RESUMEN
Objective Dentritic cell-specific ICAM-3 grabbing nonintegrin (DC-SIGN) is an important receptor for pathogenic microbes, and it acts as pathogen-recognition receptor (PAMP) and provides a bridge between the innate immunity and acquired immunity. It is meaningful to clarify whether DC-SIGN takes part in the course of cutaneous Trichosporon asahii infection and how it manages the other cytokines. Methods Twenty-five male mice were hypodermically injected with 3.2?107 CFU/ml of Trichosporon asahii suspension on one side of the back, the other side of the back received no injection to serve as control. Another five mice were treated with 0.9% saline solution as control. The cutaneous specimens were obtained on the 1st, 3rd, 7th and 14th day after inoculation. The expression of DC-SIGN gene and the other genes related to cutaneous immunity after cutaneous infection of Trichosporon asahii were investigated by RT-PCR and microarray. Results The DC-SIGN products containing 242 bp of nucleic acid from the skin specimens of the inoculated sites were amplified with RT-PCR on the 3rd, 7th and 14th day after inoculation. The results of microarray showed that a series of genes were down-regulated, including complement component 2, TNF-inducible protein cg12-1 (CG12-1), interferon-induced protein with tetratricopeptide repeats 3 (Ifit3), CD53 antigen, CD22 antigen, and prostaglandin E receptor 4. Conclusions The results suggest that DC-SIGN takes part in the course of Trichosporon asahii infection. DC-SIGN not only inhibits Th1 type of cell-mediated immunity, but also inhibits some of complement factors, prostaglandin E receptor and immunoglobulin binding protein 1b, thus resulting in chronic and intractable infection of Trichosporon asahii. The detailed roles of DC-SIGN in the course need to be further studied.