It is well known that adoptive transfer of donor‐derived tolerogenic dendritic cells (DC) helps to reduce acute allograft rejection. However, this method cannot effectively prevent grafts from infiltration of inflammatory cells and fibrosis, and thus has minimal effect on chronic allograft rejection. In this study, we used mitomycin C (MMC) to generate tolerogenic DC and demonstrated that donor (Balb/c)‐derived MMC‐DC could induce hyporesponsiveness of recipient (C57BL/6) T cells in vitro, potentially by inducing T‐cell apoptosis, decreasing IL‐2 and IL‐12 secretion, and increasing regulatory T‐cell numbers and IL‐10 secretion. Furthermore, anti‐CD154 monoclonal antibody (mAb) treatment combined with donor‐derived MMC‐DC prolonged the survival of the allografts in vivo. The mechanisms were similar to those in vitro. Impressively, both acute and chronic rejection were prevented when donor and F1 generation (Balb/c × C57BL/6) derived MMC‐DC were injected together with anti‐CD154 mAb into recipients before heart allotransplantation. In summary, we showed that donor and F1‐derived tolerogenic DC have a synergistic effect on induction and maintenance of T‐cell regulation and the secretion of immunosuppressive cytokines. Moreover, adoptive transfer of these two types of DC could inhibit both acute and chronic transplant rejection in mice.
NU-T2 is a mouse monoclonal IgG1 antibody to the CD1b molecule, (cross-)reacting with an antigen of the dermal-epidermal junction (NU-T2 DEJ AG). Further immunohistochemical characterization of the NU-T2 DEJ AG showed it to display unique properties that differentiate it from other known antigens of the dermal-epidermal junction. Indeed, the NU-T2 DEJ AG is primate-specific and present only in epithelial basement membranes. In normal human skin it is expressed within the lowermost lamina lucida of the dermal-epidermal junction but not in the deep part of epidermal appendages nor in the deep part of epidermal appendages nor in the basement membrane of dermal vessels, smooth muscles or nerves. In diseases with intraepidermal or intradermal cleavage, NU-T2 reactivity was observed at the floor of the blister. In various skin specimens with a cleavage through the lamina lucida (NaCl--or dispase-split skin, bullous pemphigoid, junctional epidermolysis bullosa), NU-T2 immunoreactivity seemed reduced, being localized at the dermal side of the cleavage. These results suggest that the antigen recognized by NU-T2 is a novel component of the lamina lucida of the dermal-epidermal junction, that seems to be important for dermal-epidermal adhesion.
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