Dendritic cells derived from TBP‐2‐deficient mice are defective in inducing T cell responses

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Abstract
Thioredoxin‐binding protein‐2 (TBP‐2), also known as vitamin D3‐up‐regulated protein 1 (VDUP1), was identified as an endogenous molecule interacting with thioredoxin (TRX). Here, we show that dendritic cells (DC) derived from TBP‐2‐deficient mice are defective in the function of T cell activation. To compare TBP‐2–/– DC function with wild‐type (WT) DC, we stimulated DC with lipopolysaccharide (LPS). Although TBP‐2–/– DC and WT DC expressed comparable levels of MHC class II and costimulatory molecules such as CD40, CD80 and CD86, the IL‐12p40, IL‐12p70 and IL‐6 productions of TBP‐2–/– DC were attenuated. In a mixed leukocyte reaction (MLR), the concentrations of IL‐2, IFN‐γ, IL‐4 and IL‐10 in the culture supernatant of MLR with TBP‐2–/– DC were significantly lower than those in the cultures with WT DC. In MLR also, as with LPS stimulation, IL‐12p40 and IL‐12p70 production from TBP‐2–/– DC was less than that from WT DC. Proliferation of T cells cultured with TBP‐2–/– DC was poorer than that with WT DC. In vivo delayed‐type hypersensitivity responses in TBP‐2–/– mice immunized with ovalbumin were significantly reduced compared to WT mice. These results indicate that TBP‐2 plays a crucial role in DC to induce T cell responses.