allergic encephalomyeli
105 n of antigen-specific regulatory T cells; or immune deviation in favor of TH1 responses.
106  is highly effective in producing Th1 to Th2 immune deviation in several model systems (i.e., fully M
107 t increased c-Maf sumoylation contributes to immune deviation in T1D by reducing c-Maf access to and
108       Disease suppression is associated with immune deviation in the periphery and with suppression o
109 with OVA in the presence of TGF-beta2 induce immune deviation in vivo (impaired delayed hypersensitiv
110  with our previous reports, indicate that an immune deviation in which intragraft Th1-type cytokines
111 nnate immune defects as a cause for systemic immune deviations in response to otherwise innocuous inf
112 w (BM) cell apoptosis associated with innate immune deviations in the BM in response to Pneumocystis
113                             We suggest that "immune deviation" in NOD-IL-4 mice is mediated by the pa
114                The eye itself contributes to immune deviation, in part by displaying unique immunoreg
115 mechanisms, and instead display a peripheral immune deviation including differentiation into IL-10-se
116 D4+ and CD8+ T cells before and after type 2 immune deviation induced by IL-4 plus anti-IFN-gamma Ab.
117                                              Immune deviation induced by intraocular injection of sol
118 okine assays, there were similarities to the immune deviation induced by intraocular inoculation in t
119                                          Th2 immune deviation induced with keyhole limpet hemocyanin
120                                              Immune deviation-inducing hybridomas up-regulated expres
121                                In this study immune deviation into a Th2 (IL-4) response was associat
122 D4+ Th1 cell-mediated autoimmune disease via immune deviation is an attractive potential therapeutic
123 e efferent CD8(+) Tr cell in a.c.-associated immune deviation is dependent on IL-10-producing, CD1d-r
124                  Anterior chamber-associated immune deviation may contribute to the maintenance of co
125 is actively maintained and is mediated by an immune deviation mechanism that differs from eye-derived
126 enotype, to test whether either apoptotic or immune deviation mechanisms apply to cytokine-producing
127           In patients with AD, an underlying immune deviation might result in higher susceptibility o
128 0 days of survival) demonstrated evidence of immune deviation; mixed lymphocyte reaction to ACI stimu
129  specific hyporesponsiveness to IRBP without immune deviation, no evidence for apoptosis either by th
130 underlying mechanisms indicated that neither immune deviation nor induction of regulatory cells was a
131        Thus, neonatal "tolerization" induces immune deviation, not tolerance in the immunological sen
132                                       Type 2 immune deviation of allospecific CD4+ T cells resulted i
133                               Differences in immune deviation of CD4(+) T cells cannot be explained b
134 s promote desensitization rely on a profound immune deviation of pathogenic T- and B-cell responses.
135 olerogenic functional phenotype, and 2) that immune deviation of responses to an inflammatory epitope
136 he hypothesis that oral tolerance induces an immune deviation of T cells, peripheral blood mononuclea
137                                              Immune deviation of T-cell responses to the beta-cell au
138                    Protection is mediated by immune deviation of the anti-myelin basic protein (MBP)
139 , CRAg-sensitized mice is coincident with an immune deviation of the lung inflammatory response, inde
140  capacity of the corneal allograft to induce immune deviation of the systemic immune response.
141 onjunctivitis to evaluate the effects of Th2 immune deviation on corneal allograft survival and possi
142  mice were used to determine the presence of immune deviation or other evidence of immunoregulation,
143 rticularly in anatomical sites which exhibit immune deviation or privilege.
144                             Thus, Th1 to Th2 immune deviation produces prolonged engraftment as compa
145                            Hence, Th1-to-Th2 immune deviation provides only a partial explanation for
146 utic strategies that aim at the induction of immune deviation show little efficacy in the established
147 phage hybridoma no. 63, both of which induce immune deviation similar to anterior chamber-associated
148 ransforming growth factor (TGF)-beta2 induce immune deviation similar to that evoked by injection of
149 by immature dendritic cells can result in an immune deviation similar to that produced by transient T
150 gest that the ultimate success of Th2-to-Th1 immune deviation strategies will rely on the efficient a
151                                       Ocular immune deviation studies have relied on intraocular inje
152 nisms, including induction of T-cell anergy, immune deviation, T regulatory cell activity, and promot
153 on of regulatory T cell activity, Th2 to Th1 immune deviation, Th1 crossregulation of Th2 immune resp
154 ization is mediated more through Ag-specific immune deviation than via suppression of allergic sensit
155 skin condition, as well as on the underlying immune deviation that might play a role in comorbidities
156 nse to antigens in the diet and the basis of immune deviation that results in immunoglobulin E (IgE)
157  IL-10 are responsible for the activation of immune deviation through interaction with antigen-presen
158                    This was achieved through immune deviation to a T-helper-cell response with increa
159 E protected them from developing EAE through immune deviation to a Th2 response.
160 n a variety of autoimmune disorders in which immune deviation to a Th2 type of response is desirable.
161 f the subretinal space and the VC to support immune deviation to antigens injected locally.
162 basis for the frequent failure of Th1 to Th2 immune deviation to blunt the severity of allograft reje
163 leviation of allergy is not achieved through immune deviation to Th1, but is linked to expansion of r
164                         From 8 wk onwards an immune deviation to the p38-specific response was observ
165 aft cytokine gene expression to test whether immune deviation to the T helper (Th) 2 response is asso
166 loligands in the graft may all contribute to immune deviation to the Th2 response.
167 h2 cell functions, it has been proposed that immune deviation toward Th1 can protect against asthma a
168 hether cyclophosphamide-treated patients had immune deviation toward Th2 responses.
169                                              Immune deviation toward type 2 (Th2, Tc2) response has b
170 ntial use of therapeutic approaches based on immune deviation toward type 2 responses.
171 nse and the associated cytokines (p < 0.05), immune deviation towards a Th1 response (p < 0.05), and
172 Th17 pro-inflammatory allergic responses and immune deviation towards Th1 responses.
173 nctions in several ways, it is believed that immune deviation towards Th2 can prevent or cure autoimm
174 on systems there would seem to be a phase of immune deviation towards Th2 cytokines, like IL-4 and IL
175 ulmonary immune activation, causing systemic immune deviations triggering BMF in this model.
176                  Importantly, GAD65-specific immune deviation was dependent on pDNA-encoded IL-4.
177                                              Immune deviation was not dependent on NK or B cells.
178                                     However, immune deviation was unsuccessful in the latter animals,
179 y of pDNA vaccination to mediate Ag-specific immune deviation, we examined the immunotherapeutic effi
180 re essential for anterior chamber-associated immune deviation, we postulated that the survival of C57
181 c cells, modulation of B-cell responses, and immune deviation were proposed to be responsible for the
182 at are pulsed with Ag into cells that induce immune deviation when injected into naive mice.
183 s, and to induce anterior chamber associated immune deviation when injected into the eye of naive all
184 grafts to induce anterior chamber associated immune deviation when placed in the anterior chamber, no
185                 Here, we report on a type of immune deviation whereby an opportunistic pathogen, Pseu
186  donor T cells induce less GVHD due to a Th2 immune deviation while GVL activity is slightly diminish

 
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