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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
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
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
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
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
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
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
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
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
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
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
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
101 the severity of allograft rejection, as such immune deviation has proven highly effective in the trea
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
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
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
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.
118 okine assays, there were similarities to the immune deviation induced by intraocular inoculation in t
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
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
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
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
139 , CRAg-sensitized mice is coincident with an immune deviation of the lung inflammatory response, inde
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,
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
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
160 n a variety of autoimmune disorders in which immune deviation to a Th2 type of response is desirable.
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
165 aft cytokine gene expression to test whether immune deviation to the T helper (Th) 2 response is asso
167 h2 cell functions, it has been proposed that immune deviation toward Th1 can protect against asthma a
171 nse and the associated cytokines (p < 0.05), immune deviation towards a Th1 response (p < 0.05), and
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
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
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
186 donor T cells induce less GVHD due to a Th2 immune deviation while GVL activity is slightly diminish