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1 st that engineered cells are able to promote bystander suppression.
2 with both parasite Ag-specific tolerance and bystander suppression.
3 t antigens induces Tregs that are capable of bystander suppression.
4 tration and identifying strategies to induce bystander suppression.
5  and the other gluten epitope, demonstrating bystander suppression.
6 mmune neuritis), indicating they function by bystander suppression.
7 eta, IL-10, or both) was the primary mode of bystander suppression.
8        One hallmark of acquired tolerance is bystander suppression, a process whereby Ag-specific (ad
9 DCs, was found to mediate both tolerance and bystander suppression against diverse T cell specificiti
10  in vivo by delayed-type hypersensitivity or bystander suppression against mycobacterial Ags in CFA.
11 lonotypic TCR in vivo, but failed to mediate bystander suppression and did not prevent Th17 cells usi
12  to create a regulatory milieu that promotes bystander suppression and infectious tolerance.
13        Low-dose tolerance is associated with bystander suppression and requires IL-10, which indicate
14 (+) T cells to examine the cellular basis of bystander suppression associated with oral tolerance in
15 This effect is specific and does not involve bystander suppression because treatment with MBP-IgG doe
16 fashion, the expanded T(reg) were capable of bystander suppression both in vitro and in vivo.
17 ese results shed light upon the mechanism of bystander suppression by donor Ag-specific TR in patient
18                                        Thus, bystander suppression does not reflect clonal deletion o
19 as assessed using a linked unresponsiveness (bystander suppression) DTH assay.
20                                     Although bystander suppression has been described in oral toleran
21                        Notably, NLPs induced bystander suppression in the EAE model established in C5
22 vated polyclonal Treg cells that would exert bystander suppression in the target tissue.
23 tigen-dependent linked DTH unresponsiveness (bystander suppression) in allograft recipients requires
24 the release of interleukin-10, implicating a bystander suppression mechanism that holds promise for t
25 e profoundly anergic and exhibit nonspecific bystander suppression mediated by IL-10 secretion.
26 uced by continuous OVA exposure demonstrated bystander suppression of cockroach allergen-mediated air
27  induction of regulatory T cells, leading to bystander suppression of EAE.
28 s (DC), but not monocyte APCs, could mediate bystander suppression of EBV-specific recall response.
29 ngTreg cells that mediated robust direct and bystander suppression of effector T (Teff) cells recogni
30 ores normoglycemia, most likely by localized bystander suppression of pathogenic IL-17-producing cell
31        NIMA(d)-exposed splenocytes exhibited bystander suppression of tetanus-specific delayed-type h
32 xtures of plasmacytoid DC (pDC) and T cells, bystander suppression of the response to a colocalized r
33 ot act as an antagonist in vivo but mediates bystander suppression, probably by the generation of reg
34 o CIX and CII were specific, suggesting that bystander suppression, rather than cross-reactivity with
35 suboptimal costimulatory molecules and IL-10 bystander suppression to drive a dual-modal T cell modul
36 strategy for generating autoantigen-specific bystander suppression useful for treatment of complex au
37                                              Bystander suppression via mDC was reversed not only by A
38                             The induction of bystander suppression, whereby the response against one