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CTLA4 ligation on Tregs results in a significant decrease in the presentation capacity of antigen-presenting cells and effector T cell downregulation in mice [ 5].

In the present study aortic murine smooth muscle cell (SMC) antigen presentation capacity was evaluated using the E α-GFP/Y-Ae system to visualize antigen uptake through a GFP tag and tracking of E α peptide/MHCII presentation using the Y-Ae Ab.

Treatment with CpG-SAV-exo effectively activateDC2.4.4 cells and enhanced tumor antigen presentation capacity.

More importantly, F4-PECMs enhance both the T cell stimulatory and antigen presentation capacity of DCs.

Conversely, the powerful antigen presentation capacity of DCs may promote the activation and/or differentiation of self-reactive effector T cells, either because of the defective processes of central and peripheral tolerance induction or inappropriate activation of the self-reactive T cells due to impaired/ineffective negative regulation.

The RLN of both naive and SIV-infected macaques contained high numbers of CD68 + MHC-II+ macrophages and cells expressing the co-stimulatory molecules B7-2 and CD40, as well as IgM + MHCII+ and IgM + CD40+ B cells, indicating maintenance of antigen presentation capacity.

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The in vivo and in vitro finding that the expansion of antigen-specific effector T cells is hampered in lymph nodes from s.c.-injected R-EAE mice prompted us to speculate a causal impairment of the antigen presentation capacities of professional antigen presenting cells (APC), such as DCs.

Furthermore, the observed excess of BMP-4 in lymph nodes significantly impaired the maturation and antigen presentation capacities of lymph node DCs, which, in turn, failed to sustain the expansion and full activation of effector (encephalitogenic) T cells.

Moreover, studies focusing on the effect of Dicer ablation in skin-draining lymph nodes migratory dendritic cell subset, namely, Langerhans cells, showed a disturbed expression of surface molecules and reduced antigen presentation capacities to CD4+ T cells, increased turnover, reduced half-lives, and increased rates of apoptosis [ 38].

The data suggest that antigen-presentation capacity is maintained in inductive sites of SIV-infected rectal mucosa, but immune effector functions may be altered.

After incubated with γFe2O3 NPs coated OVA protein and different inhibitors for 6 h, DCs cross-presentation capacity was strongly inhibited by velcade but not by NH4Cl (Fig. 4).

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