Silencing of PD-L2/B7-DC by Topical Application of Small Interfering RNA Inhibits Elicitation of Contact Hypersensitivity.

PD-L2 is a ligand for the immune checkpoint receptor PD-1; however, its regulatory function is unclear. We previously reported that silencing of CD86 in cutaneous dendritic cells by topical application of small interfering RNA (siRNA) inhibits the elicitation of contact hypersensitivity (CHS). Here, we investigated the effects of topical application of PD-L2 siRNA on allergic skin disease. PD-L2 was induced in dendritic cells concurrently with the elevation of major histocompatibility complex class II and CD86 expression. Topical application of PD-L2 siRNA inhibited the elicitation of CHS by suppressing early proinflammatory cytokine expression and migration of hapten-carrying dendritic cells into lymph nodes. Local injection of neutralizing anti-PD-L2 mAb inhibited CHS to the same extent. PD-L2 siRNA treatment inhibited CHS in PD-1/PD-L1 double knockout mice and in the sensitized T-cell-transferred skin. These results suggest that the effects of PD-L2 silencing are independent of PD-1 but dependent on local memory T cells. Most of the inhibitory effects of PD-L2 and CD86 silencing on CHS were comparable, but PD-L2 siRNA treatment did not inhibit atopic disease-like manifestations and T helper type 2 responses in NC/Nga mice. Our results suggest that PD-L2 in cutaneous dendritic cells acts as a costimulator rather than a regulator. Local PD-L2 silencing by topical application of siRNA represents a therapeutic approach for contact allergy.

Eruption disturbance caused by an odontoma that was partially attached to the crown of the adjacent maxillary first molar, and step lesion excavation for the tooth preservation: A case report.

Despite the partial attachment of a complex odontoma to an impacted tooth, it is possible to guide the tooth to erupt normally and preserve it by step lesion excavation and the prevention of infection.

Synthesis and enhanced bone regeneration of carbonate substituted octacalcium phosphate.

Using a wet method, we have synthesized octacalcium phosphate carbonate, in which HPO42- in octacalcium phosphate is replaced with CO32-. The physical, crystal, and chemical properties of this new material were compared to octacalcium phosphate, Ca-deficient hydroxyapatite, and Ca-deficient carbonate apatite using X-ray diffraction, Fourier-transform infrared spectroscopy, inductively coupled plasma spectroscopy, and scanning electron microscopy. Surface roughness and morphology were also characterized, along with the ability to support proliferation and differentiation of MG63 cells, as measured by MTT and alkaline phosphatase assay. We found that octacalcium phosphate carbonate enhanced osteoblast proliferation more strongly than all other materials tested. Similarly, Ca-deficient carbonate apatite, a hydrolysate of octacalcium phosphate carbonate, stimulated osteoblast differentiation to a better extent than Ca-deficient hydroxyapatite, a carbonate-free hydrolysate of octacalcium phosphate. These results indicate that octacalcium phosphate carbonate has good biocompatibility and osteoconduction, and incorporation of carbonate into octacalcium phosphate and apatite enhances bone regeneration.