Research Article

PYR-41 and Thalidomide Impair Dendritic Cell Cross-Presentation by Inhibiting Myddosome Formation and Attenuating the Endosomal Recruitments of p97 and Sec61 via NF-κB Inactivation

Figure 1

Treatment with PYR-41 or thalidomide impairs DC cross-priming. Murine bone marrow-derived DC (cultured for 4 d) conferred thalidomide (30 μM), PYR-41 (5 μM), or DMSO treatment prior to ovalbumin (50 μg/ml) or PBS pulse. (a) Mixed lymphocyte reaction was performed by incubating these cells with the same H-2 background splenocytes at the ratio of 1 : 10. The ability of T cell proliferation was accessed by BrdU cell proliferation assay. IL-12 concentration in supernatants of mixed lymphocyte reaction was determined by ELISA. (b) C57BL/6 mouse was intraperitoneally transferred with these 1 × 104 cells and Ag-specific IFN-γ ELISPOT assays, and (c) granzyme B expression determination was performed 5 d after adoptive transfer. The ELISPOT data were presented as spot-forming units per million cells. For qPCR, β-actin was used as an internal control. Data were presented as the mean ± SEM, , , and one-way ANOVA with Newman–Keuls post test. Tha: thalidomide; PYR: PYR-41.